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id="toc-Huntington's_disease-sublist" class="vector-toc-list"> </ul> </li> <li id="toc-Multiple_sclerosis" class="vector-toc-list-item vector-toc-level-2"> <a class="vector-toc-link" href="#Multiple_sclerosis"> <div class="vector-toc-text"> <span class="vector-toc-numb">1.4</span> <span>Multiple sclerosis</span> </div> </a> <ul id="toc-Multiple_sclerosis-sublist" class="vector-toc-list"> </ul> </li> <li id="toc-Amyotrophic_lateral_sclerosis" class="vector-toc-list-item vector-toc-level-2"> <a class="vector-toc-link" href="#Amyotrophic_lateral_sclerosis"> <div class="vector-toc-text"> <span class="vector-toc-numb">1.5</span> <span>Amyotrophic lateral sclerosis</span> </div> </a> <ul id="toc-Amyotrophic_lateral_sclerosis-sublist" class="vector-toc-list"> </ul> </li> <li id="toc-Batten_disease" class="vector-toc-list-item vector-toc-level-2"> <a class="vector-toc-link" href="#Batten_disease"> <div class="vector-toc-text"> <span class="vector-toc-numb">1.6</span> <span>Batten disease</span> </div> </a> <ul id="toc-Batten_disease-sublist" class="vector-toc-list"> </ul> </li> <li id="toc-Creutzfeldt–Jakob_disease" class="vector-toc-list-item vector-toc-level-2"> <a class="vector-toc-link" href="#Creutzfeldt–Jakob_disease"> <div class="vector-toc-text"> <span class="vector-toc-numb">1.7</span> <span>Creutzfeldt–Jakob disease</span> </div> </a> <ul id="toc-Creutzfeldt–Jakob_disease-sublist" class="vector-toc-list"> </ul> </li> </ul> </li> <li id="toc-Risk_factors" class="vector-toc-list-item vector-toc-level-1"> <a class="vector-toc-link" href="#Risk_factors"> <div class="vector-toc-text"> <span class="vector-toc-numb">2</span> <span>Risk factors</span> </div> </a> <button aria-controls="toc-Risk_factors-sublist" class="cdx-button cdx-button--weight-quiet cdx-button--icon-only vector-toc-toggle"> <span class="vector-icon mw-ui-icon-wikimedia-expand"></span> <span>Toggle Risk factors subsection</span> </button> <ul id="toc-Risk_factors-sublist" class="vector-toc-list"> <li id="toc-Aging" class="vector-toc-list-item vector-toc-level-2"> <a class="vector-toc-link" href="#Aging"> <div class="vector-toc-text"> <span class="vector-toc-numb">2.1</span> <span>Aging</span> </div> </a> <ul id="toc-Aging-sublist" class="vector-toc-list"> </ul> </li> <li id="toc-Infections" class="vector-toc-list-item vector-toc-level-2"> <a class="vector-toc-link" href="#Infections"> <div class="vector-toc-text"> <span class="vector-toc-numb">2.2</span> <span>Infections</span> </div> </a> <ul id="toc-Infections-sublist" class="vector-toc-list"> </ul> </li> </ul> </li> <li id="toc-Mechanisms" class="vector-toc-list-item vector-toc-level-1"> <a class="vector-toc-link" href="#Mechanisms"> <div class="vector-toc-text"> <span class="vector-toc-numb">3</span> <span>Mechanisms</span> </div> </a> <button aria-controls="toc-Mechanisms-sublist" class="cdx-button cdx-button--weight-quiet cdx-button--icon-only vector-toc-toggle"> <span class="vector-icon mw-ui-icon-wikimedia-expand"></span> <span>Toggle Mechanisms subsection</span> </button> <ul id="toc-Mechanisms-sublist" class="vector-toc-list"> <li id="toc-Genetics" class="vector-toc-list-item vector-toc-level-2"> <a class="vector-toc-link" href="#Genetics"> <div class="vector-toc-text"> <span class="vector-toc-numb">3.1</span> <span>Genetics</span> </div> </a> <ul id="toc-Genetics-sublist" class="vector-toc-list"> </ul> </li> <li id="toc-Epigenetics" class="vector-toc-list-item vector-toc-level-2"> <a class="vector-toc-link" href="#Epigenetics"> <div class="vector-toc-text"> <span class="vector-toc-numb">3.2</span> <span>Epigenetics</span> </div> </a> <ul id="toc-Epigenetics-sublist" class="vector-toc-list"> </ul> </li> <li id="toc-Protein_misfolding" class="vector-toc-list-item vector-toc-level-2"> <a class="vector-toc-link" href="#Protein_misfolding"> <div class="vector-toc-text"> <span class="vector-toc-numb">3.3</span> <span>Protein misfolding</span> </div> </a> <ul id="toc-Protein_misfolding-sublist" class="vector-toc-list"> </ul> </li> <li id="toc-Intracellular_mechanisms" class="vector-toc-list-item vector-toc-level-2"> <a class="vector-toc-link" href="#Intracellular_mechanisms"> <div class="vector-toc-text"> <span class="vector-toc-numb">3.4</span> <span>Intracellular mechanisms</span> </div> </a> <ul id="toc-Intracellular_mechanisms-sublist" class="vector-toc-list"> <li id="toc-Protein_degradation_pathways" class="vector-toc-list-item vector-toc-level-3"> <a class="vector-toc-link" href="#Protein_degradation_pathways"> <div class="vector-toc-text"> <span class="vector-toc-numb">3.4.1</span> <span>Protein degradation pathways</span> </div> </a> <ul id="toc-Protein_degradation_pathways-sublist" class="vector-toc-list"> </ul> </li> <li id="toc-Membrane_damage" class="vector-toc-list-item vector-toc-level-3"> <a class="vector-toc-link" href="#Membrane_damage"> <div class="vector-toc-text"> <span class="vector-toc-numb">3.4.2</span> <span>Membrane damage</span> </div> </a> <ul id="toc-Membrane_damage-sublist" class="vector-toc-list"> </ul> </li> <li id="toc-Mitochondrial_dysfunction" class="vector-toc-list-item vector-toc-level-3"> <a class="vector-toc-link" href="#Mitochondrial_dysfunction"> <div class="vector-toc-text"> <span class="vector-toc-numb">3.4.3</span> <span>Mitochondrial dysfunction</span> </div> </a> <ul id="toc-Mitochondrial_dysfunction-sublist" class="vector-toc-list"> </ul> </li> <li id="toc-DNA_damage" class="vector-toc-list-item vector-toc-level-3"> <a class="vector-toc-link" href="#DNA_damage"> <div class="vector-toc-text"> <span class="vector-toc-numb">3.4.4</span> <span>DNA damage</span> </div> </a> <ul id="toc-DNA_damage-sublist" class="vector-toc-list"> </ul> </li> <li id="toc-Axonal_transport" class="vector-toc-list-item vector-toc-level-3"> <a class="vector-toc-link" href="#Axonal_transport"> <div class="vector-toc-text"> <span class="vector-toc-numb">3.4.5</span> <span>Axonal transport</span> </div> </a> <ul id="toc-Axonal_transport-sublist" class="vector-toc-list"> </ul> </li> </ul> </li> <li id="toc-Programmed_cell_death" class="vector-toc-list-item vector-toc-level-2"> <a class="vector-toc-link" href="#Programmed_cell_death"> <div class="vector-toc-text"> <span class="vector-toc-numb">3.5</span> <span>Programmed cell death</span> </div> </a> <ul id="toc-Programmed_cell_death-sublist" class="vector-toc-list"> <li id="toc-Apoptosis_(type_I)" class="vector-toc-list-item vector-toc-level-3"> <a class="vector-toc-link" href="#Apoptosis_(type_I)"> <div class="vector-toc-text"> <span class="vector-toc-numb">3.5.1</span> <span>Apoptosis (type I)</span> </div> </a> <ul id="toc-Apoptosis_(type_I)-sublist" class="vector-toc-list"> </ul> </li> <li id="toc-Autophagic_(type_II)" class="vector-toc-list-item vector-toc-level-3"> <a class="vector-toc-link" href="#Autophagic_(type_II)"> <div class="vector-toc-text"> <span class="vector-toc-numb">3.5.2</span> <span>Autophagic (type II)</span> </div> </a> <ul id="toc-Autophagic_(type_II)-sublist" class="vector-toc-list"> </ul> </li> <li id="toc-Cytoplasmic_(type_III)" class="vector-toc-list-item vector-toc-level-3"> <a class="vector-toc-link" href="#Cytoplasmic_(type_III)"> <div class="vector-toc-text"> <span class="vector-toc-numb">3.5.3</span> <span>Cytoplasmic (type III)</span> </div> </a> <ul id="toc-Cytoplasmic_(type_III)-sublist" class="vector-toc-list"> </ul> </li> </ul> </li> <li id="toc-Transglutaminase" class="vector-toc-list-item vector-toc-level-2"> <a class="vector-toc-link" href="#Transglutaminase"> <div class="vector-toc-text"> <span class="vector-toc-numb">3.6</span> <span>Transglutaminase</span> </div> </a> <ul id="toc-Transglutaminase-sublist" class="vector-toc-list"> </ul> </li> </ul> </li> <li id="toc-Management" class="vector-toc-list-item vector-toc-level-1"> <a class="vector-toc-link" href="#Management"> <div class="vector-toc-text"> <span class="vector-toc-numb">4</span> <span>Management</span> </div> </a> <button aria-controls="toc-Management-sublist" class="cdx-button cdx-button--weight-quiet cdx-button--icon-only vector-toc-toggle"> <span class="vector-icon mw-ui-icon-wikimedia-expand"></span> <span>Toggle Management subsection</span> </button> <ul id="toc-Management-sublist" class="vector-toc-list"> <li id="toc-Animal_models_in_research" class="vector-toc-list-item vector-toc-level-2"> <a class="vector-toc-link" href="#Animal_models_in_research"> <div class="vector-toc-text"> <span class="vector-toc-numb">4.1</span> <span>Animal models in research</span> </div> </a> <ul id="toc-Animal_models_in_research-sublist" class="vector-toc-list"> </ul> </li> <li id="toc-Other_avenues_of_investigation" class="vector-toc-list-item vector-toc-level-2"> <a class="vector-toc-link" href="#Other_avenues_of_investigation"> <div class="vector-toc-text"> <span class="vector-toc-numb">4.2</span> <span>Other avenues of investigation</span> </div> </a> <ul id="toc-Other_avenues_of_investigation-sublist" class="vector-toc-list"> </ul> </li> </ul> </li> <li id="toc-See_also" class="vector-toc-list-item vector-toc-level-1"> <a class="vector-toc-link" href="#See_also"> <div class="vector-toc-text"> <span class="vector-toc-numb">5</span> <span>See also</span> </div> </a> <ul id="toc-See_also-sublist" class="vector-toc-list"> </ul> </li> <li id="toc-References" class="vector-toc-list-item vector-toc-level-1"> <a class="vector-toc-link" href="#References"> <div class="vector-toc-text"> <span class="vector-toc-numb">6</span> <span>References</span> </div> </a> <ul id="toc-References-sublist" class="vector-toc-list"> </ul> </li> </ul> </div> </div> </nav> </div> </div> <div class="mw-content-container"> <main id="content" class="mw-body"> <header class="mw-body-header vector-page-titlebar"> <nav aria-label="Contents" class="vector-toc-landmark"> <div id="vector-page-titlebar-toc" class="vector-dropdown vector-page-titlebar-toc vector-button-flush-left" > <input type="checkbox" id="vector-page-titlebar-toc-checkbox" role="button" aria-haspopup="true" data-event-name="ui.dropdown-vector-page-titlebar-toc" class="vector-dropdown-checkbox " aria-label="Toggle the table of contents" > <label id="vector-page-titlebar-toc-label" for="vector-page-titlebar-toc-checkbox" class="vector-dropdown-label cdx-button cdx-button--fake-button cdx-button--fake-button--enabled cdx-button--weight-quiet cdx-button--icon-only " aria-hidden="true" ><span class="vector-icon mw-ui-icon-listBullet mw-ui-icon-wikimedia-listBullet"></span> <span class="vector-dropdown-label-text">Toggle the table of contents</span> </label> <div class="vector-dropdown-content"> <div id="vector-page-titlebar-toc-unpinned-container" class="vector-unpinned-container"> </div> </div> </div> </nav> <h1 id="firstHeading" class="firstHeading mw-first-heading"><span class="mw-page-title-main">Neurodegenerative disease</span></h1> <div id="p-lang-btn" class="vector-dropdown mw-portlet mw-portlet-lang" > <input type="checkbox" id="p-lang-btn-checkbox" role="button" aria-haspopup="true" data-event-name="ui.dropdown-p-lang-btn" class="vector-dropdown-checkbox mw-interlanguage-selector" aria-label="Go to an article in another language. Available in 30 languages" > <label id="p-lang-btn-label" for="p-lang-btn-checkbox" class="vector-dropdown-label cdx-button cdx-button--fake-button cdx-button--fake-button--enabled cdx-button--weight-quiet cdx-button--action-progressive mw-portlet-lang-heading-30" aria-hidden="true" ><span class="vector-icon mw-ui-icon-language-progressive mw-ui-icon-wikimedia-language-progressive"></span> <span class="vector-dropdown-label-text">30 languages</span> </label> <div class="vector-dropdown-content"> <div class="vector-menu-content"> <ul class="vector-menu-content-list"> <li class="interlanguage-link interwiki-ar mw-list-item"><a href="https://ar.wikipedia.org/wiki/%D8%AA%D8%AD%D9%84%D9%84_%D8%B9%D8%B5%D8%A8%D9%8A" title="تحلل عصبي – Arabic" lang="ar" hreflang="ar" data-title="تحلل عصبي" data-language-autonym="العربية" data-language-local-name="Arabic" class="interlanguage-link-target"><span>العربية</span></a></li><li class="interlanguage-link interwiki-az mw-list-item"><a href="https://az.wikipedia.org/wiki/Neyrodegenerativ_x%C9%99st%C9%99lik" title="Neyrodegenerativ xəstəlik – Azerbaijani" lang="az" hreflang="az" data-title="Neyrodegenerativ xəstəlik" data-language-autonym="Azərbaycanca" data-language-local-name="Azerbaijani" class="interlanguage-link-target"><span>Azərbaycanca</span></a></li><li class="interlanguage-link interwiki-be mw-list-item"><a href="https://be.wikipedia.org/wiki/%D0%9D%D0%B5%D0%B9%D1%80%D0%B0%D0%B4%D1%8D%D0%B3%D0%B5%D0%BD%D0%B5%D1%80%D0%B0%D1%82%D1%8B%D1%9E%D0%BD%D1%8B%D1%8F_%D0%B7%D0%B0%D1%85%D0%B2%D0%BE%D1%80%D0%B2%D0%B0%D0%BD%D0%BD%D1%96" title="Нейрадэгенератыўныя захворванні – Belarusian" lang="be" hreflang="be" data-title="Нейрадэгенератыўныя захворванні" data-language-autonym="Беларуская" data-language-local-name="Belarusian" class="interlanguage-link-target"><span>Беларуская</span></a></li><li class="interlanguage-link interwiki-bs mw-list-item"><a href="https://bs.wikipedia.org/wiki/Neurodegenerativna_bolest" title="Neurodegenerativna bolest – Bosnian" lang="bs" hreflang="bs" data-title="Neurodegenerativna bolest" data-language-autonym="Bosanski" data-language-local-name="Bosnian" class="interlanguage-link-target"><span>Bosanski</span></a></li><li class="interlanguage-link interwiki-ca mw-list-item"><a href="https://ca.wikipedia.org/wiki/Neurodegeneraci%C3%B3" title="Neurodegeneració – Catalan" lang="ca" hreflang="ca" data-title="Neurodegeneració" data-language-autonym="Català" data-language-local-name="Catalan" class="interlanguage-link-target"><span>Català</span></a></li><li class="interlanguage-link interwiki-de mw-list-item"><a href="https://de.wikipedia.org/wiki/Neurodegenerative_Erkrankung" title="Neurodegenerative Erkrankung – German" lang="de" hreflang="de" data-title="Neurodegenerative Erkrankung" data-language-autonym="Deutsch" data-language-local-name="German" class="interlanguage-link-target"><span>Deutsch</span></a></li><li class="interlanguage-link interwiki-es mw-list-item"><a href="https://es.wikipedia.org/wiki/Enfermedad_neurodegenerativa" title="Enfermedad neurodegenerativa – Spanish" lang="es" hreflang="es" data-title="Enfermedad neurodegenerativa" data-language-autonym="Español" data-language-local-name="Spanish" class="interlanguage-link-target"><span>Español</span></a></li><li class="interlanguage-link interwiki-eo mw-list-item"><a href="https://eo.wikipedia.org/wiki/Ne%C5%ADrodegenera_malsano" title="Neŭrodegenera malsano – Esperanto" lang="eo" hreflang="eo" data-title="Neŭrodegenera malsano" data-language-autonym="Esperanto" data-language-local-name="Esperanto" class="interlanguage-link-target"><span>Esperanto</span></a></li><li class="interlanguage-link interwiki-eu mw-list-item"><a href="https://eu.wikipedia.org/wiki/Gaixotasun_neurodegeneratibo" title="Gaixotasun neurodegeneratibo – Basque" lang="eu" hreflang="eu" data-title="Gaixotasun neurodegeneratibo" data-language-autonym="Euskara" data-language-local-name="Basque" class="interlanguage-link-target"><span>Euskara</span></a></li><li class="interlanguage-link interwiki-fa mw-list-item"><a href="https://fa.wikipedia.org/wiki/%D8%B2%D9%88%D8%A7%D9%84_%D8%B9%D8%B5%D8%A8%DB%8C" title="زوال عصبی – Persian" lang="fa" hreflang="fa" data-title="زوال عصبی" data-language-autonym="فارسی" data-language-local-name="Persian" class="interlanguage-link-target"><span>فارسی</span></a></li><li class="interlanguage-link interwiki-fr mw-list-item"><a href="https://fr.wikipedia.org/wiki/Maladie_neuro-%C3%A9volutive" title="Maladie neuro-évolutive – French" lang="fr" hreflang="fr" data-title="Maladie neuro-évolutive" data-language-autonym="Français" data-language-local-name="French" class="interlanguage-link-target"><span>Français</span></a></li><li class="interlanguage-link interwiki-hi mw-list-item"><a href="https://hi.wikipedia.org/wiki/%E0%A4%A4%E0%A4%82%E0%A4%A4%E0%A5%8D%E0%A4%B0%E0%A4%BF%E0%A4%95%E0%A4%BE_%E0%A4%85%E0%A4%AA%E0%A4%B5%E0%A4%BF%E0%A4%95%E0%A4%BE%E0%A4%B8" title="तंत्रिका अपविकास – Hindi" lang="hi" hreflang="hi" data-title="तंत्रिका अपविकास" data-language-autonym="हिन्दी" data-language-local-name="Hindi" class="interlanguage-link-target"><span>हिन्दी</span></a></li><li class="interlanguage-link interwiki-it mw-list-item"><a href="https://it.wikipedia.org/wiki/Malattie_neurodegenerative" title="Malattie neurodegenerative – Italian" lang="it" hreflang="it" data-title="Malattie neurodegenerative" data-language-autonym="Italiano" data-language-local-name="Italian" class="interlanguage-link-target"><span>Italiano</span></a></li><li class="interlanguage-link interwiki-la mw-list-item"><a href="https://la.wikipedia.org/wiki/Neurodegeneratio" title="Neurodegeneratio – Latin" lang="la" hreflang="la" data-title="Neurodegeneratio" data-language-autonym="Latina" data-language-local-name="Latin" class="interlanguage-link-target"><span>Latina</span></a></li><li class="interlanguage-link interwiki-mk mw-list-item"><a href="https://mk.wikipedia.org/wiki/%D0%9D%D0%B5%D0%B2%D1%80%D0%BE%D0%B4%D0%B5%D0%B3%D0%B5%D0%BD%D0%B5%D1%80%D0%B0%D1%86%D0%B8%D1%98%D0%B0" title="Невродегенерација – Macedonian" lang="mk" hreflang="mk" data-title="Невродегенерација" data-language-autonym="Македонски" data-language-local-name="Macedonian" class="interlanguage-link-target"><span>Македонски</span></a></li><li class="interlanguage-link interwiki-ml mw-list-item"><a href="https://ml.wikipedia.org/wiki/%E0%B4%A8%E0%B5%8D%E0%B4%AF%E0%B5%81%E0%B4%B1%E0%B5%8B_%E0%B4%A1%E0%B4%BF%E0%B4%9C%E0%B5%86%E0%B4%A8%E0%B5%86%E0%B4%B0%E0%B5%86%E0%B4%B1%E0%B5%8D%E0%B4%B1%E0%B5%80%E0%B4%B5%E0%B5%8D_%E0%B4%B0%E0%B5%8B%E0%B4%97%E0%B4%99%E0%B5%8D%E0%B4%99%E0%B5%BE" title="ന്യുറോ ഡിജെനെരെറ്റീവ് രോഗങ്ങൾ – Malayalam" lang="ml" hreflang="ml" data-title="ന്യുറോ ഡിജെനെരെറ്റീവ് രോഗങ്ങൾ" data-language-autonym="മലയാളം" data-language-local-name="Malayalam" class="interlanguage-link-target"><span>മലയാളം</span></a></li><li class="interlanguage-link interwiki-ms mw-list-item"><a href="https://ms.wikipedia.org/wiki/Neurodegenerasi" title="Neurodegenerasi – Malay" lang="ms" hreflang="ms" data-title="Neurodegenerasi" data-language-autonym="Bahasa Melayu" data-language-local-name="Malay" class="interlanguage-link-target"><span>Bahasa Melayu</span></a></li><li class="interlanguage-link interwiki-nl mw-list-item"><a href="https://nl.wikipedia.org/wiki/Neurodegeneratie" title="Neurodegeneratie – Dutch" lang="nl" hreflang="nl" data-title="Neurodegeneratie" data-language-autonym="Nederlands" data-language-local-name="Dutch" class="interlanguage-link-target"><span>Nederlands</span></a></li><li class="interlanguage-link interwiki-ja mw-list-item"><a href="https://ja.wikipedia.org/wiki/%E7%A5%9E%E7%B5%8C%E5%A4%89%E6%80%A7%E7%96%BE%E6%82%A3" title="神経変性疾患 – Japanese" lang="ja" hreflang="ja" data-title="神経変性疾患" data-language-autonym="日本語" data-language-local-name="Japanese" class="interlanguage-link-target"><span>日本語</span></a></li><li class="interlanguage-link interwiki-pl mw-list-item"><a href="https://pl.wikipedia.org/wiki/Choroby_neurodegeneracyjne" title="Choroby neurodegeneracyjne – Polish" lang="pl" hreflang="pl" data-title="Choroby neurodegeneracyjne" data-language-autonym="Polski" data-language-local-name="Polish" class="interlanguage-link-target"><span>Polski</span></a></li><li class="interlanguage-link interwiki-pt mw-list-item"><a href="https://pt.wikipedia.org/wiki/Neurodegenera%C3%A7%C3%A3o" title="Neurodegeneração – Portuguese" lang="pt" hreflang="pt" data-title="Neurodegeneração" data-language-autonym="Português" data-language-local-name="Portuguese" class="interlanguage-link-target"><span>Português</span></a></li><li class="interlanguage-link interwiki-ru mw-list-item"><a href="https://ru.wikipedia.org/wiki/%D0%9D%D0%B5%D0%B9%D1%80%D0%BE%D0%B4%D0%B5%D0%B3%D0%B5%D0%BD%D0%B5%D1%80%D0%B0%D1%82%D0%B8%D0%B2%D0%BD%D0%BE%D0%B5_%D0%B7%D0%B0%D0%B1%D0%BE%D0%BB%D0%B5%D0%B2%D0%B0%D0%BD%D0%B8%D0%B5" title="Нейродегенеративное заболевание – Russian" lang="ru" hreflang="ru" data-title="Нейродегенеративное заболевание" data-language-autonym="Русский" data-language-local-name="Russian" class="interlanguage-link-target"><span>Русский</span></a></li><li class="interlanguage-link interwiki-simple mw-list-item"><a href="https://simple.wikipedia.org/wiki/Neurodegeneration" title="Neurodegeneration – Simple English" lang="en-simple" hreflang="en-simple" data-title="Neurodegeneration" data-language-autonym="Simple English" data-language-local-name="Simple English" class="interlanguage-link-target"><span>Simple English</span></a></li><li class="interlanguage-link interwiki-sr mw-list-item"><a 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.hatnote{display:none!important}}</style><div role="note" class="hatnote navigation-not-searchable">For the medical journal, see <a href="/wiki/Experimental_Neurology" title="Experimental Neurology">Experimental Neurology</a>.</div> <div class="shortdescription nomobile noexcerpt noprint searchaux" style="display:none">Medical condition</div><style data-mw-deduplicate="TemplateStyles:r1257001546">.mw-parser-output .infobox-subbox{padding:0;border:none;margin:-3px;width:auto;min-width:100%;font-size:100%;clear:none;float:none;background-color:transparent}.mw-parser-output .infobox-3cols-child{margin:auto}.mw-parser-output .infobox .navbar{font-size:100%}@media screen{html.skin-theme-clientpref-night .mw-parser-output .infobox-full-data:not(.notheme)>div:not(.notheme)[style]{background:#1f1f23!important;color:#f8f9fa}}@media screen and (prefers-color-scheme:dark){html.skin-theme-clientpref-os .mw-parser-output .infobox-full-data:not(.notheme) div:not(.notheme){background:#1f1f23!important;color:#f8f9fa}}@media(min-width:640px){body.skin--responsive .mw-parser-output .infobox-table{display:table!important}body.skin--responsive .mw-parser-output .infobox-table>caption{display:table-caption!important}body.skin--responsive .mw-parser-output .infobox-table>tbody{display:table-row-group}body.skin--responsive .mw-parser-output .infobox-table tr{display:table-row!important}body.skin--responsive .mw-parser-output .infobox-table th,body.skin--responsive .mw-parser-output .infobox-table td{padding-left:inherit;padding-right:inherit}}</style><table class="infobox ib-medical-condition"><tbody><tr><th colspan="2" class="infobox-above" style="background:#ccc">Neurodegenerative disease</th></tr><tr style="background-color: #f8f9fa;"><td colspan="2" class="infobox-full-data"><span class="mw-default-size" typeof="mw:File/Frameless"><a href="/wiki/File:Alzheimer%27s_disease_brain_comparison.jpg" class="mw-file-description"><img src="//upload.wikimedia.org/wikipedia/commons/thumb/a/a5/Alzheimer%27s_disease_brain_comparison.jpg/220px-Alzheimer%27s_disease_brain_comparison.jpg" decoding="async" width="220" height="99" class="mw-file-element" srcset="//upload.wikimedia.org/wikipedia/commons/thumb/a/a5/Alzheimer%27s_disease_brain_comparison.jpg/330px-Alzheimer%27s_disease_brain_comparison.jpg 1.5x, //upload.wikimedia.org/wikipedia/commons/thumb/a/a5/Alzheimer%27s_disease_brain_comparison.jpg/440px-Alzheimer%27s_disease_brain_comparison.jpg 2x" data-file-width="3984" data-file-height="1800" /></a></span></td></tr><tr><td colspan="2" class="infobox-full-data">Normal <a href="/wiki/Human_brain" title="Human brain">brain</a> on left contrasted with structural changes shown in brain on right of person with <a href="/wiki/Alzheimer%27s_disease" title="Alzheimer's disease">Alzheimer's disease</a>, the most common neurodegenerative disease<sup id="cite_ref-CSHPB-Apr18_1-0" class="reference"><a href="#cite_note-CSHPB-Apr18-1"><span class="cite-bracket">[</span>1<span class="cite-bracket">]</span></a></sup></td></tr><tr><th scope="row" class="infobox-label"><a href="/wiki/Medical_specialty" title="Medical specialty">Specialty</a></th><td class="infobox-data"><a href="/wiki/Neurology" title="Neurology">Neurology</a>, <a href="/wiki/Psychiatry" title="Psychiatry">Psychiatry</a></td></tr></tbody></table> <p>A <b>neurodegenerative disease</b> is caused by the progressive loss of <a href="/wiki/Neuron" title="Neuron">neurons</a>, in the process known as <b>neurodegeneration</b>.<sup id="cite_ref-Lamptey_2-0" class="reference"><a href="#cite_note-Lamptey-2"><span class="cite-bracket">[</span>2<span class="cite-bracket">]</span></a></sup><sup id="cite_ref-NINDS_3-0" class="reference"><a href="#cite_note-NINDS-3"><span class="cite-bracket">[</span>3<span class="cite-bracket">]</span></a></sup> Neuronal damage may also ultimately result in their <a href="/wiki/Cell_death" title="Cell death">death</a>. Neurodegenerative diseases include <a href="/wiki/Amyotrophic_lateral_sclerosis" class="mw-redirect" title="Amyotrophic lateral sclerosis">amyotrophic lateral sclerosis</a>, <a href="/wiki/Multiple_sclerosis" title="Multiple sclerosis">multiple sclerosis</a>, <a href="/wiki/Parkinson%27s_disease" title="Parkinson's disease">Parkinson's disease</a>, <a href="/wiki/Alzheimer%27s_disease" title="Alzheimer's disease">Alzheimer's disease</a>, <a href="/wiki/Huntington%27s_disease" title="Huntington's disease">Huntington's disease</a>, <a href="/wiki/Multiple_system_atrophy" title="Multiple system atrophy">multiple system atrophy</a>, <a href="/wiki/Tauopathy" title="Tauopathy">tauopathies</a>, and <a href="/wiki/Prion_diseases" class="mw-redirect" title="Prion diseases">prion diseases</a>. Neurodegeneration can be found in the brain at many different levels of neuronal circuitry, ranging from molecular to systemic.<sup id="cite_ref-4" class="reference"><a href="#cite_note-4"><span class="cite-bracket">[</span>4<span class="cite-bracket">]</span></a></sup> Because there is no known way to reverse the progressive degeneration of neurons, these diseases are considered to be incurable; however research has shown that the two major contributing factors to neurodegeneration are oxidative stress and inflammation.<sup id="cite_ref-Pereira_5-0" class="reference"><a href="#cite_note-Pereira-5"><span class="cite-bracket">[</span>5<span class="cite-bracket">]</span></a></sup><sup id="cite_ref-Stephenson_6-0" class="reference"><a href="#cite_note-Stephenson-6"><span class="cite-bracket">[</span>6<span class="cite-bracket">]</span></a></sup><sup id="cite_ref-Singh_7-0" class="reference"><a href="#cite_note-Singh-7"><span class="cite-bracket">[</span>7<span class="cite-bracket">]</span></a></sup><sup id="cite_ref-JPND_8-0" class="reference"><a href="#cite_note-JPND-8"><span class="cite-bracket">[</span>8<span class="cite-bracket">]</span></a></sup> Biomedical research has revealed many similarities between these diseases at the <a href="/wiki/Subcellular" class="mw-redirect" title="Subcellular">subcellular</a> level, including atypical protein assemblies (like <a href="/wiki/Proteinopathy" title="Proteinopathy">proteinopathy</a>) and induced cell death.<sup id="cite_ref-rubinsztein_9-0" class="reference"><a href="#cite_note-rubinsztein-9"><span class="cite-bracket">[</span>9<span class="cite-bracket">]</span></a></sup><sup id="cite_ref-bredesen_10-0" class="reference"><a href="#cite_note-bredesen-10"><span class="cite-bracket">[</span>10<span class="cite-bracket">]</span></a></sup> These similarities suggest that <a href="/wiki/Therapy" title="Therapy">therapeutic</a> advances against one neurodegenerative disease might ameliorate other diseases as well. </p><p>Within neurodegenerative diseases, it is estimated that 55 million people worldwide had <a href="/wiki/Dementia" title="Dementia">dementia</a> in 2019, and that by 2050 this figure will increase to 139 million people.<sup id="cite_ref-WHO_dementia_report_11-0" class="reference"><a href="#cite_note-WHO_dementia_report-11"><span class="cite-bracket">[</span>11<span class="cite-bracket">]</span></a></sup> </p> <meta property="mw:PageProp/toc" /> <div class="mw-heading mw-heading2"><h2 id="Specific_disorders">Specific disorders</h2><span class="mw-editsection"><span class="mw-editsection-bracket">[</span><a href="/w/index.php?title=Neurodegenerative_disease&action=edit&section=1" title="Edit section: Specific disorders"><span>edit</span></a><span class="mw-editsection-bracket">]</span></span></div> <p>The consequences of neurodegeneration can vary widely depending on the specific region affected, ranging from issues related to movement to the development of dementia.<sup id="cite_ref-12" class="reference"><a href="#cite_note-12"><span class="cite-bracket">[</span>12<span class="cite-bracket">]</span></a></sup><sup id="cite_ref-13" class="reference"><a href="#cite_note-13"><span class="cite-bracket">[</span>13<span class="cite-bracket">]</span></a></sup> </p> <div class="mw-heading mw-heading3"><h3 id="Alzheimer's_disease"><span id="Alzheimer.27s_disease"></span>Alzheimer's disease</h3><span class="mw-editsection"><span class="mw-editsection-bracket">[</span><a href="/w/index.php?title=Neurodegenerative_disease&action=edit&section=2" title="Edit section: Alzheimer's disease"><span>edit</span></a><span class="mw-editsection-bracket">]</span></span></div> <figure class="mw-default-size" typeof="mw:File/Thumb"><a href="/wiki/File:Alzheimers_brain.jpg" class="mw-file-description"><img src="//upload.wikimedia.org/wikipedia/commons/thumb/c/cc/Alzheimers_brain.jpg/220px-Alzheimers_brain.jpg" decoding="async" width="220" height="216" class="mw-file-element" srcset="//upload.wikimedia.org/wikipedia/commons/thumb/c/cc/Alzheimers_brain.jpg/330px-Alzheimers_brain.jpg 1.5x, //upload.wikimedia.org/wikipedia/commons/thumb/c/cc/Alzheimers_brain.jpg/440px-Alzheimers_brain.jpg 2x" data-file-width="500" data-file-height="492" /></a><figcaption>Comparison of brain tissue between healthy individual and Alzheimer's disease patient, demonstrating extent of neuronal death</figcaption></figure> <link rel="mw-deduplicated-inline-style" href="mw-data:TemplateStyles:r1236090951"><div role="note" class="hatnote navigation-not-searchable">Main article: <a href="/wiki/Alzheimer%27s_disease" title="Alzheimer's disease">Alzheimer's disease</a></div> <p><a href="/wiki/Alzheimer%27s_disease" title="Alzheimer's disease">Alzheimer's disease</a> (AD) is a chronic neurodegenerative disease that results in the loss of <a href="/wiki/Neuron" title="Neuron">neurons</a> and <a href="/wiki/Synapse" title="Synapse">synapses</a> in the <a href="/wiki/Cerebral_cortex" title="Cerebral cortex">cerebral cortex</a> and certain subcortical structures, resulting in gross <a href="/wiki/Atrophy" title="Atrophy">atrophy</a> of the <a href="/wiki/Temporal_lobe" title="Temporal lobe">temporal lobe</a>, <a href="/wiki/Parietal_lobe" title="Parietal lobe">parietal lobe</a>, and parts of the <a href="/wiki/Frontal_cortex" class="mw-redirect" title="Frontal cortex">frontal cortex</a> and <a href="/wiki/Cingulate_gyrus" class="mw-redirect" title="Cingulate gyrus">cingulate gyrus</a>.<sup id="cite_ref-pmid12934968_14-0" class="reference"><a href="#cite_note-pmid12934968-14"><span class="cite-bracket">[</span>14<span class="cite-bracket">]</span></a></sup> It is the most common neurodegenerative disease.<sup id="cite_ref-CSHPB-Apr18_1-1" class="reference"><a href="#cite_note-CSHPB-Apr18-1"><span class="cite-bracket">[</span>1<span class="cite-bracket">]</span></a></sup> Even with billions of dollars being used to find a treatment for Alzheimer's disease, no effective treatments have been found.<sup id="cite_ref-15" class="reference"><a href="#cite_note-15"><span class="cite-bracket">[</span>15<span class="cite-bracket">]</span></a></sup> Within clinical trials stable and effective AD therapeutic strategies have a 99.5% failure rate.<sup id="cite_ref-16" class="reference"><a href="#cite_note-16"><span class="cite-bracket">[</span>16<span class="cite-bracket">]</span></a></sup> Reasons for this failure rate include inappropriate drug doses, invalid target and participant selection, and inadequate knowledge of pathophysiology of AD. Currently, diagnoses of Alzheimer's is subpar, and better methods need to be utilized for various aspects of clinical diagnoses.<sup id="cite_ref-Archer-2017_17-0" class="reference"><a href="#cite_note-Archer-2017-17"><span class="cite-bracket">[</span>17<span class="cite-bracket">]</span></a></sup> Alzheimer's has a 20% misdiagnosis rate.<sup id="cite_ref-Archer-2017_17-1" class="reference"><a href="#cite_note-Archer-2017-17"><span class="cite-bracket">[</span>17<span class="cite-bracket">]</span></a></sup> </p><p>AD pathology is primarily characterized by the presence of <a href="/wiki/Amyloid_plaques" title="Amyloid plaques">amyloid plaques</a> and <a href="/wiki/Neurofibrillary_tangle" title="Neurofibrillary tangle">neurofibrillary tangles</a>. Plaques are made up of small <a href="/wiki/Peptide" title="Peptide">peptides</a>, typically 39–43 amino acids in length, called <a href="/wiki/Amyloid_beta" title="Amyloid beta">amyloid beta</a> (also written as A-beta or Aβ). Amyloid beta is a fragment from a larger protein called <a href="/wiki/Amyloid_precursor_protein" class="mw-redirect" title="Amyloid precursor protein">amyloid precursor protein</a> (APP), a <a href="/wiki/Transmembrane_protein" title="Transmembrane protein">transmembrane protein</a> that penetrates through the neuron's membrane. APP appears to play roles in normal neuron growth, survival and post-injury repair.<sup id="cite_ref-pmid16822978_18-0" class="reference"><a href="#cite_note-pmid16822978-18"><span class="cite-bracket">[</span>18<span class="cite-bracket">]</span></a></sup><sup id="cite_ref-pmid12927332_19-0" class="reference"><a href="#cite_note-pmid12927332-19"><span class="cite-bracket">[</span>19<span class="cite-bracket">]</span></a></sup> APP is <a href="/wiki/Proteolysis" title="Proteolysis">cleaved</a> into smaller fragments by <a href="/wiki/Enzymes" class="mw-redirect" title="Enzymes">enzymes</a> such as <a href="/wiki/Gamma_secretase" title="Gamma secretase">gamma secretase</a> and <a href="/wiki/Beta_secretase" class="mw-redirect" title="Beta secretase">beta secretase</a>.<sup id="cite_ref-pmid15787600_20-0" class="reference"><a href="#cite_note-pmid15787600-20"><span class="cite-bracket">[</span>20<span class="cite-bracket">]</span></a></sup> One of these fragments gives rise to fibrils of amyloid beta which can self-assemble into the dense extracellular amyloid plaques.<sup id="cite_ref-pmid15184601_21-0" class="reference"><a href="#cite_note-pmid15184601-21"><span class="cite-bracket">[</span>21<span class="cite-bracket">]</span></a></sup><sup id="cite_ref-pmid15004691_22-0" class="reference"><a href="#cite_note-pmid15004691-22"><span class="cite-bracket">[</span>22<span class="cite-bracket">]</span></a></sup> </p> <div class="mw-heading mw-heading3"><h3 id="Parkinson's_disease"><span id="Parkinson.27s_disease"></span>Parkinson's disease</h3><span class="mw-editsection"><span class="mw-editsection-bracket">[</span><a href="/w/index.php?title=Neurodegenerative_disease&action=edit&section=3" title="Edit section: Parkinson's disease"><span>edit</span></a><span class="mw-editsection-bracket">]</span></span></div> <link rel="mw-deduplicated-inline-style" href="mw-data:TemplateStyles:r1236090951"><div role="note" class="hatnote navigation-not-searchable">Main article: <a href="/wiki/Parkinson%27s_disease" title="Parkinson's disease">Parkinson's disease</a></div> <p><a href="/wiki/Parkinson%27s_disease" title="Parkinson's disease">Parkinson's disease</a> (PD) is the second most common neurodegenerative disorder.<sup id="cite_ref-23" class="reference"><a href="#cite_note-23"><span class="cite-bracket">[</span>23<span class="cite-bracket">]</span></a></sup> It typically manifests as <a href="/wiki/Bradykinesia" class="mw-redirect" title="Bradykinesia">bradykinesia</a>, rigidity, resting tremor and posture instability. The crude prevalence rate of PD has been reported to range from 15 per 100,000 to 12,500 per 100,000, and the incidence of PD from 15 per 100,000 to 328 per 100,000, with the disease being less common in Asian countries. </p><p>PD is primarily characterized by death of <a href="/wiki/Dopaminergic" title="Dopaminergic">dopaminergic</a> neurons in the <a href="/wiki/Substantia_nigra" title="Substantia nigra">substantia nigra</a>, a region of the <a href="/wiki/Midbrain" title="Midbrain">midbrain</a>. The cause of this selective cell death is unknown. Notably, <a href="/wiki/Alpha-synuclein" title="Alpha-synuclein">alpha-synuclein</a>-<a href="/wiki/Ubiquitin" title="Ubiquitin">ubiquitin</a> complexes and aggregates are observed to accumulate in <a href="/wiki/Lewy_bodies" class="mw-redirect" title="Lewy bodies">Lewy bodies</a> within affected neurons. It is thought that defects in protein transport machinery and regulation, such as <a href="/wiki/RAB1" title="RAB1">RAB1</a>, may play a role in this disease mechanism.