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has-post-thumbnail hentry category-neurodegenerative-diseases tag-alzheimers-disease tag-genetic-bottleneck tag-heteroplasmy tag-leigh-syndrome tag-mitochondrial-dna tag-mitochondrial-dysfunction tag-mitochondrial-replacement-therapy tag-neurodegenerative-diseases tag-oxidative-stress tag-parkinsons-disease" itemtype="https://schema.org/CreativeWork" itemscope> <div class="inside-article"> <div class="featured-image page-header-image-single "> <img width="800" height="419" src="https://mutation.blog/archive/wp-content/uploads/2024/10/banner-01-2.jpg" class="attachment-full size-full" alt="" itemprop="image" decoding="async" fetchpriority="high" srcset="https://mutation.blog/archive/wp-content/uploads/2024/10/banner-01-2.jpg 800w, https://mutation.blog/archive/wp-content/uploads/2024/10/banner-01-2-300x157.jpg 300w, https://mutation.blog/archive/wp-content/uploads/2024/10/banner-01-2-768x402.jpg 768w" sizes="(max-width: 800px) 100vw, 800px" /> </div> <header class="entry-header"> <h1 class="entry-title" itemprop="headline">The Role of Mitochondrial DNA in Neurodegenerative Diseases</h1> <div class="entry-meta"> <span class="posted-on"><time class="entry-date published" datetime="2024-10-28T14:48:45+05:30" itemprop="datePublished">October 28, 2024</time></span> <span class="byline">by <span class="author vcard" itemprop="author" itemtype="https://schema.org/Person" itemscope><a class="url fn n" href="https://mutation.blog/archive/author/mutation/" title="View all posts by mutation" rel="author" itemprop="url"><span class="author-name" itemprop="name">mutation</span></a></span></span> </div> </header> <div class="entry-content" itemprop="text"> <h4><b>Introduction</b></h4> <p><span style="font-weight: 400;">Heterochromatin and its known role in energy production and management of the cells make it vital in the body, hence mtDNA. Therefore, unlike nuclear DNA, mitochondrial DNA, or mtDNA, is inherited in a maternal mode, and it is duplicated and located within the mitochondrion in virtually all the body’s cells. As for the mtDNA mutations or variations, the correlation between them and neurodegenerative diseases has drawn more attention in recent research. Such diseases as Alzheimer’s, Parkinson’s, and Leigh syndrome indicate a gradual degeneration of neurons and subsequent diminished mental and motor function, as well as the manifestation of many other symptoms. By defining the role of mtDNA in these diseases, people not only have an idea about how these diseases occur but also could find ways to diagnose, prevent, or cure these diseases. Therefore, this article aims to focus on the connection between mtDNA and neurodegenerative diseases, the latest investigations, and their potential for further advancement in the field and management of discs.</span></p> <h4><b>Mitochondrial DNA: Structure and Function</b></h4> <p><span style="font-weight: 400;">Mitochondria, sometimes called the energy factories of the cell, are in charge of creating energy that is necessary for various cellular activities. They do this through oxidative phosphorylation, which is a series of enzymes and protein complexes situated in the inner mitochondrial membrane with their codes from both nuclear and mitochondrial DNA. In the same way that it differs from the nuclear genome, which is a parental blend of both the mother and the father, mtDNA can only be inherited from the mother. This circular DNA measuring 16,569 base pairs contains 37 genes, which code for proteins involved in the synthesis of the components of the respiratory chain and other mitochondrial tRNAs and rRNAs.</span></p> <p><span style="font-weight: 400;">The primary reason why mtDNA usually acquires more mutations than nuclear DNA is the fact that mtDNA is iteratively duplicated and is located adjacent to the source of oxidative stress, ROS. These mutations can add up over time and also lead to dysfunctions of the cell, particularly if the cell is in a tissue that has high energy requirements, like the brain tissue. Besides, there is the coexistence of different populations of mtDNA called heteroplasmy that makes its involvement in disease even more complex. The degree of heteroplasmy is capable of impacting the progression and the age of onset of mtDNA-associated disorders, such as neurodegenerative diseases.</span></p> <p></div></div> <div style="background: #f7f7f7;border: 1px solid rgba(0, 0, 0, 0.07);"> <div style="padding: 30px;"><div class="Adblock-main"> <div class="Adblock-head"> <h2>Yearwise