<sup id="cite_ref-24" class="reference"><a href="#cite_note-24"><span class="cite-bracket">[</span>24<span class="cite-bracket">]</span></a></sup> Impaired axonal transport of alpha-synuclein may also lead to its accumulation in Lewy bodies. Experiments have revealed reduced transport rates of both wild-type and two familial Parkinson's disease-associated mutant alpha-synucleins through axons of cultured neurons.<sup id="cite_ref-devos_25-0" class="reference"><a href="#cite_note-devos-25"><span class="cite-bracket">[</span>25<span class="cite-bracket">]</span></a></sup> Membrane damage by alpha-synuclein could be another Parkinson's disease mechanism.<sup id="cite_ref-curvature_26-0" class="reference"><a href="#cite_note-curvature-26"><span class="cite-bracket">[</span>26<span class="cite-bracket">]</span></a></sup> </p><p>The main known risk factor is age. Mutations in genes such as α-synuclein (SNCA), <a href="/wiki/LRRK2" title="LRRK2">leucine-rich repeat kinase 2</a> (LRRK2), <a href="/wiki/Glucocerebrosidase" title="Glucocerebrosidase">glucocerebrosidase</a> (GBA), and <a href="/wiki/Tau_protein" title="Tau protein">tau protein</a> (MAPT) can also cause hereditary PD or increase PD risk.<sup id="cite_ref-pmid26601739_27-0" class="reference"><a href="#cite_note-pmid26601739-27"><span class="cite-bracket">[</span>27<span class="cite-bracket">]</span></a></sup> While PD is the second most common neurodegenerative disorder, problems with diagnoses still persist.<sup id="cite_ref-Schmidt-2020_28-0" class="reference"><a href="#cite_note-Schmidt-2020-28"><span class="cite-bracket">[</span>28<span class="cite-bracket">]</span></a></sup> Problems with the sense of smell is a widespread symptom of Parkinson's disease (PD), however, some neurologists question its efficacy.<sup id="cite_ref-Schmidt-2020_28-1" class="reference"><a href="#cite_note-Schmidt-2020-28"><span class="cite-bracket">[</span>28<span class="cite-bracket">]</span></a></sup> This assessment method is a source of controversy among medical professionals.<sup id="cite_ref-Schmidt-2020_28-2" class="reference"><a href="#cite_note-Schmidt-2020-28"><span class="cite-bracket">[</span>28<span class="cite-bracket">]</span></a></sup> The <a href="/wiki/Gut_microbiome" class="mw-redirect" title="Gut microbiome">gut microbiome</a> might play a role in the diagnosis of PD, and research suggests various ways that could revolutionize the future of PD treatment.<sup id="cite_ref-29" class="reference"><a href="#cite_note-29"><span class="cite-bracket">[</span>29<span class="cite-bracket">]</span></a></sup> </p> <div class="mw-heading mw-heading3"><h3 id="Huntington's_disease"><span id="Huntington.27s_disease"></span>Huntington's disease</h3><span class="mw-editsection"><span class="mw-editsection-bracket">[</span><a href="/w/index.php?title=Neurodegenerative_disease&action=edit&section=4" title="Edit section: Huntington's disease"><span>edit</span></a><span class="mw-editsection-bracket">]</span></span></div> <link rel="mw-deduplicated-inline-style" href="mw-data:TemplateStyles:r1236090951"><div role="note" class="hatnote navigation-not-searchable">Main article: <a href="/wiki/Huntington%27s_disease" title="Huntington's disease">Huntington's disease</a></div> <p><a href="/wiki/Huntington%27s_disease" title="Huntington's disease">Huntington's disease</a> (HD) is a rare <a href="/wiki/Autosomal_dominant" class="mw-redirect" title="Autosomal dominant">autosomal dominant</a> neurodegenerative disorder caused by mutations in the <a href="/wiki/Huntingtin_gene" class="mw-redirect" title="Huntingtin gene">huntingtin gene</a> <i>(HTT)</i>. HD is characterized by loss of <a href="/wiki/Medium_spiny_neuron" title="Medium spiny neuron">medium spiny neurons</a> and <a href="/wiki/Astrogliosis" title="Astrogliosis">astrogliosis</a>.<sup id="cite_ref-30" class="reference"><a href="#cite_note-30"><span class="cite-bracket">[</span>30<span class="cite-bracket">]</span></a></sup><sup id="cite_ref-pmid18279698_31-0" class="reference"><a href="#cite_note-pmid18279698-31"><span class="cite-bracket">[</span>31<span class="cite-bracket">]</span></a></sup><sup id="cite_ref-pmid17965655_32-0" class="reference"><a href="#cite_note-pmid17965655-32"><span class="cite-bracket">[</span>32<span class="cite-bracket">]</span></a></sup> The first brain region to be substantially affected is the <a href="/wiki/Striatum" title="Striatum">striatum</a>, followed by degeneration of the <a href="/wiki/Frontal_lobe" title="Frontal lobe">frontal</a> and <a href="/wiki/Temporal_lobe" title="Temporal lobe">temporal</a> cortices.<sup id="cite_ref-33" class="reference"><a href="#cite_note-33"><span class="cite-bracket">[</span>33<span class="cite-bracket">]</span></a></sup> The striatum's <a href="/wiki/Subthalamic_nucleus" title="Subthalamic nucleus">subthalamic nuclei</a> send control signals to the <a href="/wiki/Globus_pallidus" title="Globus pallidus">globus pallidus</a>, which initiates and modulates motion. The weaker signals from subthalamic nuclei thus cause reduced initiation and modulation of movement, resulting in the characteristic movements of the disorder, notably <a href="/wiki/Chorea" title="Chorea">chorea</a>.<sup id="cite_ref-pmid10923984_34-0" class="reference"><a href="#cite_note-pmid10923984-34"><span class="cite-bracket">[</span>34<span class="cite-bracket">]</span></a></sup> Huntington's disease presents itself later in life even though the proteins that cause the disease works towards manifestation from their early stages in the humans affected by the proteins.<sup id="cite_ref-Barnat-2020_35-0" class="reference"><a href="#cite_note-Barnat-2020-35"><span class="cite-bracket">[</span>35<span class="cite-bracket">]</span></a></sup> Along with being a neurodegenerative disorder, HD has links to problems with neurodevelopment.<sup id="cite_ref-Barnat-2020_35-1" class="reference"><a href="#cite_note-Barnat-2020-35"><span class="cite-bracket">[</span>35<span class="cite-bracket">]</span></a></sup> </p><p>HD is caused by <a href="/wiki/Polyglutamine_tract" title="Polyglutamine tract">polyglutamine tract</a> expansion in the huntingtin gene, resulting in the mutant huntingtin. Aggregates of mutant huntingtin form as <a href="/wiki/Inclusion_bodies" title="Inclusion bodies">inclusion bodies</a> in neurons, and may be directly toxic. Additionally, they may damage molecular motors and microtubules to interfere with normal <a href="/wiki/Axonal_transport" title="Axonal transport">axonal transport</a>, leading to impaired transport of important cargoes such as <a href="/wiki/BDNF" class="mw-redirect" title="BDNF">BDNF</a>.<sup id="cite_ref-devos_25-1" class="reference"><a href="#cite_note-devos-25"><span class="cite-bracket">[</span>25<span class="cite-bracket">]</span></a></sup> Huntington's disease currently has no effective treatments that would modify the disease.<sup id="cite_ref-36" class="reference"><a href="#cite_note-36"><span class="cite-bracket">[</span>36<span class="cite-bracket">]</span></a></sup> </p> <div class="mw-heading mw-heading3"><h3 id="Multiple_sclerosis">Multiple sclerosis</h3><span class="mw-editsection"><span class="mw-editsection-bracket">[</span><a href="/w/index.php?title=Neurodegenerative_disease&action=edit&section=5" title="Edit section: Multiple sclerosis"><span>edit</span></a><span class="mw-editsection-bracket">]</span></span></div> <link rel="mw-deduplicated-inline-style" href="mw-data:TemplateStyles:r1236090951"><div role="note" class="hatnote navigation-not-searchable">Main article: <a href="/wiki/Multiple_sclerosis" title="Multiple sclerosis">Multiple sclerosis</a></div> <p><a href="/wiki/Multiple_sclerosis" title="Multiple sclerosis">Multiple sclerosis</a> (MS) is a chronic debilitating <a href="/wiki/Demyelinating_disease" title="Demyelinating disease">demyelinating disease</a> of the <a href="/wiki/Central_nervous_system" title="Central nervous system">central nervous system</a>, caused by an autoimmune attack resulting in the progressive loss of myelin sheath on neuronal axons.<sup id="cite_ref-ninds.nih.gov_37-0" class="reference"><a href="#cite_note-ninds.nih.gov-37"><span class="cite-bracket">[</span>37<span class="cite-bracket">]</span></a></sup> The resultant decrease in the speed of signal transduction leads to a loss of functionality that includes both cognitive and motor impairment depending on the location of the lesion.<sup id="cite_ref-ninds.nih.gov_37-1" class="reference"><a href="#cite_note-ninds.nih.gov-37"><span class="cite-bracket">[</span>37<span class="cite-bracket">]</span></a></sup> The progression of MS occurs due to episodes of increasing inflammation, which is proposed to be due to the release of antigens such as <a href="/wiki/Myelin_oligodendrocyte_glycoprotein" title="Myelin oligodendrocyte glycoprotein">myelin oligodendrocyte glycoprotein</a>, <a href="/wiki/Myelin_basic_protein" title="Myelin basic protein">myelin basic protein</a>, and <a href="/wiki/Proteolipid_protein" class="mw-redirect" title="Proteolipid protein">proteolipid protein</a>, causing an autoimmune response.<sup id="cite_ref-38" class="reference"><a href="#cite_note-38"><span class="cite-bracket">[</span>38<span class="cite-bracket">]</span></a></sup> This sets off a cascade of signaling molecules that result in T cells, B cells, and <a href="/wiki/Macrophage" title="Macrophage">macrophages</a> to cross the blood-brain barrier and attack myelin on neuronal axons leading to inflammation.<sup id="cite_ref-Stys-2019_39-0" class="reference"><a href="#cite_note-Stys-2019-39"><span class="cite-bracket">[</span>39<span class="cite-bracket">]</span></a></sup> Further release of antigens drives subsequent degeneration causing increased inflammation.<sup id="cite_ref-40" class="reference"><a href="#cite_note-40"><span class="cite-bracket">[</span>40<span class="cite-bracket">]</span></a></sup> Multiple sclerosis presents itself as a spectrum based on the degree of inflammation, a majority of patients experience early relapsing and remitting episodes of neuronal deterioration following a period of recovery. Some of these individuals may transition to a more linear progression of the disease, while about 15% of others begin with a progressive course on the onset of multiple sclerosis. The inflammatory response contributes to the loss of the grey matter, and as a result current literature devotes itself to combatting the auto-inflammatory aspect of the disease.<sup id="cite_ref-Stys-2019_39-1" class="reference"><a href="#cite_note-Stys-2019-39"><span class="cite-bracket">[</span>39<span class="cite-bracket">]</span></a></sup> While there are several proposed causal links between EBV and the <i>HLA-DRB1*15:01</i> allele to the onset of MS – they may contribute to the degree of autoimmune attack and the resultant inflammation – they do not determine the onset of MS.<sup id="cite_ref-Stys-2019_39-2" class="reference"><a href="#cite_note-Stys-2019-39"><span class="cite-bracket">[</span>39<span class="cite-bracket">]</span></a></sup> </p> <div class="mw-heading mw-heading3"><h3 id="Amyotrophic_lateral_sclerosis">Amyotrophic lateral sclerosis</h3><span class="mw-editsection"><span class="mw-editsection-bracket">[</span><a href="/w/index.php?title=Neurodegenerative_disease&action=edit&section=6" title="Edit section: Amyotrophic lateral sclerosis"><span>edit</span></a><span class="mw-editsection-bracket">]</span></span></div> <link rel="mw-deduplicated-inline-style" href="mw-data:TemplateStyles:r1236090951"><div role="note" class="hatnote navigation-not-searchable">Main article: <a href="/wiki/Amyotrophic_lateral_sclerosis" class="mw-redirect" title="Amyotrophic lateral sclerosis">Amyotrophic lateral sclerosis</a></div> <p><a href="/wiki/Amyotrophic_lateral_sclerosis" class="mw-redirect" title="Amyotrophic lateral sclerosis">Amyotrophic lateral sclerosis</a> (ALS), commonly referred to <a href="/wiki/Lou_Gehrig" title="Lou Gehrig">Lou Gehrig's</a> disease, is a rare neurodegenerative disorder characterized by the gradual loss of both <a href="/wiki/Upper_motor_neuron" title="Upper motor neuron">upper motor neurons</a> (UMNs) and <a href="/wiki/Lower_motor_neuron" title="Lower motor neuron">lower motor neurons</a> (LMNs).<sup id="cite_ref-Min-2020_41-0" class="reference"><a href="#cite_note-Min-2020-41"><span class="cite-bracket">[</span>41<span class="cite-bracket">]</span></a></sup> Although initial symptoms may vary, most patients develop skeletal muscle weakness that progresses to involve the entire body.<sup id="cite_ref-Min-2020_41-1" class="reference"><a href="#cite_note-Min-2020-41"><span class="cite-bracket">[</span>41<span class="cite-bracket">]</span></a></sup> The precise etiology of ALS remains unknown. In 1993, missense mutations in the gene encoding the antioxidant enzyme <a href="/wiki/SOD1" title="SOD1">superoxide dismutase 1 (SOD1)</a> were discovered in a subset of patients with familial ALS. More recently, <a href="/wiki/TDP-43" class="mw-redirect" title="TDP-43">TAR DNA-binding protein 43 (TDP-43)</a> and <a href="/wiki/FUS_(gene)" class="mw-redirect" title="FUS (gene)">Fused in Sarcoma (FUS)</a> protein aggregates have been implicated in some cases of the disease, and a mutation in chromosome 9 (<a href="/wiki/C9orf72" title="C9orf72">C9orf72</a>) is thought to be the most common known cause of sporadic ALS. Early diagnosis of ALS is harder than with other neurodegenerative diseases as there are no highly effective means of determining its early onset.<sup id="cite_ref-Min-2020_41-2" class="reference"><a href="#cite_note-Min-2020-41"><span class="cite-bracket">[</span>41<span class="cite-bracket">]</span></a></sup> Currently, there is research being done regarding the diagnosis of ALS through upper motor neuron tests.<sup id="cite_ref-Quinn-2020_42-0" class="reference"><a href="#cite_note-Quinn-2020-42"><span class="cite-bracket">[</span>42<span class="cite-bracket">]</span></a></sup> The Penn Upper Motor Neuron Score (PUMNS) consists of 28 criteria with a score range of 0–32.<sup id="cite_ref-Quinn-2020_42-1" class="reference"><a href="#cite_note-Quinn-2020-42"><span class="cite-bracket">[</span>42<span class="cite-bracket">]</span></a></sup> A higher score indicates a higher level of burden present on the upper motor neurons.<sup id="cite_ref-Quinn-2020_42-2" class="reference"><a href="#cite_note-Quinn-2020-42"><span class="cite-bracket">[</span>42<span class="cite-bracket">]</span></a></sup> The PUMNS has proven quite effective in determining the burden that exists on upper motor neurons in affected patients.<sup id="cite_ref-Quinn-2020_42-3" class="reference"><a href="#cite_note-Quinn-2020-42"><span class="cite-bracket">[</span>42<span class="cite-bracket">]</span></a></sup> </p><p>Independent research provided <i>in vitro</i> evidence that the primary cellular sites where SOD1 mutations act are located on <a href="/wiki/Astrocyte" title="Astrocyte">astrocytes</a>.<sup id="cite_ref-nagai_43-0" class="reference"><a href="#cite_note-nagai-43"><span class="cite-bracket">[</span>43<span class="cite-bracket">]</span></a></sup><sup id="cite_ref-digiorgio_44-0" class="reference"><a href="#cite_note-digiorgio-44"><span class="cite-bracket">[</span>44<span class="cite-bracket">]</span></a></sup> Astrocytes then cause the toxic effects on the <a href="/wiki/Motor_neurons" class="mw-redirect" title="Motor neurons">motor neurons</a>.<sup id="cite_ref-45" class="reference"><a href="#cite_note-45"><span class="cite-bracket">[</span>45<span class="cite-bracket">]</span></a></sup> The specific mechanism of toxicity still needs to be investigated, but the findings are significant because they implicate cells other than neuron cells in neurodegeneration.<sup id="cite_ref-julien_46-0" class="reference"><a href="#cite_note-julien-46"><span class="cite-bracket">[</span>46<span class="cite-bracket">]</span></a></sup> </p> <div class="mw-heading mw-heading3"><h3 id="Batten_disease">Batten disease</h3><span class="mw-editsection"><span class="mw-editsection-bracket">[</span><a href="/w/index.php?title=Neurodegenerative_disease&action=edit&section=7" title="Edit section: Batten disease"><span>edit</span></a><span class="mw-editsection-bracket">]</span></span></div> <link rel="mw-deduplicated-inline-style" href="mw-data:TemplateStyles:r1236090951"><div role="note" class="hatnote navigation-not-searchable">Main article: <a href="/wiki/Batten_disease" title="Batten disease">Batten disease</a></div> <p><a href="/wiki/Batten_disease" title="Batten disease">Batten disease</a> is a rare and fatal recessive neurodegenerative disorder that begins in childhood.<sup id="cite_ref-NIH_47-0" class="reference"><a href="#cite_note-NIH-47"><span class="cite-bracket">[</span>47<span class="cite-bracket">]</span></a></sup> Batten disease is the common name for a group of <a href="/wiki/Lysosomal_storage_disorder" class="mw-redirect" title="Lysosomal storage disorder">lysosomal storage disorders</a> known as <a href="/wiki/Neuronal_ceroid_lipofuscinosis" title="Neuronal ceroid lipofuscinosis">neuronal ceroid lipofuscinoses</a> (NCLs) – each caused by a specific gene mutation,<sup id="cite_ref-NIH_47-1" class="reference"><a href="#cite_note-NIH-47"><span class="cite-bracket">[</span>47<span class="cite-bracket">]</span></a></sup> of which there are thirteen.<sup id="cite_ref-Johnson19_48-0" class="reference"><a href="#cite_note-Johnson19-48"><span class="cite-bracket">[</span>48<span class="cite-bracket">]</span></a></sup> Since Batten disease is quite rare, its worldwide prevalence is about 1 in every 100,000 live births.<sup id="cite_ref-Johnson19_48-1" class="reference"><a href="#cite_note-Johnson19-48"><span class="cite-bracket">[</span>48<span class="cite-bracket">]</span></a></sup> In North America, NCL3 disease (juvenile NCL) typically manifests between the ages of 4 and 7.<sup id="cite_ref-Masten-2020_49-0" class="reference"><a href="#cite_note-Masten-2020-49"><span class="cite-bracket">[</span>49<span class="cite-bracket">]</span></a></sup> Batten disease is characterized by motor impairment, <a href="/wiki/Epilepsy" title="Epilepsy">epilepsy</a>, <a href="/wiki/Dementia" title="Dementia">dementia</a>, vision loss, and shortened lifespan.<sup id="cite_ref-50" class="reference"><a href="#cite_note-50"><span class="cite-bracket">[</span>50<span class="cite-bracket">]</span></a></sup> A loss of vision is common first sign of Batten disease.<sup id="cite_ref-Masten-2020_49-1" class="reference"><a href="#cite_note-Masten-2020-49"><span class="cite-bracket">[</span>49<span class="cite-bracket">]</span></a></sup> Loss of vision is typically preceded by cognitive and behavioral changes, seizures, and loss of the ability to walk.<sup id="cite_ref-Masten-2020_49-2" class="reference"><a href="#cite_note-Masten-2020-49"><span class="cite-bracket">[</span>49<span class="cite-bracket">]</span></a></sup> It is common for people to establish cardiac arrhythmias and difficulties eating food as the disease progresses.<sup id="cite_ref-Masten-2020_49-3" class="reference"><a href="#cite_note-Masten-2020-49"><span class="cite-bracket">[</span>49<span class="cite-bracket">]</span></a></sup> Batten disease diagnosis depends on a conflation of many criteria: clinical signs and symptoms, evaluations of the eye, electroencephalograms (EEG), and brain magnetic resonance imaging (MRI) results.<sup id="cite_ref-Johnson19_48-2" class="reference"><a href="#cite_note-Johnson19-48"><span class="cite-bracket">[</span>48<span class="cite-bracket">]</span></a></sup> The diagnosis provided by these results are corroborated by genetic and biochemical testing.<sup id="cite_ref-Johnson19_48-3" class="reference"><a href="#cite_note-Johnson19-48"><span class="cite-bracket">[</span>48<span class="cite-bracket">]</span></a></sup> No effective treatments were available to prevent the disease from being widespread before the past few years.<sup id="cite_ref-Johnson19_48-4" class="reference"><a href="#cite_note-Johnson19-48"><span class="cite-bracket">[</span>48<span class="cite-bracket">]</span></a></sup> In recent years, more models have been created to expedite the research process for methods to treat Batten disease.<sup id="cite_ref-Johnson19_48-5" class="reference"><a href="#cite_note-Johnson19-48"><span class="cite-bracket">[</span>48<span class="cite-bracket">]</span></a></sup> </p> <div class="mw-heading mw-heading3"><h3 id="Creutzfeldt–Jakob_disease"><span id="Creutzfeldt.E2.80.93Jakob_disease"></span>Creutzfeldt–Jakob disease</h3><span class="mw-editsection"><span class="mw-editsection-bracket">[</span><a href="/w/index.php?title=Neurodegenerative_disease&action=edit&section=8" title="Edit section: Creutzfeldt–Jakob disease"><span>edit</span></a><span class="mw-editsection-bracket">]</span></span></div> <link rel="mw-deduplicated-inline-style" href="mw-data:TemplateStyles:r1236090951"><div role="note" class="hatnote navigation-not-searchable">Main article: <a href="/wiki/Creutzfeldt-Jakob_disease" class="mw-redirect" title="Creutzfeldt-Jakob disease">Creutzfeldt-Jakob disease</a></div> <p><a href="/wiki/Creutzfeldt%E2%80%93Jakob_disease" title="Creutzfeldt–Jakob disease">Creutzfeldt–Jakob disease</a> (CJD) is a <a href="/wiki/Prion" title="Prion">prion</a> disease that is characterized by rapidly progressive dementia.<sup id="cite_ref-51" class="reference"><a href="#cite_note-51"><span class="cite-bracket">[</span>51<span class="cite-bracket">]</span></a></sup> Misfolded proteins called prions aggregate in brain tissue leading to nerve cell death.<sup id="cite_ref-52" class="reference"><a href="#cite_note-52"><span class="cite-bracket">[</span>52<span class="cite-bracket">]</span></a></sup> <a href="/wiki/Variant_Creutzfeldt%E2%80%93Jakob_disease" title="Variant Creutzfeldt–Jakob disease">Variant Creutzfeldt–Jakob disease</a> (vCJD) is the infectious form that comes from the meat of a cow that was infected with <a href="/wiki/Bovine_spongiform_encephalopathy" title="Bovine spongiform encephalopathy">bovine spongiform encephalopathy</a>, also called mad cow disease.<sup id="cite_ref-53" class="reference"><a href="#cite_note-53"><span class="cite-bracket">[</span>53<span class="cite-bracket">]</span></a></sup> </p> <div class="mw-heading mw-heading2"><h2 id="Risk_factors">Risk factors</h2><span class="mw-editsection"><span class="mw-editsection-bracket">[</span><a href="/w/index.php?title=Neurodegenerative_disease&action=edit&section=9" title="Edit section: Risk factors"><span>edit</span></a><span class="mw-editsection-bracket">]</span></span></div> <div class="mw-heading mw-heading3"><h3 id="Aging">Aging</h3><span class="mw-editsection"><span class="mw-editsection-bracket">[</span><a href="/w/index.php?title=Neurodegenerative_disease&action=edit&section=10" title="Edit section: Aging"><span>edit</span></a><span class="mw-editsection-bracket">]</span></span></div> <link rel="mw-deduplicated-inline-style" href="mw-data:TemplateStyles:r1236090951"><div role="note" class="hatnote navigation-not-searchable">Further information: <a href="/wiki/Aging_brain" title="Aging brain">Aging brain</a></div> <p>The greatest risk factor for neurodegenerative diseases is <a href="/wiki/Ageing" title="Ageing">aging</a>. <a href="/wiki/Free-radical_theory_of_aging#Mitochondria" title="Free-radical theory of aging">Mitochondrial DNA mutations</a> as well as <a href="/wiki/Oxidative_stress" title="Oxidative stress">oxidative stress</a> both contribute to aging.<sup id="cite_ref-lin_54-0" class="reference"><a href="#cite_note-lin-54"><span class="cite-bracket">[</span>54<span class="cite-bracket">]</span></a></sup> Many of these diseases are late-onset, meaning there is some factor that changes as a person ages for each disease.<sup id="cite_ref-rubinsztein_9-1" class="reference"><a href="#cite_note-rubinsztein-9"><span class="cite-bracket">[</span>9<span class="cite-bracket">]</span></a></sup> One constant factor is that in each disease, neurons gradually lose function as the disease progresses with age. It has been proposed that <a href="/wiki/DNA_damage_(naturally_occurring)" title="DNA damage (naturally occurring)">DNA damage</a> accumulation provides the underlying causative link between aging and neurodegenerative disease.<sup id="cite_ref-Bernsteinbook_55-0" class="reference"><a href="#cite_note-Bernsteinbook-55"><span class="cite-bracket">[</span>55<span class="cite-bracket">]</span></a></sup><sup id="cite_ref-pmid26385091_56-0" class="reference"><a href="#cite_note-pmid26385091-56"><span class="cite-bracket">[</span>56<span class="cite-bracket">]</span></a></sup> About 20–40% of healthy people between 60 and 78 years old experience discernable decrements in cognitive performance in several domains including working, spatial, and episodic memory, and processing speed.<sup id="cite_ref-pmid28438892_57-0" class="reference"><a href="#cite_note-pmid28438892-57"><span class="cite-bracket">[</span>57<span class="cite-bracket">]</span></a></sup> </p> <div class="mw-heading mw-heading3"><h3 id="Infections">Infections</h3><span class="mw-editsection"><span class="mw-editsection-bracket">[</span><a href="/w/index.php?title=Neurodegenerative_disease&action=edit&section=11" title="Edit section: Infections"><span>edit</span></a><span class="mw-editsection-bracket">]</span></span></div> <figure typeof="mw:File/Thumb"><a href="/wiki/File:Hazard_ratio_lag_for_replicated_viral_infection%E2%80%93neurodegenerative_disease_pairs.jpg" class="mw-file-description"><img src="//upload.wikimedia.org/wikipedia/commons/thumb/b/ba/Hazard_ratio_lag_for_replicated_viral_infection%E2%80%93neurodegenerative_disease_pairs.jpg/180px-Hazard_ratio_lag_for_replicated_viral_infection%E2%80%93neurodegenerative_disease_pairs.jpg" decoding="async" width="180" height="170" class="mw-file-element" srcset="//upload.wikimedia.org/wikipedia/commons/thumb/b/ba/Hazard_ratio_lag_for_replicated_viral_infection%E2%80%93neurodegenerative_disease_pairs.jpg/270px-Hazard_ratio_lag_for_replicated_viral_infection%E2%80%93neurodegenerative_disease_pairs.jpg 1.5x, //upload.wikimedia.org/wikipedia/commons/thumb/b/ba/Hazard_ratio_lag_for_replicated_viral_infection%E2%80%93neurodegenerative_disease_pairs.jpg/360px-Hazard_ratio_lag_for_replicated_viral_infection%E2%80%93neurodegenerative_disease_pairs.jpg 2x" data-file-width="3362" data-file-height="3181" /></a><figcaption>Risks from viral exposures according to one biobank study<sup id="cite_ref-10.1016/j.neuron.2022.12.029_58-0" class="reference"><a href="#cite_note-10.1016/j.neuron.2022.12.029-58"><span class="cite-bracket">[</span>58<span class="cite-bracket">]</span></a></sup></figcaption></figure> <p>A study using <a href="/wiki/Electronic_health_record" title="Electronic health record">electronic health records</a> indicates that 45 (with 22 of these being replicated with the <a href="/wiki/UK_Biobank" title="UK Biobank">UK Biobank</a>) viral exposures can significantly elevate risks of neurodegenerative disease, including up to 15 years after infection.<sup id="cite_ref-10.1016/j.neuron.2022.12.029_58-1" class="reference"><a href="#cite_note-10.1016/j.neuron.2022.12.029-58"><span class="cite-bracket">[</span>58<span class="cite-bracket">]</span></a></sup><sup id="cite_ref-59" class="reference"><a href="#cite_note-59"><span class="cite-bracket">[</span>59<span class="cite-bracket">]</span></a></sup> </p> <div class="mw-heading mw-heading2"><h2 id="Mechanisms">Mechanisms</h2><span class="mw-editsection"><span class="mw-editsection-bracket">[</span><a href="/w/index.php?title=Neurodegenerative_disease&action=edit&section=12" title="Edit section: Mechanisms"><span>edit</span></a><span class="mw-editsection-bracket">]</span></span></div> <div class="mw-heading mw-heading3"><h3 id="Genetics">Genetics</h3><span class="mw-editsection"><span class="mw-editsection-bracket">[</span><a href="/w/index.php?title=Neurodegenerative_disease&action=edit&section=13" title="Edit section: Genetics"><span>edit</span></a><span class="mw-editsection-bracket">]</span></span></div> <link rel="mw-deduplicated-inline-style" href="mw-data:TemplateStyles:r1236090951"><div role="note" class="hatnote navigation-not-searchable">See also: <a href="/wiki/Trinucleotide_repeat_disorder" title="Trinucleotide repeat disorder">Trinucleotide repeat disorder</a> and <a href="/wiki/Epigenetics_of_neurodegenerative_diseases" title="Epigenetics of neurodegenerative diseases">Epigenetics of neurodegenerative diseases</a></div> <p>Many neurodegenerative diseases are caused by <a href="/wiki/Genetic_mutation" class="mw-redirect" title="Genetic mutation">genetic mutations</a>, most of which are located in completely unrelated genes. In many of the different diseases, the mutated gene has a common feature: a repeat of the CAG nucleotide triplet. CAG codes for the amino acid <a href="/wiki/Glutamine" title="Glutamine">glutamine</a>. A repeat of CAG results in a <a href="/wiki/Polyglutamine_tract" title="Polyglutamine tract">polyglutamine (polyQ) tract</a>. Diseases associated with such mutations are known as <a href="/wiki/Trinucleotide_repeat_disorder" title="Trinucleotide repeat disorder">trinucleotide repeat disorders</a>.<sup id="cite_ref-thompson_60-0" class="reference"><a href="#cite_note-thompson-60"><span class="cite-bracket">[</span>60<span class="cite-bracket">]</span></a></sup><sup id="cite_ref-marsh_61-0" class="reference"><a href="#cite_note-marsh-61"><span class="cite-bracket">[</span>61<span class="cite-bracket">]</span></a></sup> </p><p>Polyglutamine repeats typically cause dominant pathogenesis. Extra glutamine residues can acquire toxic properties through a variety of ways, including irregular protein folding and degradation pathways, altered subcellular localization, and abnormal interactions with other cellular proteins.<sup id="cite_ref-thompson_60-1" class="reference"><a href="#cite_note-thompson-60"><span class="cite-bracket">[</span>60<span class="cite-bracket">]</span></a></sup> PolyQ studies often use a variety of animal models because there is such a clearly defined trigger – repeat expansion. Extensive research has been done using the <a href="/wiki/Model_organism" title="Model organism">models</a> of <a href="/wiki/Nematode" title="Nematode">nematode</a> (<i>C. elegans</i>), and fruit fly (<i>Drosophila</i>), mice, and non-human primates.<sup id="cite_ref-marsh_61-1" class="reference"><a href="#cite_note-marsh-61"><span class="cite-bracket">[</span>61<span class="cite-bracket">]</span></a></sup><sup id="cite_ref-orr_62-0" class="reference"><a href="#cite_note-orr-62"><span class="cite-bracket">[</span>62<span class="cite-bracket">]</span></a></sup> </p><p>Nine inherited neurodegenerative diseases are caused by the expansion of the CAG trinucleotide and polyQ tract, including <a href="/wiki/Huntington%27s_disease" title="Huntington's disease">Huntington's disease</a> and the <a href="/wiki/Spinocerebellar_ataxia" title="Spinocerebellar ataxia">spinocerebellar ataxias</a>.<sup id="cite_ref-63" class="reference"><a href="#cite_note-63"><span class="cite-bracket">[</span>63<span class="cite-bracket">]</span></a></sup> </p> <div class="mw-heading mw-heading3"><h3 id="Epigenetics">Epigenetics</h3><span class="mw-editsection"><span class="mw-editsection-bracket">[</span><a href="/w/index.php?title=Neurodegenerative_disease&action=edit&section=14" title="Edit section: Epigenetics"><span>edit</span></a><span class="mw-editsection-bracket">]</span></span></div> <p>The presence of epigenetic modifications for certain genes has been demonstrated in this type of pathology. An example is <a href="/wiki/FKBP5" title="FKBP5">FKBP5</a> gene, which progressively increases its expression with age and has been related to <a href="/wiki/Braak_staging" title="Braak staging">Braak staging</a> and increased tau pathology both in vitro and in mouse models of AD.<sup id="cite_ref-64" class="reference"><a href="#cite_note-64"><span class="cite-bracket">[</span>64<span class="cite-bracket">]</span></a></sup> </p> <div class="mw-heading mw-heading3"><h3 id="Protein_misfolding">Protein misfolding</h3><span class="mw-editsection"><span class="mw-editsection-bracket">[</span><a href="/w/index.php?title=Neurodegenerative_disease&action=edit&section=15" title="Edit section: Protein misfolding"><span>edit</span></a><span class="mw-editsection-bracket">]</span></span></div> <link rel="mw-deduplicated-inline-style" href="mw-data:TemplateStyles:r1236090951"><div role="note" class="hatnote navigation-not-searchable">See also: <a href="/wiki/Stress_granule" title="Stress granule">Stress granule</a></div> <p>Several neurodegenerative diseases are classified as <a href="/wiki/Proteopathy" class="mw-redirect" title="Proteopathy">proteopathies</a> as they are associated with the <a href="/wiki/Protein_aggregation" title="Protein aggregation">aggregation</a> of <a href="/wiki/Protein_folding" title="Protein folding">misfolded proteins</a>. Protein toxicity is one of the key mechanisms of many neurodegenrative diseases.<sup id="cite_ref-Chung_65-0" class="reference"><a href="#cite_note-Chung-65"><span class="cite-bracket">[</span>65<span class="cite-bracket">]</span></a></sup> </p> <ul><li><b><a href="/wiki/Alpha-synuclein" title="Alpha-synuclein">alpha-synuclein</a>:</b> can aggregate to form insoluble fibrils in pathological conditions characterized by <a href="/wiki/Lewy_bodies" class="mw-redirect" title="Lewy bodies">Lewy bodies</a>, such as Parkinson's disease, <a href="/wiki/Dementia_with_Lewy_bodies" title="Dementia with Lewy bodies">dementia with Lewy bodies</a>, and <a href="/wiki/Multiple_system_atrophy" title="Multiple system atrophy">multiple system atrophy</a>. Alpha-synuclein is the primary structural component of Lewy body fibrils. In addition, an alpha-synuclein fragment, known as the non-Abeta component (NAC), is found in <a href="/wiki/Amyloid_plaques" title="Amyloid plaques">amyloid plaques</a> in <a href="/wiki/Alzheimer%27s_disease" title="Alzheimer's disease">Alzheimer's disease</a>.</li> <li><b><a href="/wiki/Tau_protein" title="Tau protein">tau</a>:</b> <a href="/wiki/Hyperphosphorylated" class="mw-redirect" title="Hyperphosphorylated">hyperphosphorylated</a> <a href="/wiki/Tau_protein" title="Tau protein">tau protein</a> is the main component of <a href="/wiki/Neurofibrillary_tangles" class="mw-redirect" title="Neurofibrillary tangles">neurofibrillary tangles</a> in Alzheimer's disease; tau fibrils are the main component of <a href="/wiki/Pick_bodies" class="mw-redirect" title="Pick bodies">Pick bodies</a> found in <a href="/wiki/Behavioral_variant_frontotemporal_dementia" class="mw-redirect" title="Behavioral variant frontotemporal dementia">behavioral variant frontotemporal dementia</a>.</li> <li><b><a href="/wiki/Amyloid_beta" title="Amyloid beta">amyloid beta</a>:</b> the major component of amyloid plaques in Alzheimer's disease.</li> <li><b><a href="/wiki/Prion" title="Prion">prion</a>:</b> main component of <a href="/wiki/Prion_diseases" class="mw-redirect" title="Prion diseases">prion diseases</a> and <a href="/wiki/Transmissible_spongiform_encephalopathy" title="Transmissible spongiform encephalopathy">transmissible spongiform encephalopathy</a>.</li></ul> <div class="mw-heading mw-heading3"><h3 id="Intracellular_mechanisms">Intracellular mechanisms</h3><span class="mw-editsection"><span class="mw-editsection-bracket">[</span><a href="/w/index.php?title=Neurodegenerative_disease&action=edit&section=16" title="Edit section: Intracellular mechanisms"><span>edit</span></a><span class="mw-editsection-bracket">]</span></span></div> <div class="mw-heading mw-heading4"><h4 id="Protein_degradation_pathways">Protein degradation pathways</h4><span class="mw-editsection"><span class="mw-editsection-bracket">[</span><a href="/w/index.php?title=Neurodegenerative_disease&action=edit&section=17" title="Edit section: Protein degradation pathways"><span>edit</span></a><span class="mw-editsection-bracket">]</span></span></div> <p>Parkinson's disease and Huntington's disease are both late-onset and associated with the accumulation of intracellular toxic proteins. Diseases caused by the aggregation of proteins are known as <a href="/wiki/Proteopathies" class="mw-redirect" title="Proteopathies">proteopathies</a>, and they are primarily caused by aggregates in the following structures:<sup id="cite_ref-rubinsztein_9-2" class="reference"><a href="#cite_note-rubinsztein-9"><span class="cite-bracket">[</span>9<span class="cite-bracket">]</span></a></sup> </p> <ul><li>cytosol, e.g. Parkinson's and Huntington's</li> <li>nucleus, e.g. <a href="/wiki/Spinocerebellar_ataxia_type_1" title="Spinocerebellar ataxia type 1">Spinocerebellar ataxia type 1</a> (SCA1)</li> <li>endoplasmic reticulum (ER), (as seen with neuroserpin mutations that cause familial encephalopathy with neuroserpin inclusion bodies)</li> <li>extracellularly excreted proteins, amyloid-beta in Alzheimer's disease</li></ul> <p>There are two main avenues eukaryotic cells use to remove troublesome proteins or organelles: </p> <ul><li><b>ubiquitin–proteasome:</b> protein <a href="/wiki/Ubiquitin" title="Ubiquitin">ubiquitin</a> along with enzymes is key for the degradation of many proteins that cause proteopathies including polyQ expansions and alpha-synucleins. Research indicates proteasome enzymes may not be able to correctly cleave these irregular proteins, which could possibly result in a more toxic species. This is the primary route cells use to degrade proteins.<sup id="cite_ref-rubinsztein_9-3" class="reference"><a href="#cite_note-rubinsztein-9"><span class="cite-bracket">[</span>9<span class="cite-bracket">]</span></a></sup> <ul><li>Decreased proteasome activity is consistent with models in which intracellular protein aggregates form. It is still unknown whether or not these aggregates are a cause or a result of neurodegeneration.<sup id="cite_ref-rubinsztein_9-4" class="reference"><a href="#cite_note-rubinsztein-9"><span class="cite-bracket">[</span>9<span class="cite-bracket">]</span></a></sup></li></ul></li> <li><b>autophagy–lysosome pathways:</b> a form of <a href="/wiki/Programmed_cell_death" title="Programmed cell death">programmed cell death</a> (PCD), this becomes the favorable route when a protein is aggregate-prone meaning it is a poor proteasome substrate. This can be split into two forms of autophagy: <b><a href="/wiki/Macroautophagy" class="mw-redirect" title="Macroautophagy">macroautophagy</a></b> and <b>chaperone-mediated autophagy (CMA)</b>.<sup id="cite_ref-rubinsztein_9-5" class="reference"><a href="#cite_note-rubinsztein-9"><span class="cite-bracket">[</span>9<span class="cite-bracket">]</span></a></sup> <ul><li><b>macroautophagy</b> is involved with nutrient recycling of macromolecules under conditions of starvation, certain apoptotic pathways, and if absent, leads to the formation of ubiquinated inclusions. Experiments in mice with neuronally confined macroautophagy-gene knockouts develop intraneuronal aggregates leading to neurodegeneration.<sup id="cite_ref-rubinsztein_9-6" class="reference"><a href="#cite_note-rubinsztein-9"><span class="cite-bracket">[</span>9<span class="cite-bracket">]</span></a></sup></li> <li><b>chaperone-mediated autophagy</b> defects may also lead to neurodegeneration. Research has shown that mutant proteins bind to the CMA-pathway receptors on lysosomal membrane and in doing so block their own degradation as well as the degradation of other substrates.<sup id="cite_ref-rubinsztein_9-7" class="reference"><a href="#cite_note-rubinsztein-9"><span class="cite-bracket">[</span>9<span class="cite-bracket">]</span></a></sup></li></ul></li></ul> <div class="mw-heading mw-heading4"><h4 id="Membrane_damage">Membrane damage</h4><span class="mw-editsection"><span class="mw-editsection-bracket">[</span><a href="/w/index.php?title=Neurodegenerative_disease&action=edit&section=18" title="Edit section: Membrane damage"><span>edit</span></a><span class="mw-editsection-bracket">]</span></span></div> <p>Damage to the membranes of organelles by monomeric or oligomeric proteins could also contribute to these diseases. Alpha-synuclein can damage membranes by inducing membrane curvature,<sup id="cite_ref-curvature_26-1" class="reference"><a href="#cite_note-curvature-26"><span class="cite-bracket">[</span>26<span class="cite-bracket">]</span></a></sup> and cause extensive tubulation and vesiculation when incubated with artificial phospholipid vesicles.<sup id="cite_ref-curvature_26-2" class="reference"><a href="#cite_note-curvature-26"><span class="cite-bracket">[</span>26<span class="cite-bracket">]</span></a></sup> <a rel="nofollow" class="external text" href="http://www.jbc.org/content/287/35/29301.long">The tubes formed from these lipid vesicles consist of both micellar as well as bilayer tubes. Extensive induction of membrane curvature is deleterious to the cell and would eventually lead to cell death.</a> <a rel="nofollow" class="external text" href="http://www.jbc.org/content/288/24/17620.long">Apart from tubular structures, alpha-synuclein can also form lipoprotein nanoparticles similar to apolipoproteins.</a> </p> <div class="mw-heading mw-heading4"><h4 id="Mitochondrial_dysfunction">Mitochondrial dysfunction</h4><span class="mw-editsection"><span class="mw-editsection-bracket">[</span><a href="/w/index.php?title=Neurodegenerative_disease&action=edit&section=19" title="Edit section: Mitochondrial dysfunction"><span>edit</span></a><span class="mw-editsection-bracket">]</span></span></div> <p>The most common form of cell death in neurodegeneration is through the intrinsic mitochondrial apoptotic pathway. This pathway controls the activation of caspase-9 by regulating the release of <a href="/wiki/Cytochrome_c" title="Cytochrome c">cytochrome c</a> from the <a href="/wiki/Mitochondrion#Intermembrane_space" title="Mitochondrion">mitochondrial intermembrane space</a>. <a href="/wiki/Reactive_oxygen_species" title="Reactive oxygen species">Reactive oxygen species</a> (ROS) are normal byproducts of mitochondrial respiratory chain activity. ROS concentration is mediated by mitochondrial antioxidants such as manganese superoxide dismutase (SOD2) and <a href="/wiki/Glutathione_peroxidase" title="Glutathione peroxidase">glutathione peroxidase</a>. Over production of ROS (<a href="/wiki/Oxidative_stress" title="Oxidative stress">oxidative stress</a>) is a central feature of all neurodegenerative disorders. In addition to the generation of ROS, mitochondria are also involved with life-sustaining functions including calcium homeostasis, PCD, <a href="/wiki/Mitochondrial_fission" title="Mitochondrial fission">mitochondrial fission</a> and <a href="/wiki/Mitochondrial_fusion" title="Mitochondrial fusion">fusion</a>, lipid concentration of the mitochondrial membranes, and the mitochondrial permeability transition. <a href="/wiki/Mitochondrial_disease" title="Mitochondrial disease">Mitochondrial disease</a> leading to neurodegeneration is likely, at least on some level, to involve all of these functions.<sup id="cite_ref-dimauro_66-0" class="reference"><a href="#cite_note-dimauro-66"><span class="cite-bracket">[</span>66<span class="cite-bracket">]</span></a></sup> </p><p>There is strong evidence that mitochondrial dysfunction and oxidative stress play a causal role in neurodegenerative disease pathogenesis, including in four of the more well known diseases <a href="/wiki/Alzheimer%27s" class="mw-redirect" title="Alzheimer's">Alzheimer's</a>, <a href="/wiki/Parkinson%27s" class="mw-redirect" title="Parkinson's">Parkinson's</a>, <a href="/wiki/Huntington%27s" class="mw-redirect" title="Huntington's">Huntington's</a>, and <a href="/wiki/Amyotrophic_lateral_sclerosis" class="mw-redirect" title="Amyotrophic lateral sclerosis">amyotrophic lateral sclerosis</a>.<sup id="cite_ref-lin_54-1" class="reference"><a href="#cite_note-lin-54"><span class="cite-bracket">[</span>54<span class="cite-bracket">]</span></a></sup> </p><p><a href="/wiki/Neuron" title="Neuron">Neurons</a> are particularly vulnerable to <a href="/wiki/Oxidative_stress" title="Oxidative stress">oxidative damage</a> due to their strong metabolic activity associated with high <a href="/wiki/Transcription_(biology)" title="Transcription (biology)">transcription</a> levels, high oxygen consumption, and weak <a href="/wiki/Antioxidant" title="Antioxidant">antioxidant</a> defense.<sup id="cite_ref-pmid28785371_67-0" class="reference"><a href="#cite_note-pmid28785371-67"><span class="cite-bracket">[</span>67<span class="cite-bracket">]</span></a></sup><sup id="cite_ref-pmid27663141_68-0" class="reference"><a href="#cite_note-pmid27663141-68"><span class="cite-bracket">[</span>68<span class="cite-bracket">]</span></a></sup> </p> <div class="mw-heading mw-heading4"><h4 id="DNA_damage">DNA damage</h4><span class="mw-editsection"><span class="mw-editsection-bracket">[</span><a href="/w/index.php?title=Neurodegenerative_disease&action=edit&section=20" title="Edit section: DNA damage"><span>edit</span></a><span class="mw-editsection-bracket">]</span></span></div> <p>The brain metabolizes as much as a fifth of consumed oxygen, and <a href="/wiki/Reactive_oxygen_species" title="Reactive oxygen species">reactive oxygen species</a> produced by oxidative metabolism are a major source of <a href="/wiki/DNA_damage_(naturally_occurring)" title="DNA damage (naturally occurring)">DNA damage</a> in the <a href="/wiki/Brain" title="Brain">brain</a>. Damage to a cell's <a href="/wiki/DNA" title="DNA">DNA</a> is particularly harmful because DNA is the blueprint for protein production and unlike other molecules it cannot simply be replaced by re-synthesis. The vulnerability of post-mitotic neurons to DNA damage (such as oxidative lesions or certain types of DNA strand breaks), coupled with a gradual decline in the activities of <a href="/wiki/DNA_repair" title="DNA repair">repair mechanisms</a>, could lead to accumulation of DNA damage with age and contribute to brain aging and neurodegeneration.<sup id="cite_ref-pmid25033177_69-0" class="reference"><a href="#cite_note-pmid25033177-69"><span class="cite-bracket">[</span>69<span class="cite-bracket">]</span></a></sup> DNA single-strand breaks are common and are associated with the neurodegenerative disease ataxia-<a href="/wiki/Oculomotor_apraxia" title="Oculomotor apraxia">oculomotor apraxia</a>.<sup id="cite_ref-pmid21550379_70-0" class="reference"><a href="#cite_note-pmid21550379-70"><span class="cite-bracket">[</span>70<span class="cite-bracket">]</span></a></sup><sup id="cite_ref-pmid27663141_68-1" class="reference"><a href="#cite_note-pmid27663141-68"><span class="cite-bracket">[</span>68<span class="cite-bracket">]</span></a></sup> Increased oxidative DNA damage in the brain is associated with <a href="/wiki/Biochemistry_of_Alzheimer%27s_disease" title="Biochemistry of Alzheimer's disease">Alzheimer's disease</a> and <a href="/wiki/Pathophysiology_of_Parkinson%27s_disease" title="Pathophysiology of Parkinson's disease">Parkinson's disease</a>.<sup id="cite_ref-pmid21550379_70-1" class="reference"><a href="#cite_note-pmid21550379-70"><span class="cite-bracket">[</span>70<span class="cite-bracket">]</span></a></sup> Defective DNA repair has been linked to neurodegenerative disorders such as Alzheimer's disease, <a href="/wiki/Genetics_of_amyotrophic_lateral_sclerosis" title="Genetics of amyotrophic lateral sclerosis">amyotrophic lateral sclerosis</a>, <a href="/wiki/Ataxia_telangiectasia" class="mw-redirect" title="Ataxia telangiectasia">ataxia telangiectasia</a>, <a href="/wiki/Cockayne_syndrome" title="Cockayne syndrome">Cockayne syndrome</a>, Parkinson's disease and <a href="/wiki/Xeroderma_pigmentosum" title="Xeroderma pigmentosum">xeroderma pigmentosum</a>.<sup id="cite_ref-pmid21550379_70-2" class="reference"><a href="#cite_note-pmid21550379-70"><span class="cite-bracket">[</span>70<span class="cite-bracket">]</span></a></sup><sup id="cite_ref-pmid25033177_69-1" class="reference"><a href="#cite_note-pmid25033177-69"><span class="cite-bracket">[</span>69<span class="cite-bracket">]</span></a></sup> </p> <div class="mw-heading mw-heading4"><h4 id="Axonal_transport">Axonal transport</h4><span class="mw-editsection"><span class="mw-editsection-bracket">[</span><a href="/w/index.php?title=Neurodegenerative_disease&action=edit&section=21" title="Edit section: Axonal transport"><span>edit</span></a><span class="mw-editsection-bracket">]</span></span></div> <link rel="mw-deduplicated-inline-style" href="mw-data:TemplateStyles:r1236090951"><div role="note" class="hatnote navigation-not-searchable">Main article: <a href="/wiki/Axonal_transport" title="Axonal transport">Axonal transport</a></div> <p>Axonal swelling, and <a href="/wiki/Axonal_spheroid" class="mw-redirect" title="Axonal spheroid">axonal spheroids</a> have been observed in many different neurodegenerative diseases. This suggests that defective axons are not only present in diseased neurons, but also that they may cause certain pathological insult due to accumulation of organelles. <a href="/wiki/Axonal_transport" title="Axonal transport">Axonal transport</a> can be disrupted by a variety of mechanisms including damage to: <a href="/wiki/Kinesin" title="Kinesin">kinesin</a> and <a href="/wiki/Cytoplasmic_dynein" class="mw-redirect" title="Cytoplasmic dynein">cytoplasmic dynein</a>, <a href="/wiki/Microtubules" class="mw-redirect" title="Microtubules">microtubules</a>, cargoes, and <a href="/wiki/Mitochondria" class="mw-redirect" title="Mitochondria">mitochondria</a>.<sup id="cite_ref-devos_25-2" class="reference"><a href="#cite_note-devos-25"><span class="cite-bracket">[</span>25<span class="cite-bracket">]</span></a></sup> When axonal transport is severely disrupted a degenerative pathway known as <a href="/wiki/Wallerian_degeneration" title="Wallerian degeneration">Wallerian-like degeneration</a> is often triggered.<sup id="cite_ref-71" class="reference"><a href="#cite_note-71"><span class="cite-bracket">[</span>71<span class="cite-bracket">]</span></a></sup> </p> <div class="mw-heading mw-heading3"><h3 id="Programmed_cell_death">Programmed cell death</h3><span class="mw-editsection"><span class="mw-editsection-bracket">[</span><a href="/w/index.php?title=Neurodegenerative_disease&action=edit&section=22" title="Edit section: Programmed cell death"><span>edit</span></a><span class="mw-editsection-bracket">]</span></span></div> <p><a href="/wiki/Programmed_cell_death" title="Programmed cell death">Programmed cell death</a> (PCD) is death of a <a href="/wiki/Cell_(biology)" title="Cell (biology)">cell</a> in any form, mediated by an intracellular program.<sup id="cite_ref-engelberg_72-0" class="reference"><a href="#cite_note-engelberg-72"><span class="cite-bracket">[</span>72<span class="cite-bracket">]</span></a></sup> This process can be activated in neurodegenerative diseases including Parkinson's disease, amytrophic lateral sclerosis, Alzheimer's disease and Huntington's disease.<sup id="cite_ref-Nature_73-0" class="reference"><a href="#cite_note-Nature-73"><span class="cite-bracket">[</span>73<span class="cite-bracket">]</span></a></sup> PCD observed in neurodegenerative diseases may be directly pathogenic; alternatively, PCD may occur in response to other injury or disease processes.<sup id="cite_ref-bredesen_10-1" class="reference"><a href="#cite_note-bredesen-10"><span class="cite-bracket">[</span>10<span class="cite-bracket">]</span></a></sup> </p> <div class="mw-heading mw-heading4"><h4 id="Apoptosis_(type_I)"><span id="Apoptosis_.28type_I.29"></span>Apoptosis (type I)</h4><span class="mw-editsection"><span class="mw-editsection-bracket">[</span><a href="/w/index.php?title=Neurodegenerative_disease&action=edit&section=23" title="Edit section: Apoptosis (type I)"><span>edit</span></a><span class="mw-editsection-bracket">]</span></span></div> <p><a href="/wiki/Apoptosis" title="Apoptosis">Apoptosis</a> is a form of programmed cell death in multicellular organisms. It is one of the main types of programmed cell death (PCD) and involves a series of biochemical events leading to a characteristic cell morphology and death. </p> <ul><li><b>Extrinsic apoptotic pathways:</b> Occur when factors outside the cell activate cell surface death receptors (e.g., Fas) that result in the activation of <a href="/wiki/Caspases" class="mw-redirect" title="Caspases">caspases</a>-8 or -10.<sup id="cite_ref-bredesen_10-2" class="reference"><a href="#cite_note-bredesen-10"><span class="cite-bracket">[</span>10<span class="cite-bracket">]</span></a></sup></li> <li><b>Intrinsic apoptotic pathways:</b> Result from mitochondrial release of <a href="/wiki/Cytochrome_c" title="Cytochrome c">cytochrome c</a> or endoplasmic reticulum malfunctions, each leading to the activation of caspase-9. The <a href="/wiki/Cell_nucleus" title="Cell nucleus">nucleus</a> and <a href="/wiki/Golgi_apparatus" title="Golgi apparatus">Golgi apparatus</a> are other organelles that have damage sensors, which can lead the cells down apoptotic pathways.<sup id="cite_ref-bredesen_10-3" class="reference"><a href="#cite_note-bredesen-10"><span class="cite-bracket">[</span>10<span class="cite-bracket">]</span></a></sup><sup id="cite_ref-green_74-0" class="reference"><a href="#cite_note-green-74"><span class="cite-bracket">[</span>74<span class="cite-bracket">]</span></a></sup></li></ul> <p><a href="/wiki/Caspases" class="mw-redirect" title="Caspases">Caspases</a> (cysteine-aspartic acid proteases) cleave at very specific <a href="/wiki/Amino_acid" title="Amino acid">amino acid</a> residues. There are two types of caspases: <b>initiators</b> and <b>effectors</b>. Initiator caspases cleave inactive forms of effector caspases. This activates the effectors that in turn cleave other proteins resulting in apoptotic initiation.<sup id="cite_ref-bredesen_10-4" class="reference"><a href="#cite_note-bredesen-10"><span class="cite-bracket">[</span>10<span class="cite-bracket">]</span></a></sup> </p> <div class="mw-heading mw-heading4"><h4 id="Autophagic_(type_II)"><span id="Autophagic_.28type_II.29"></span>Autophagic (type II)</h4><span class="mw-editsection"><span class="mw-editsection-bracket">[</span><a href="/w/index.php?title=Neurodegenerative_disease&action=edit&section=24" title="Edit section: Autophagic (type II)"><span>edit</span></a><span class="mw-editsection-bracket">]</span></span></div> <p>Autophagy is a form of intracellular <a href="/wiki/Phagocytosis" title="Phagocytosis">phagocytosis</a> in which a cell actively consumes damaged organelles or misfolded proteins by encapsulating them into an <a href="/wiki/Autophagosome" title="Autophagosome">autophagosome</a>, which fuses with a lysosome to destroy the contents of the autophagosome. Because many neurodegenerative diseases show unusual protein aggregates, it is hypothesized that defects in autophagy could be a common mechanism of neurodegeneration.<sup id="cite_ref-bredesen_10-5" class="reference"><a href="#cite_note-bredesen-10"><span class="cite-bracket">[</span>10<span class="cite-bracket">]</span></a></sup> </p> <div class="mw-heading mw-heading4"><h4 id="Cytoplasmic_(type_III)"><span id="Cytoplasmic_.28type_III.29"></span>Cytoplasmic (type III)</h4><span class="mw-editsection"><span class="mw-editsection-bracket">[</span><a href="/w/index.php?title=Neurodegenerative_disease&action=edit&section=25" title="Edit section: Cytoplasmic (type III)"><span>edit</span></a><span class="mw-editsection-bracket">]</span></span></div> <p>PCD can also occur via non-apoptotic processes, also known as Type III or cytoplasmic cell death. For example, type III PCD might be caused by trophotoxicity, or hyperactivation of trophic factor receptors. Cytotoxins that induce PCD can cause <a href="/wiki/Necrosis" title="Necrosis">necrosis</a> at low concentrations, or aponecrosis (combination of apoptosis and necrosis) at higher concentrations. It is still unclear exactly what combination of apoptosis, non-apoptosis, and necrosis causes different kinds of aponecrosis.<sup id="cite_ref-bredesen_10-6" class="reference"><a href="#cite_note-bredesen-10"><span class="cite-bracket">[</span>10<span class="cite-bracket">]</span></a></sup> </p> <div class="mw-heading mw-heading3"><h3 id="Transglutaminase">Transglutaminase</h3><span class="mw-editsection"><span class="mw-editsection-bracket">[</span><a href="/w/index.php?title=Neurodegenerative_disease&action=edit&section=26" title="Edit section: Transglutaminase"><span>edit</span></a><span class="mw-editsection-bracket">]</span></span></div> <p><a href="/wiki/Transglutaminase" title="Transglutaminase">Transglutaminases</a> are human <a href="/wiki/Enzymes" class="mw-redirect" title="Enzymes">enzymes</a> <a href="/wiki/Ubiquitously" class="mw-redirect" title="Ubiquitously">ubiquitously</a> present in the human body and in the brain in particular.<sup id="cite_ref-caccamo_75-0" class="reference"><a href="#cite_note-caccamo-75"><span class="cite-bracket">[</span>75<span class="cite-bracket">]</span></a></sup> </p><p>The main function of transglutaminases is <a href="/wiki/Molecular_binding" title="Molecular binding">bind</a> proteins and peptides intra- and intermolecularly, by a type of <a href="/wiki/Covalent_bonds" class="mw-redirect" title="Covalent bonds">covalent bonds</a> termed <a href="/wiki/Isopeptide_bond" title="Isopeptide bond">isopeptide bonds</a>, in a reaction termed <a href="/wiki/Isopeptide_bond" title="Isopeptide bond">transamidation</a> or <a href="/wiki/Isopeptide_bond" title="Isopeptide bond">crosslinking</a>.<sup id="cite_ref-caccamo_75-1" class="reference"><a href="#cite_note-caccamo-75"><span class="cite-bracket">[</span>75<span class="cite-bracket">]</span></a></sup> </p><p>Transglutaminase <a href="/wiki/Chemical_bond" title="Chemical bond">binding</a> of these proteins and peptides make them clump together. The resulting structures are turned extremely resistant to chemical and mechanical disruption.<sup id="cite_ref-caccamo_75-2" class="reference"><a href="#cite_note-caccamo-75"><span class="cite-bracket">[</span>75<span class="cite-bracket">]</span></a></sup> </p><p>Most relevant human neurodegenerative diseases share the property of having <a href="/wiki/Protein_aggregation" title="Protein aggregation">abnormal structures made up of proteins and peptides</a>.<sup id="cite_ref-caccamo_75-3" class="reference"><a href="#cite_note-caccamo-75"><span class="cite-bracket">[</span>75<span class="cite-bracket">]</span></a></sup> </p><p>Each of these neurodegenerative diseases have one (or several) specific main protein or peptide. In <a href="/wiki/Alzheimer%27s_disease" title="Alzheimer's disease">Alzheimer's disease</a>, these are <a href="/wiki/Amyloid-beta" class="mw-redirect" title="Amyloid-beta">amyloid-beta</a> and <a href="/wiki/Tau" title="Tau">tau</a>. In <a href="/wiki/Parkinson%27s" class="mw-redirect" title="Parkinson's">Parkinson's</a> disease, it is <a href="/wiki/Alpha-synuclein" title="Alpha-synuclein">alpha-synuclein</a>. In <a href="/wiki/Huntington%27s" class="mw-redirect" title="Huntington's">Huntington's</a> disease, it is <a href="/wiki/Huntingtin" title="Huntingtin">huntingtin</a>.<sup id="cite_ref-caccamo_75-4" class="reference"><a href="#cite_note-caccamo-75"><span class="cite-bracket">[</span>75<span class="cite-bracket">]</span></a></sup> </p><p><b><a href="/wiki/Transglutaminase" title="Transglutaminase">Transglutaminase</a> <a href="/wiki/Substrate_(chemistry)" title="Substrate (chemistry)">substrates</a>:</b> <a href="/wiki/Amyloid-beta" class="mw-redirect" title="Amyloid-beta">Amyloid-beta</a>, <a href="/wiki/Tau" title="Tau">tau</a>, <a href="/wiki/Alpha-synuclein" title="Alpha-synuclein">alpha-synuclein</a> and <a href="/wiki/Huntingtin" title="Huntingtin">huntingtin</a> have been proved to be <a href="/wiki/Substrate_(chemistry)" title="Substrate (chemistry)">substrates</a> of <a href="/wiki/Transglutaminases" class="mw-redirect" title="Transglutaminases">transglutaminases</a> in vitro or in vivo, that is, they can be <a href="/wiki/Chemical_bond" title="Chemical bond">bonded</a> by trasglutaminases by <a href="/wiki/Covalent_bonds" class="mw-redirect" title="Covalent bonds">covalent bonds</a> to each other and potentially to any other transglutaminase substrate in the brain.<sup id="cite_ref-caccamo_75-5" class="reference"><a href="#cite_note-caccamo-75"><span class="cite-bracket">[</span>75<span class="cite-bracket">]</span></a></sup> </p><p><b><a href="/wiki/Transglutaminase" title="Transglutaminase">Transglutaminase</a> augmented expression:</b> It has been proved that in these neurodegenerative diseases (Alzheimer's disease, Parkinson's disease, and Huntington's disease) the <a href="/wiki/Gene_expression" title="Gene expression">expression</a> of the <a href="/wiki/Transglutaminase" title="Transglutaminase">transglutaminase</a> <a href="/wiki/Enzyme" title="Enzyme">enzyme</a> is increased.<sup id="cite_ref-caccamo_75-6" class="reference"><a href="#cite_note-caccamo-75"><span class="cite-bracket">[</span>75<span class="cite-bracket">]</span></a></sup> </p><p><b>Presence of <a href="/wiki/Isopeptide_bond" title="Isopeptide bond">isopeptide bonds</a> in these structures:</b> The presence of <a href="/wiki/Isopeptide_bond" title="Isopeptide bond">isopeptide bonds</a> (the result of the <a href="/wiki/Transglutaminase" title="Transglutaminase">transglutaminase</a> reaction) have been detected in the <a href="/wiki/Protein_aggregation" title="Protein aggregation">abnormal structures that are characteristic of these neurodegenerative diseases</a>.<sup id="cite_ref-caccamo_75-7" class="reference"><a href="#cite_note-caccamo-75"><span class="cite-bracket">[</span>75<span class="cite-bracket">]</span></a></sup> </p><p><b>Co-localization:</b> Co-localization of transglutaminase mediated <a href="/wiki/Isopeptide_bond" title="Isopeptide bond">isopeptide bonds</a> with these <a href="/wiki/Protein_aggregation" title="Protein aggregation">abnormal structures</a> has been detected in the autopsy of brains of patients with these diseases.<sup id="cite_ref-caccamo_75-8" class="reference"><a href="#cite_note-caccamo-75"><span class="cite-bracket">[</span>75<span class="cite-bracket">]</span></a></sup> </p> <div class="mw-heading mw-heading2"><h2 id="Management">Management</h2><span class="mw-editsection"><span class="mw-editsection-bracket">[</span><a href="/w/index.php?title=Neurodegenerative_disease&action=edit&section=27" title="Edit section: Management"><span>edit</span></a><span class="mw-editsection-bracket">]</span></span></div> <p>The process of neurodegeneration is not well understood, so the diseases that stem from it have, as yet, no cures. </p> <div class="mw-heading mw-heading3"><h3 id="Animal_models_in_research">Animal models in research</h3><span class="mw-editsection"><span class="mw-editsection-bracket">[</span><a href="/w/index.php?title=Neurodegenerative_disease&action=edit&section=28" title="Edit section: Animal models in research"><span>edit</span></a><span class="mw-editsection-bracket">]</span></span></div> <p>In the search for effective treatments (as opposed to <a href="/wiki/Palliative_care" title="Palliative care">palliative care</a>), investigators employ <a href="/wiki/Animal_model" class="mw-redirect" title="Animal model">animal models</a> of disease to test potential therapeutic agents. Model organisms provide an inexpensive and relatively quick means to perform two main functions: target identification and target validation. Together, these help show the value of any specific therapeutic strategies and drugs when attempting to ameliorate disease severity. An example is the drug <a href="/wiki/Dimebon" class="mw-redirect" title="Dimebon">Dimebon</a> by Medivation, Inc. In 2009 this drug was in phase III clinical trials for use in Alzheimer's disease, and also phase II clinical trials for use in Huntington's disease.<sup id="cite_ref-marsh_61-2" class="reference"><a href="#cite_note-marsh-61"><span class="cite-bracket">[</span>61<span class="cite-bracket">]</span></a></sup> In March 2010, the results of a clinical trial phase III were released; the investigational Alzheimer's disease drug Dimebon failed in the pivotal CONNECTION trial of patients with mild-to-moderate disease.<sup id="cite_ref-76" class="reference"><a href="#cite_note-76"><span class="cite-bracket">[</span>76<span class="cite-bracket">]</span></a></sup> With CONCERT, the remaining Pfizer and Medivation Phase III trial for Dimebon (latrepirdine) in Alzheimer's disease failed in 2012, effectively ending the development in this indication.<sup id="cite_ref-Sweetlove12_77-0" class="reference"><a href="#cite_note-Sweetlove12-77"><span class="cite-bracket">[</span>77<span class="cite-bracket">]</span></a></sup> </p><p>In another experiment using a rat model of Alzheimer's disease, it was demonstrated that systemic administration of hypothalamic proline-rich peptide (PRP)-1 offers neuroprotective effects and can prevent neurodegeneration in hippocampus <a href="/wiki/Amyloid-beta" class="mw-redirect" title="Amyloid-beta">amyloid-beta</a> 25–35. This suggests that there could be therapeutic value to PRP-1.<sup id="cite_ref-galoyan_78-0" class="reference"><a href="#cite_note-galoyan-78"><span class="cite-bracket">[</span>78<span class="cite-bracket">]</span></a></sup> </p> <div class="mw-heading mw-heading3"><h3 id="Other_avenues_of_investigation">Other avenues of investigation</h3><span class="mw-editsection"><span class="mw-editsection-bracket">[</span><a href="/w/index.php?title=Neurodegenerative_disease&action=edit&section=29" title="Edit section: Other avenues of investigation"><span>edit</span></a><span class="mw-editsection-bracket">]</span></span></div> <p>Protein degradation offers therapeutic options both in preventing the synthesis and degradation of irregular proteins. There is also interest in upregulating autophagy to help clear protein aggregates implicated in neurodegeneration. Both of these options involve very complex pathways that we are only beginning to understand.<sup id="cite_ref-rubinsztein_9-8" class="reference"><a href="#cite_note-rubinsztein-9"><span class="cite-bracket">[</span>9<span class="cite-bracket">]</span></a></sup> </p><p>The goal of <a href="/wiki/Immunotherapy" title="Immunotherapy">immunotherapy</a> is to enhance aspects of the immune system. Both active and passive vaccinations have been proposed for Alzheimer's disease and other conditions; however, more research must be done to prove safety and efficacy in humans.<sup id="cite_ref-brody_79-0" class="reference"><a href="#cite_note-brody-79"><span class="cite-bracket">[</span>79<span class="cite-bracket">]</span></a></sup> </p><p>A current therapeutic target for the treatment of Alzheimer's disease is the protease β-secretase<sup id="cite_ref-80" class="reference"><a href="#cite_note-80"><span class="cite-bracket">[</span>80<span class="cite-bracket">]</span></a></sup><sup class="noprint Inline-Template noprint Template-Fact" style="white-space:nowrap;">[<i><a href="/wiki/Wikipedia:No_original_research#Primary,_secondary_and_tertiary_sources" title="Wikipedia:No original research"><span title="This claim needs references to reliable secondary sources. (May 2020)">non-primary source needed</span></a></i>]</sup>, which is involved in the amyloidogenic processing pathway that leads to the pathological accumulation of proteins in the brain. When the gene that encodes for amyloid precursor protein (APP) is spliced by α-secretase<sup id="cite_ref-81" class="reference"><a href="#cite_note-81"><span class="cite-bracket">[</span>81<span class="cite-bracket">]</span></a></sup><sup class="noprint Inline-Template noprint Template-Fact" style="white-space:nowrap;">[<i><a href="/wiki/Wikipedia:No_original_research#Primary,_secondary_and_tertiary_sources" title="Wikipedia:No original research"><span title="This claim needs references to reliable secondary sources. (May 2020)">non-primary source needed</span></a></i>]</sup> rather than β-secretase, the toxic protein β amyloid is not produced. Targeted inhibition<sup id="cite_ref-82" class="reference"><a href="#cite_note-82"><span class="cite-bracket">[</span>82<span class="cite-bracket">]</span></a></sup> of β-secretase can potentially prevent the neuronal death that is responsible for the symptoms of Alzheimer's disease. </p><p>Dr. Antonio Barbera, a former <a href="/wiki/Obstetrics_and_gynaecology" title="Obstetrics and gynaecology">obstetrics and gynaecology</a> doctor, is prescribing <a href="/wiki/Table_tennis" title="Table tennis">table tennis</a> for patients who are suffering from a serious <a href="/wiki/Neurological_disorder" title="Neurological disorder">neurological disorder</a>.<sup id="cite_ref-83" class="reference"><a href="#cite_note-83"><span class="cite-bracket">[</span>83<span class="cite-bracket">]</span></a></sup> </p> <div class="mw-heading mw-heading2"><h2 id="See_also">See also</h2><span class="mw-editsection"><span class="mw-editsection-bracket">[</span><a href="/w/index.php?title=Neurodegenerative_disease&action=edit&section=30" title="Edit section: See also"><span>edit</span></a><span class="mw-editsection-bracket">]</span></span></div> <ul><li><a href="/wiki/Amyloid" title="Amyloid">Amyloid</a></li> <li><a href="/wiki/JUNQ_and_IPOD" title="JUNQ and IPOD">JUNQ and IPOD</a></li> <li><a href="/wiki/Neurodegeneration_with_brain_iron_accumulation" title="Neurodegeneration with brain iron accumulation">Neurodegeneration with brain iron accumulation</a></li> <li><a href="/wiki/Prevention_of_dementia" title="Prevention of dementia">Prevention of dementia</a></li></ul> <div class="mw-heading mw-heading2"><h2 id="References">References</h2><span class="mw-editsection"><span class="mw-editsection-bracket">[</span><a href="/w/index.php?title=Neurodegenerative_disease&action=edit&section=31" title="Edit section: References"><span>edit</span></a><span class="mw-editsection-bracket">]</span></span></div> <style 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January 12, 2024.</cite><span title="ctx_ver=Z39.88-2004&rft_val_fmt=info%3Aofi%2Ffmt%3Akev%3Amtx%3Ajournal&rft.genre=article&rft.atitle=Colorado+doctor+prescribes+ping+pong+treatment+for+neurodegenerative+disorders%3A+%27Doing+something+good%27&rft.date=2024-01-12&rft_id=https%3A%2F%2Fwww.foxnews.com%2Fhealth%2Fcolorado-doctor-prescribes-pingpong-treatment-neurodegenerative-disorders-something-good&rfr_id=info%3Asid%2Fen.wikipedia.org%3ANeurodegenerative+disease" class="Z3988"></span></span> </li> </ol></div></div> <div class="navbox-styles"><style data-mw-deduplicate="TemplateStyles:r1236075235">.mw-parser-output .navbox{box-sizing:border-box;border:1px solid #a2a9b1;width:100%;clear:both;font-size:88%;text-align:center;padding:1px;margin:1em auto 0}.mw-parser-output .navbox .navbox{margin-top:0}.mw-parser-output .navbox+.navbox,.mw-parser-output .navbox+.navbox-styles+.navbox{margin-top:-1px}.mw-parser-output .navbox-inner,.mw-parser-output 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ol>li:first-child::before,.mw-parser-output .hlist dt ol>li:first-child::before,.mw-parser-output .hlist li ol>li:first-child::before{content:" ("counter(listitem)"\a0 "}</style></div><div role="navigation" class="navbox" aria-label="Navbox" style="width:100%; margin:0.5em 0 0.5em 0;;padding:3px"><table class="nowraplinks navbox-inner" style="border-spacing:0;background:transparent;color:inherit"><tbody><tr><th scope="row" class="navbox-group" style="width:1%;background: #EAECF0;color:black;">Classification</th><td class="navbox-list-with-group navbox-list navbox-odd" style="width:100%;padding:0"><div style="padding:0 0.25em"><div style="position:relative; float:right; font-size:0.8em;"><a href="https://www.wikidata.org/wiki/Q1755122" class="extiw" title="d:Q1755122">D</a></div><div class="hlist" style="text-align:left;"><ul><li><b><a href="/wiki/International_Statistical_Classification_of_Diseases_and_Related_Health_Problems" class="mw-redirect" title="International Statistical Classification of Diseases and Related Health Problems">ICD</a>-<a href="/wiki/ICD-10" title="ICD-10">10</a></b>: <a rel="nofollow" class="external text" href="https://icd.who.int/browse10/2019/en#/G30">G30</a>-<a rel="nofollow" class="external text" href="https://icd.who.int/browse10/2019/en#/G32">G32</a></li><li><b><a href="/wiki/Medical_Subject_Headings" title="Medical Subject Headings">MeSH</a></b>: <a rel="nofollow" class="external text" href="https://meshb.nlm.nih.gov/record/ui?ui=D019636">D019636</a></li></ul></div></div></td></tr></tbody></table></div> <div class="navbox-styles"><link rel="mw-deduplicated-inline-style" href="mw-data:TemplateStyles:r1129693374"><link rel="mw-deduplicated-inline-style" href="mw-data:TemplateStyles:r1236075235"></div><div role="navigation" class="navbox" aria-labelledby="Diseases_of_the_nervous_system,_primarily_CNS" style="padding:3px"><table class="nowraplinks mw-collapsible autocollapse navbox-inner" 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.navbar-ct-full{font-size:114%;margin:0 7em}.mw-parser-output .navbar-ct-mini{font-size:114%;margin:0 4em}html.skin-theme-clientpref-night .mw-parser-output .navbar li a abbr{color:var(--color-base)!important}@media(prefers-color-scheme:dark){html.skin-theme-clientpref-os .mw-parser-output .navbar li a abbr{color:var(--color-base)!important}}@media print{.mw-parser-output .navbar{display:none!important}}</style><div class="navbar plainlinks hlist navbar-mini"><ul><li class="nv-view"><a href="/wiki/Template:Central_nervous_system_disease" title="Template:Central nervous system disease"><abbr title="View this template">v</abbr></a></li><li class="nv-talk"><a href="/wiki/Template_talk:Central_nervous_system_disease" title="Template talk:Central nervous system disease"><abbr title="Discuss this template">t</abbr></a></li><li class="nv-edit"><a href="/wiki/Special:EditPage/Template:Central_nervous_system_disease" title="Special:EditPage/Template:Central nervous system disease"><abbr title="Edit this template">e</abbr></a></li></ul></div><div id="Diseases_of_the_nervous_system,_primarily_CNS" style="font-size:114%;margin:0 4em">Diseases of the <a href="/wiki/Nervous_system" title="Nervous system">nervous system</a>, primarily <a href="/wiki/Central_nervous_system_disease" title="Central nervous system disease">CNS</a></div></th></tr><tr><th scope="row" class="navbox-group" style="width:1%"><a href="/wiki/Inflammation" title="Inflammation">Inflammation</a></th><td class="navbox-list-with-group navbox-list navbox-odd hlist" style="width:100%;padding:0"><div style="padding:0 0.25em"></div><table class="nowraplinks navbox-subgroup" style="border-spacing:0"><tbody><tr><th id="Brain" scope="row" class="navbox-group" style="width:1%"><a href="/wiki/Human_brain" title="Human brain">Brain</a></th><td class="navbox-list-with-group navbox-list navbox-odd" style="width:100%;padding:0"><div style="padding:0 0.25em"> <ul><li><a href="/wiki/Encephalitis" title="Encephalitis">Encephalitis</a> <ul><li><a href="/wiki/Viral_encephalitis" title="Viral encephalitis">Viral encephalitis</a></li> <li><a href="/wiki/Herpesviral_encephalitis" class="mw-redirect" title="Herpesviral encephalitis">Herpesviral encephalitis</a></li> <li><a href="/wiki/Limbic_encephalitis" title="Limbic encephalitis">Limbic encephalitis</a></li> <li><a href="/wiki/Encephalitis_lethargica" title="Encephalitis lethargica">Encephalitis lethargica</a></li></ul></li> <li><a href="/wiki/Cavernous_sinus_thrombosis" title="Cavernous sinus thrombosis">Cavernous sinus thrombosis</a></li> <li><a href="/wiki/Brain_abscess" title="Brain abscess">Brain abscess</a> <ul><li><a href="/wiki/Amoebic_brain_abscess" title="Amoebic brain abscess">Amoebic</a></li></ul></li></ul> </div></td></tr><tr><th scope="row" class="navbox-group" style="width:1%">Brain and <a href="/wiki/Spinal_cord" title="Spinal cord">spinal cord</a></th><td class="navbox-list-with-group navbox-list navbox-even" style="width:100%;padding:0"><div style="padding:0 0.25em"> <ul><li><a href="/wiki/Encephalomyelitis" title="Encephalomyelitis">Encephalomyelitis</a> <ul><li><a href="/wiki/Acute_disseminated_encephalomyelitis" title="Acute disseminated encephalomyelitis">Acute disseminated</a></li></ul></li> <li><a href="/wiki/Meningitis" title="Meningitis">Meningitis</a></li> <li><a href="/wiki/Meningoencephalitis" title="Meningoencephalitis">Meningoencephalitis</a></li></ul> </div></td></tr></tbody></table><div></div></td></tr><tr><th scope="row" class="navbox-group" style="width:1%"><a href="/wiki/Human_brain" title="Human brain">Brain</a>/<br /><a href="/wiki/Encephalopathy" title="Encephalopathy">encephalopathy</a></th><td class="navbox-list-with-group navbox-list navbox-odd hlist" style="width:100%;padding:0"><div style="padding:0 0.25em"></div><table class="nowraplinks navbox-subgroup" style="border-spacing:0"><tbody><tr><th scope="row" class="navbox-group" style="width:1%"><a class="mw-selflink selflink">Degenerative</a></th><td class="navbox-list-with-group navbox-list navbox-odd" style="width:100%;padding:0"><div style="padding:0 0.25em"></div><table class="nowraplinks navbox-subgroup" style="border-spacing:0"><tbody><tr><th scope="row" class="navbox-group" style="width:1%"><a href="/wiki/Extrapyramidal_system" title="Extrapyramidal system">Extrapyramidal</a> and<br /><a href="/wiki/Movement_disorders" class="mw-redirect" title="Movement disorders">movement disorders</a></th><td class="navbox-list-with-group navbox-list navbox-odd" style="width:100%;padding:0"><div style="padding:0 0.25em"> <ul><li><a href="/wiki/Basal_ganglia_disease" title="Basal ganglia disease">Basal ganglia disease</a> <ul><li><a href="/wiki/Parkinsonism" title="Parkinsonism">Parkinsonism</a> <ul><li><a href="/wiki/Parkinson%27s_disease" title="Parkinson's disease">PD</a></li> <li><a href="/wiki/Postencephalitic_parkinsonism" class="mw-redirect" title="Postencephalitic parkinsonism">Postencephalitic</a></li> <li><a href="/wiki/Neuroleptic_malignant_syndrome" title="Neuroleptic malignant syndrome">NMS</a></li></ul></li> <li><a href="/wiki/Neurodegeneration_with_brain_iron_accumulation" title="Neurodegeneration with brain iron accumulation">NBIA</a> <ul><li><a href="/wiki/Pantothenate_kinase-associated_neurodegeneration" title="Pantothenate kinase-associated neurodegeneration">PKAN</a></li></ul></li> <li><a href="/wiki/Tauopathy" title="Tauopathy">Tauopathy</a> <ul><li><a href="/wiki/Progressive_supranuclear_palsy" title="Progressive supranuclear palsy">PSP</a></li></ul></li> <li><a href="/wiki/Multiple_system_atrophy" title="Multiple system atrophy">Striatonigral degeneration</a></li> <li><a href="/wiki/Hemiballismus" title="Hemiballismus">Hemiballismus</a></li> <li><a href="/wiki/Huntington%27s_disease" title="Huntington's disease">HD</a></li> <li><a href="/wiki/Olivopontocerebellar_atrophy" class="mw-redirect" title="Olivopontocerebellar atrophy">OA</a></li></ul></li></ul> <ul><li><a href="/wiki/Dyskinesia" title="Dyskinesia">Dyskinesia</a> <ul><li><a href="/wiki/Dystonia" title="Dystonia">Dystonia</a> <ul><li><a href="/wiki/Status_dystonicus" title="Status dystonicus">Status dystonicus</a></li> <li><a href="/wiki/Spasmodic_torticollis" title="Spasmodic torticollis">Spasmodic torticollis</a></li> <li><a href="/wiki/Meige%27s_syndrome" title="Meige's syndrome">Meige's</a></li> <li><a href="/wiki/Blepharospasm" title="Blepharospasm">Blepharospasm</a></li></ul></li> <li><a href="/wiki/Athetosis" title="Athetosis">Athetosis</a></li> <li><a href="/wiki/Chorea" title="Chorea">Chorea</a> <ul><li><a href="/wiki/Choreoathetosis" title="Choreoathetosis">Choreoathetosis</a></li></ul></li> <li><a href="/wiki/Myoclonus" title="Myoclonus">Myoclonus</a> <ul><li><a href="/wiki/Myoclonic_epilepsy" title="Myoclonic epilepsy">Myoclonic epilepsy</a></li></ul></li> <li><a href="/wiki/Akathisia" title="Akathisia">Akathisia</a></li></ul></li></ul> <ul><li><a href="/wiki/Tremor" title="Tremor">Tremor</a> <ul><li><a href="/wiki/Essential_tremor" title="Essential tremor">Essential tremor</a></li> <li><a href="/wiki/Intention_tremor" title="Intention tremor">Intention tremor</a></li></ul></li> <li><a href="/wiki/Restless_legs_syndrome" title="Restless legs syndrome">Restless legs</a></li> <li><a href="/wiki/Stiff-person_syndrome" title="Stiff-person syndrome">Stiff-person</a></li></ul> </div></td></tr><tr><th scope="row" class="navbox-group" style="width:1%"><a href="/wiki/Dementia" title="Dementia">Dementia</a></th><td class="navbox-list-with-group navbox-list navbox-even" style="width:100%;padding:0"><div style="padding:0 0.25em"> <ul><li><a href="/wiki/Tauopathy" title="Tauopathy">Tauopathy</a> <ul><li><a href="/wiki/Alzheimer%27s_disease" title="Alzheimer's disease">Alzheimer's</a> <ul><li><a href="/wiki/Early-onset_Alzheimer%27s_disease" title="Early-onset Alzheimer's disease">Early-onset</a></li></ul></li> <li><a href="/wiki/Primary_progressive_aphasia" title="Primary progressive aphasia">Primary progressive aphasia</a></li></ul></li> <li><a href="/wiki/Frontotemporal_dementia" title="Frontotemporal dementia">Frontotemporal dementia</a>/<a href="/wiki/Frontotemporal_lobar_degeneration" title="Frontotemporal lobar degeneration">Frontotemporal lobar degeneration</a> <ul><li><a href="/wiki/Pick%27s_disease" class="mw-redirect" title="Pick's disease">Pick's</a></li></ul></li> <li><a href="/wiki/Lewy_bodies_dementia" class="mw-redirect" title="Lewy bodies dementia">Lewy bodies dementia</a></li> <li><a href="/wiki/Posterior_cortical_atrophy" title="Posterior cortical atrophy">Posterior cortical atrophy</a></li></ul> <p><a href="/wiki/Creutzfeldt%E2%80%93Jakob_disease" title="Creutzfeldt–Jakob disease">Creutzfeldt–Jakob disease</a> </p> <ul><li><a href="/wiki/Vascular_dementia" title="Vascular dementia">Vascular dementia</a></li></ul> </div></td></tr><tr><th scope="row" class="navbox-group" style="width:1%"><a href="/wiki/Mitochondrial_disease" title="Mitochondrial disease">Mitochondrial disease</a></th><td class="navbox-list-with-group navbox-list navbox-odd" style="width:100%;padding:0"><div style="padding:0 0.25em"> <ul><li><a href="/wiki/Leigh_syndrome" title="Leigh syndrome">Leigh syndrome</a></li></ul> </div></td></tr></tbody></table><div></div></td></tr><tr><th scope="row" class="navbox-group" style="width:1%"><a href="/wiki/Demyelinating_disease" title="Demyelinating disease">Demyelinating</a></th><td class="navbox-list-with-group navbox-list navbox-even" style="width:100%;padding:0"><div style="padding:0 0.25em"> <ul><li><a href="/wiki/CNS_demyelinating_autoimmune_diseases" title="CNS demyelinating autoimmune diseases">Autoimmune</a></li> <li><a href="/wiki/Inflammatory_demyelinating_diseases_of_the_central_nervous_system" title="Inflammatory demyelinating diseases of the central nervous system">Inflammatory</a></li> <li><a href="/wiki/Multiple_sclerosis" title="Multiple sclerosis">Multiple sclerosis</a></li> <li>For more detailed coverage, see <a href="/wiki/Template:Demyelinating_diseases_of_CNS" title="Template:Demyelinating diseases of CNS">Template:Demyelinating diseases of CNS</a></li></ul> </div></td></tr><tr><th scope="row" class="navbox-group" style="width:1%">Episodic/<br /><a href="/wiki/Paroxysmal_attack" title="Paroxysmal attack">paroxysmal</a></th><td class="navbox-list-with-group navbox-list navbox-odd" style="width:100%;padding:0"><div style="padding:0 0.25em"></div><table class="nowraplinks navbox-subgroup" style="border-spacing:0"><tbody><tr><th scope="row" class="navbox-group" style="width:1%"><a href="/wiki/Epileptic_seizure" class="mw-redirect" title="Epileptic seizure">Seizures</a> and <a href="/wiki/Epilepsy" title="Epilepsy">epilepsy</a></th><td class="navbox-list-with-group navbox-list navbox-odd" style="width:100%;padding:0"><div style="padding:0 0.25em"> <ul><li><a href="/wiki/Focal_seizure" title="Focal seizure">Focal</a></li> <li><a href="/wiki/Generalized_epilepsy" title="Generalized epilepsy">Generalised</a></li> <li><a href="/wiki/Status_epilepticus" title="Status epilepticus">Status epilepticus</a></li> <li>For more detailed coverage, see <a href="/wiki/Template:Epilepsy" class="mw-redirect" title="Template:Epilepsy">Template:Epilepsy</a></li></ul> </div></td></tr><tr><th scope="row" class="navbox-group" style="width:1%"><a href="/wiki/Headache" title="Headache">Headache</a></th><td class="navbox-list-with-group navbox-list navbox-even" style="width:100%;padding:0"><div style="padding:0 0.25em"> <ul><li><a href="/wiki/Migraine" title="Migraine">Migraine</a></li> <li><a href="/wiki/Cluster_headache" title="Cluster headache">Cluster</a></li> <li><a href="/wiki/Tension_headache" title="Tension headache">Tension</a></li> <li>For more detailed coverage, see <a href="/wiki/Template:Headache" title="Template:Headache">Template:Headache</a></li></ul> </div></td></tr><tr><th scope="row" class="navbox-group" style="width:1%"><a href="/wiki/Cerebrovascular_disease" title="Cerebrovascular disease">Cerebrovascular</a></th><td class="navbox-list-with-group navbox-list navbox-odd" style="width:100%;padding:0"><div style="padding:0 0.25em"> <ul><li><a href="/wiki/Transient_ischemic_attack" title="Transient ischemic attack">TIA</a></li> <li><a href="/wiki/Stroke" title="Stroke">Stroke</a></li> <li>For more detailed coverage, see <a href="/wiki/Template:Cerebrovascular_diseases" title="Template:Cerebrovascular diseases">Template:Cerebrovascular diseases</a></li></ul> </div></td></tr><tr><th scope="row" class="navbox-group" style="width:1%">Other</th><td class="navbox-list-with-group navbox-list navbox-even" style="width:100%;padding:0"><div style="padding:0 0.25em"> <ul><li><a href="/wiki/Sleep_disorders" class="mw-redirect" title="Sleep disorders">Sleep disorders</a> <ul><li>For more detailed coverage, see <a href="/wiki/Template:Sleep" title="Template:Sleep">Template:Sleep</a></li></ul></li></ul> </div></td></tr></tbody></table><div></div></td></tr><tr><th scope="row" class="navbox-group" style="width:1%"><a href="/wiki/Cerebrospinal_fluid" title="Cerebrospinal fluid">CSF</a></th><td class="navbox-list-with-group navbox-list navbox-odd" style="width:100%;padding:0"><div style="padding:0 0.25em"> <ul><li><a href="/wiki/Intracranial_pressure" title="Intracranial pressure">Intracranial hypertension</a> <ul><li><a href="/wiki/Hydrocephalus" title="Hydrocephalus">Hydrocephalus</a></li> <li><a href="/wiki/Normal_pressure_hydrocephalus" title="Normal pressure hydrocephalus">Normal pressure hydrocephalus</a></li> <li><a href="/wiki/Choroid_plexus_papilloma" title="Choroid plexus papilloma">Choroid plexus papilloma</a></li> <li><a href="/wiki/Idiopathic_intracranial_hypertension" title="Idiopathic intracranial hypertension">Idiopathic intracranial hypertension</a></li></ul></li> <li><a href="/wiki/Cerebral_edema" title="Cerebral edema">Cerebral edema</a></li> <li><a href="/wiki/Spontaneous_cerebrospinal_fluid_leak" class="mw-redirect" title="Spontaneous cerebrospinal fluid leak">Intracranial hypotension</a></li></ul> </div></td></tr><tr><th scope="row" class="navbox-group" style="width:1%">Other</th><td class="navbox-list-with-group navbox-list navbox-even" style="width:100%;padding:0"><div style="padding:0 0.25em"> <ul><li><a href="/wiki/Brain_herniation" title="Brain herniation">Brain herniation</a></li> <li><a href="/wiki/Reye_syndrome" title="Reye syndrome">Reye syndrome</a></li> <li><a href="/wiki/Hepatic_encephalopathy" title="Hepatic encephalopathy">Hepatic encephalopathy</a></li> <li><a href="/wiki/Toxic_encephalopathy" title="Toxic encephalopathy">Toxic encephalopathy</a></li> <li><a href="/wiki/Hashimoto%27s_encephalopathy" title="Hashimoto's encephalopathy">Hashimoto's encephalopathy</a></li> <li><a href="/wiki/Fetal_alcohol_spectrum_disorder" title="Fetal alcohol spectrum disorder">Static encephalopathy</a></li></ul> </div></td></tr></tbody></table><div></div></td></tr><tr><th scope="row" class="navbox-group" style="width:1%">Both/either</th><td class="navbox-list-with-group navbox-list navbox-odd hlist" style="width:100%;padding:0"><div style="padding:0 0.25em"></div><table class="nowraplinks navbox-subgroup" style="border-spacing:0"><tbody><tr><th id="Degenerative" scope="row" class="navbox-group" style="width:1%"><a class="mw-selflink selflink">Degenerative</a></th><td class="navbox-list-with-group navbox-list navbox-odd" style="width:100%;padding:0"><div style="padding:0 0.25em"></div><table class="nowraplinks navbox-subgroup" style="border-spacing:0"><tbody><tr><th scope="row" class="navbox-group" style="width:1%"><a href="/wiki/Spinocerebellar_ataxia" title="Spinocerebellar ataxia">SA</a></th><td class="navbox-list-with-group navbox-list navbox-odd" style="width:100%;padding:0"><div style="padding:0 0.25em"> <ul><li><a href="/wiki/Friedreich%27s_ataxia" title="Friedreich's ataxia">Friedreich's ataxia</a></li> <li><a href="/wiki/Ataxia%E2%80%93telangiectasia" title="Ataxia–telangiectasia">Ataxia–telangiectasia</a></li></ul> </div></td></tr><tr><th scope="row" class="navbox-group" style="width:1%"><a href="/wiki/Motor_neuron_diseases" title="Motor neuron diseases">MND</a></th><td class="navbox-list-with-group navbox-list navbox-even" style="width:100%;padding:0"><div style="padding:0 0.25em"> <ul><li><i><a href="/wiki/Upper_motor_neuron" title="Upper motor neuron">UMN</a> only:</i> <ul><li><a href="/wiki/Primary_lateral_sclerosis" title="Primary lateral sclerosis">Primary lateral sclerosis</a></li> <li><a href="/wiki/Pseudobulbar_palsy" title="Pseudobulbar palsy">Pseudobulbar palsy</a></li> <li><a href="/wiki/Hereditary_spastic_paraplegia" title="Hereditary spastic paraplegia">Hereditary spastic paraplegia</a></li></ul></li></ul> <ul><li><i><a href="/wiki/Lower_motor_neuron" title="Lower motor neuron">LMN</a> only:</i> <ul><li><a href="/wiki/Distal_hereditary_motor_neuronopathies" title="Distal hereditary motor neuronopathies">Distal hereditary motor neuronopathies</a></li> <li><a href="/wiki/Spinal_muscular_atrophies" title="Spinal muscular atrophies">Spinal muscular atrophies</a> <ul><li><a href="/wiki/Spinal_muscular_atrophy" title="Spinal muscular atrophy">SMA</a></li> <li><a href="/wiki/Spinal_and_bulbar_muscular_atrophy" title="Spinal and bulbar muscular atrophy">SMAX1</a></li> <li><a href="/wiki/X-linked_spinal_muscular_atrophy_type_2" title="X-linked spinal muscular atrophy type 2">SMAX2</a></li> <li><a href="/wiki/Distal_spinal_muscular_atrophy_type_1" title="Distal spinal muscular atrophy type 1">DSMA1</a></li> <li><a href="/wiki/Congenital_distal_spinal_muscular_atrophy" title="Congenital distal spinal muscular atrophy">Congenital DSMA</a></li> <li>Spinal muscular atrophy with lower extremity predominance (SMALED) <ul><li><a href="/wiki/Spinal_muscular_atrophy_with_lower_extremity_predominance_1" title="Spinal muscular atrophy with lower extremity predominance 1">SMALED1</a></li> <li><a href="/wiki/Spinal_muscular_atrophy_with_lower_extremity_predominance_2A" title="Spinal muscular atrophy with lower extremity predominance 2A">SMALED2A</a></li> <li><a href="/wiki/Spinal_muscular_atrophy_with_lower_extremity_predominance_2B" title="Spinal muscular atrophy with lower extremity predominance 2B">SMALED2B</a></li></ul></li> <li><a href="/wiki/Pontocerebellar_hypoplasia" title="Pontocerebellar hypoplasia">SMA-PCH</a></li> <li><a href="/wiki/Spinal_muscular_atrophy_with_progressive_myoclonic_epilepsy" title="Spinal muscular atrophy with progressive myoclonic epilepsy">SMA-PME</a></li></ul></li> <li><a href="/wiki/Progressive_muscular_atrophy" title="Progressive muscular atrophy">Progressive muscular atrophy</a></li> <li><a href="/wiki/Progressive_bulbar_palsy" title="Progressive bulbar palsy">Progressive bulbar palsy</a> <ul><li><a href="/wiki/Fazio%E2%80%93Londe_disease" title="Fazio–Londe disease">Fazio–Londe</a></li> <li><a href="/wiki/Infantile_progressive_bulbar_palsy" title="Infantile progressive bulbar palsy">Infantile progressive bulbar palsy</a></li></ul></li></ul></li></ul> <ul><li><i>both:</i> <ul><li><a href="/wiki/Amyotrophic_lateral_sclerosis" class="mw-redirect" title="Amyotrophic lateral sclerosis">Amyotrophic lateral sclerosis</a></li></ul></li></ul> </div></td></tr></tbody></table><div></div></td></tr></tbody></table><div></div></td></tr></tbody></table></div> <div class="navbox-styles"><link rel="mw-deduplicated-inline-style" href="mw-data:TemplateStyles:r1129693374"><link rel="mw-deduplicated-inline-style" href="mw-data:TemplateStyles:r1236075235"></div><div role="navigation" class="navbox" aria-labelledby="Neuroscience" style="padding:3px"><table class="nowraplinks hlist mw-collapsible autocollapse navbox-inner" style="border-spacing:0;background:transparent;color:inherit"><tbody><tr><th scope="col" class="navbox-title" colspan="3"><link rel="mw-deduplicated-inline-style" href="mw-data:TemplateStyles:r1129693374"><link rel="mw-deduplicated-inline-style" href="mw-data:TemplateStyles:r1239400231"><div class="navbar plainlinks hlist navbar-mini"><ul><li class="nv-view"><a href="/wiki/Template:Neuroscience" title="Template:Neuroscience"><abbr title="View this template">v</abbr></a></li><li class="nv-talk"><a href="/wiki/Template_talk:Neuroscience" title="Template talk:Neuroscience"><abbr title="Discuss this template">t</abbr></a></li><li class="nv-edit"><a href="/wiki/Special:EditPage/Template:Neuroscience" title="Special:EditPage/Template:Neuroscience"><abbr title="Edit this template">e</abbr></a></li></ul></div><div id="Neuroscience" style="font-size:114%;margin:0 4em"><a href="/wiki/Neuroscience" title="Neuroscience">Neuroscience</a></div></th></tr><tr><td class="navbox-abovebelow" colspan="3"><div> <ul><li><a href="/wiki/Outline_of_neuroscience" title="Outline of neuroscience">Outline</a></li> <li><a href="/wiki/History_of_neuroscience" title="History of neuroscience">History</a></li></ul> </div></td></tr><tr><th scope="row" class="navbox-group" style="width:1%"><a href="/wiki/Basic_research" title="Basic research">Basic<br />science</a></th><td class="navbox-list-with-group navbox-list navbox-odd" style="width:100%;padding:0"><div style="padding:0 0.25em"> <ul><li><a href="/wiki/Behavioral_epigenetics" title="Behavioral epigenetics">Behavioral epigenetics</a></li> <li><a href="/wiki/Behavioural_genetics" title="Behavioural genetics">Behavioral genetics</a></li> <li><a href="/wiki/Brain_mapping" title="Brain mapping">Brain mapping</a></li> <li><a href="/wiki/Brain-reading" title="Brain-reading">Brain-reading</a></li> <li><a href="/wiki/Cellular_neuroscience" title="Cellular neuroscience">Cellular neuroscience</a></li> <li><a href="/wiki/Computational_neuroscience" title="Computational neuroscience">Computational neuroscience</a></li> <li><a href="/wiki/Connectomics" title="Connectomics">Connectomics</a></li> <li><a href="/wiki/Imaging_genetics" title="Imaging genetics">Imaging genetics</a></li> <li><a href="/wiki/Integrative_neuroscience" title="Integrative neuroscience">Integrative neuroscience</a></li> <li><a href="/wiki/Molecular_neuroscience" title="Molecular neuroscience">Molecular neuroscience</a></li> <li><a href="/wiki/Neural_decoding" title="Neural decoding">Neural decoding</a></li> <li><a href="/wiki/Neural_engineering" title="Neural engineering">Neural engineering</a></li> <li><a href="/wiki/Neuroanatomy" title="Neuroanatomy">Neuroanatomy</a></li> <li><a href="/wiki/Neurobiology" class="mw-redirect" title="Neurobiology">Neurobiology</a></li> <li><a href="/wiki/Neurochemistry" title="Neurochemistry">Neurochemistry</a></li> <li><a href="/wiki/Neuroendocrinology" title="Neuroendocrinology">Neuroendocrinology</a></li> <li><a href="/wiki/Neurogenetics" title="Neurogenetics">Neurogenetics</a></li> <li><a href="/wiki/Neuroinformatics" title="Neuroinformatics">Neuroinformatics</a></li> <li><a href="/wiki/Neurometrics" title="Neurometrics">Neurometrics</a></li> <li><a href="/wiki/Neuromorphology" title="Neuromorphology">Neuromorphology</a></li> <li><a href="/wiki/Neurophysics" title="Neurophysics">Neurophysics</a></li> <li><a href="/wiki/Neurophysiology" title="Neurophysiology">Neurophysiology</a></li> <li><a href="/wiki/Systems_neuroscience" title="Systems neuroscience">Systems neuroscience</a></li></ul> </div></td><td class="noviewer navbox-image" rowspan="5" style="width:1px;padding:0 0 0 2px"><div><span typeof="mw:File"><a href="/wiki/File:Gray739.png" class="mw-file-description"><img src="//upload.wikimedia.org/wikipedia/commons/thumb/9/96/Gray739.png/130px-Gray739.png" decoding="async" width="130" height="99" class="mw-file-element" srcset="//upload.wikimedia.org/wikipedia/commons/thumb/9/96/Gray739.png/195px-Gray739.png 1.5x, //upload.wikimedia.org/wikipedia/commons/thumb/9/96/Gray739.png/260px-Gray739.png 2x" data-file-width="500" data-file-height="379" /></a></span></div></td></tr><tr><th scope="row" class="navbox-group" style="width:1%"><a href="/wiki/Clinical_neuroscience" title="Clinical neuroscience">Clinical<br />neuroscience</a></th><td class="navbox-list-with-group navbox-list navbox-even" style="width:100%;padding:0"><div style="padding:0 0.25em"> <ul><li><a href="/wiki/Behavioral_neurology" title="Behavioral neurology">Behavioral neurology</a></li> <li><a href="/wiki/Clinical_neurophysiology" title="Clinical neurophysiology">Clinical neurophysiology</a></li> <li><a href="/wiki/Epileptology" class="mw-redirect" title="Epileptology">Epileptology</a></li> <li><a href="/wiki/Neurocardiology" title="Neurocardiology">Neurocardiology</a></li> <li><a href="/wiki/Neuroepidemiology" title="Neuroepidemiology">Neuroepidemiology</a></li> <li><a href="/wiki/Enteric_nervous_system#Function" title="Enteric nervous system">Neurogastroenterology</a></li> <li><a href="/wiki/Neuroimmunology" title="Neuroimmunology">Neuroimmunology</a></li> <li><a href="/wiki/Neurointensive_care" title="Neurointensive care">Neurointensive care</a></li> <li><a href="/wiki/Neurology" title="Neurology">Neurology</a></li> <li><a href="/wiki/Neuro-oncology" title="Neuro-oncology">Neuro-oncology</a></li> <li><a href="/wiki/Neuro-ophthalmology" title="Neuro-ophthalmology">Neuro-ophthalmology</a></li> <li><a href="/wiki/Neuropathology" title="Neuropathology">Neuropathology</a></li> <li><a href="/wiki/Neuropharmacology" title="Neuropharmacology">Neuropharmacology</a></li> <li><a href="/wiki/Neuroprosthetics" title="Neuroprosthetics">Neuroprosthetics</a></li> <li><a href="/wiki/Neuropsychiatry" title="Neuropsychiatry">Neuropsychiatry</a></li> <li><a href="/wiki/Neuroradiology" title="Neuroradiology">Neuroradiology</a></li> <li><a href="/wiki/Neurorehabilitation" title="Neurorehabilitation">Neurorehabilitation</a></li> <li><a href="/wiki/Neurosurgery" title="Neurosurgery">Neurosurgery</a></li> <li><a href="/wiki/Neurotology" title="Neurotology">Neurotology</a></li> <li><a href="/wiki/Neurovirology" title="Neurovirology">Neurovirology</a></li> <li><a href="/wiki/Nutritional_neuroscience" title="Nutritional neuroscience">Nutritional neuroscience</a></li> <li><a href="/wiki/Psychiatry" title="Psychiatry">Psychiatry</a></li></ul> </div></td></tr><tr><th scope="row" class="navbox-group" style="width:1%"><a href="/wiki/Cognitive_neuroscience" title="Cognitive neuroscience">Cognitive<br />neuroscience</a></th><td class="navbox-list-with-group navbox-list navbox-odd" style="width:100%;padding:0"><div style="padding:0 0.25em"> <ul><li><a href="/wiki/Affective_neuroscience" title="Affective neuroscience">Affective neuroscience</a></li> <li><a href="/wiki/Behavioral_neuroscience" title="Behavioral neuroscience">Behavioral neuroscience</a></li> <li><a href="/wiki/Chronobiology" title="Chronobiology">Chronobiology</a></li> <li><a href="/wiki/Molecular_cellular_cognition" title="Molecular cellular cognition">Molecular cellular cognition</a></li> <li><a href="/wiki/Motor_control" title="Motor control">Motor control</a></li> <li><a href="/wiki/Neurolinguistics" title="Neurolinguistics">Neurolinguistics</a></li> <li><a href="/wiki/Neuropsychology" title="Neuropsychology">Neuropsychology</a></li> <li><a href="/wiki/Sensory_neuroscience" title="Sensory neuroscience">Sensory neuroscience</a></li> <li><a href="/wiki/Social_cognitive_neuroscience" title="Social cognitive neuroscience">Social cognitive neuroscience</a></li></ul> </div></td></tr><tr><th scope="row" class="navbox-group" style="width:1%">Interdisciplinary<br />fields</th><td class="navbox-list-with-group navbox-list navbox-even" style="width:100%;padding:0"><div style="padding:0 0.25em"> <ul><li><a href="/wiki/Consumer_neuroscience" title="Consumer neuroscience">Consumer neuroscience</a></li> <li><a href="/wiki/Cultural_neuroscience" title="Cultural neuroscience">Cultural neuroscience</a></li> <li><a href="/wiki/Educational_neuroscience" title="Educational neuroscience">Educational neuroscience</a></li> <li><a href="/wiki/Evolutionary_neuroscience" title="Evolutionary neuroscience">Evolutionary neuroscience</a></li> <li><a href="/wiki/Global_neurosurgery" title="Global neurosurgery">Global neurosurgery</a></li> <li><a href="/wiki/Neuroanthropology" title="Neuroanthropology">Neuroanthropology</a></li> <li><a href="/wiki/Neural_engineering" title="Neural engineering">Neural engineering</a></li> <li><a href="/wiki/Neurotechnology" title="Neurotechnology">Neurobiotics</a></li> <li><a href="/wiki/Neurocriminology" title="Neurocriminology">Neurocriminology</a></li> <li><a href="/wiki/Neuroeconomics" title="Neuroeconomics">Neuroeconomics</a></li> <li><a href="/wiki/Neuroepistemology" title="Neuroepistemology">Neuroepistemology</a></li> <li><a href="/wiki/Neuroesthetics" title="Neuroesthetics">Neuroesthetics</a></li> <li><a href="/wiki/Neuroethics" title="Neuroethics">Neuroethics</a></li> <li><a href="/wiki/Neuroethology" title="Neuroethology">Neuroethology</a></li> <li><a href="/wiki/Neurohistory" title="Neurohistory">Neurohistory</a></li> <li><a href="/wiki/Neurolaw" title="Neurolaw">Neurolaw</a></li> <li><a href="/wiki/Neuromarketing" title="Neuromarketing">Neuromarketing</a></li> <li><a href="/wiki/Neuromorphic_engineering" class="mw-redirect" title="Neuromorphic engineering">Neuromorphic engineering</a></li> <li><a href="/wiki/Neurophenomenology" title="Neurophenomenology">Neurophenomenology</a></li> <li><a href="/wiki/Neurophilosophy" title="Neurophilosophy">Neurophilosophy</a></li> <li><a href="/wiki/Neuropolitics" title="Neuropolitics">Neuropolitics</a></li> <li><a href="/wiki/Neurorobotics" title="Neurorobotics">Neurorobotics</a></li> <li><a href="/wiki/Neuroscience_of_religion" title="Neuroscience of religion">Neurotheology</a></li> <li><a href="/wiki/Paleoneurobiology" title="Paleoneurobiology">Paleoneurobiology</a></li> <li><a href="/wiki/Social_neuroscience" title="Social neuroscience">Social neuroscience</a></li></ul> </div></td></tr><tr><th scope="row" class="navbox-group" style="width:1%">Concepts</th><td class="navbox-list-with-group navbox-list navbox-odd" style="width:100%;padding:0"><div style="padding:0 0.25em"> <ul><li><a href="/wiki/Brain%E2%80%93computer_interface" title="Brain–computer interface">Brain–computer interface</a></li> <li><a href="/wiki/Development_of_the_nervous_system" title="Development of the nervous system">Development of the nervous system</a></li> <li><a href="/wiki/Artificial_neural_network" class="mw-redirect" title="Artificial neural network">Neural network (artificial)</a></li> <li><a href="/wiki/Neural_circuit" title="Neural circuit">Neural network (biological)</a></li> <li><a href="/wiki/Detection_theory" title="Detection theory">Detection theory</a></li> <li><a href="/wiki/Intraoperative_neurophysiological_monitoring" title="Intraoperative neurophysiological monitoring">Intraoperative neurophysiological monitoring</a></li> <li><a href="/wiki/Neurochip" title="Neurochip">Neurochip</a></li> <li><a class="mw-selflink selflink">Neurodegenerative disease</a></li> <li><a href="/wiki/Neurodevelopmental_disorder" title="Neurodevelopmental disorder">Neurodevelopmental disorder</a></li> <li><a href="/wiki/Neurodiversity" title="Neurodiversity">Neurodiversity</a></li> <li><a href="/wiki/Neurogenesis" title="Neurogenesis">Neurogenesis</a></li> <li><a href="/wiki/Neuroimaging" title="Neuroimaging">Neuroimaging</a></li> <li><a href="/wiki/Neuroimmune_system" title="Neuroimmune system">Neuroimmune system</a></li> <li><a href="/wiki/Neuromanagement" title="Neuromanagement">Neuromanagement</a></li> <li><a href="/wiki/Neuromodulation" title="Neuromodulation">Neuromodulation</a></li> <li><a href="/wiki/Neuroplasticity" title="Neuroplasticity">Neuroplasticity</a></li> <li><a href="/wiki/Neurotechnology" title="Neurotechnology">Neurotechnology</a></li> <li><a href="/wiki/Neurotoxin" title="Neurotoxin">Neurotoxin</a></li> <li><a href="/wiki/Neural_basis_of_self" title="Neural basis of self">Self-awareness</a></li></ul> </div></td></tr><tr><td class="navbox-abovebelow hlist" colspan="3"><div> <ul><li><span class="noviewer" typeof="mw:File"><span title="Category"><img alt="" src="//upload.wikimedia.org/wikipedia/en/thumb/9/96/Symbol_category_class.svg/16px-Symbol_category_class.svg.png" decoding="async" width="16" height="16" class="mw-file-element" srcset="//upload.wikimedia.org/wikipedia/en/thumb/9/96/Symbol_category_class.svg/23px-Symbol_category_class.svg.png 1.5x, //upload.wikimedia.org/wikipedia/en/thumb/9/96/Symbol_category_class.svg/31px-Symbol_category_class.svg.png 2x" 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title="Help:Authority control">Authority control databases</a>: National <span class="mw-valign-text-top noprint" typeof="mw:File/Frameless"><a href="https://www.wikidata.org/wiki/Q1755122#identifiers" title="Edit this at Wikidata"><img alt="Edit this at Wikidata" src="//upload.wikimedia.org/wikipedia/en/thumb/8/8a/OOjs_UI_icon_edit-ltr-progressive.svg/10px-OOjs_UI_icon_edit-ltr-progressive.svg.png" decoding="async" width="10" height="10" class="mw-file-element" srcset="//upload.wikimedia.org/wikipedia/en/thumb/8/8a/OOjs_UI_icon_edit-ltr-progressive.svg/15px-OOjs_UI_icon_edit-ltr-progressive.svg.png 1.5x, //upload.wikimedia.org/wikipedia/en/thumb/8/8a/OOjs_UI_icon_edit-ltr-progressive.svg/20px-OOjs_UI_icon_edit-ltr-progressive.svg.png 2x" data-file-width="20" data-file-height="20" /></a></span></th><td class="navbox-list-with-group navbox-list navbox-odd" style="width:100%;padding:0"><div style="padding:0 0.25em"><ul><li><span class="uid"><span class="rt-commentedText tooltip tooltip-dotted" title="Nervendegeneration"><a rel="nofollow" class="external text" href="https://d-nb.info/gnd/4300182-8">Germany</a></span></span></li><li><span class="uid"><a rel="nofollow" class="external text" href="https://id.loc.gov/authorities/sh85090923">United States</a></span></li><li><span class="uid"><span class="rt-commentedText tooltip tooltip-dotted" title="Système nerveux -- Dégénérescence"><a rel="nofollow" class="external text" href="https://catalogue.bnf.fr/ark:/12148/cb11965374p">France</a></span></span></li><li><span class="uid"><span class="rt-commentedText tooltip tooltip-dotted" title="Système nerveux -- Dégénérescence"><a rel="nofollow" class="external text" href="https://data.bnf.fr/ark:/12148/cb11965374p">BnF data</a></span></span></li><li><span class="uid"><span class="rt-commentedText tooltip tooltip-dotted" title="neurodegenerace"><a rel="nofollow" class="external text" href="https://aleph.nkp.cz/F/?func=find-c&local_base=aut&ccl_term=ica=ph255239&CON_LNG=ENG">Czech Republic</a></span></span><ul><li><span class="uid"><span class="rt-commentedText tooltip tooltip-dotted" title="neurodegenerativní onemocnění"><a rel="nofollow" class="external text" href="https://aleph.nkp.cz/F/?func=find-c&local_base=aut&ccl_term=ica=ph123254&CON_LNG=ENG">2</a></span></span></li></ul></li><li><span class="uid"><span class="rt-commentedText tooltip tooltip-dotted" title="Degeneración (Patología)"><a rel="nofollow" class="external text" href="http://catalogo.bne.es/uhtbin/authoritybrowse.cgi?action=display&authority_id=XX548538">Spain</a></span></span></li><li><span class="uid"><span class="rt-commentedText tooltip tooltip-dotted" title="Nervu sistēmas deģenerācija"><a rel="nofollow" class="external text" href="https://kopkatalogs.lv/F?func=direct&local_base=lnc10&doc_number=000333062&P_CON_LNG=ENG">Latvia</a></span></span></li><li><span class="uid"><a rel="nofollow" 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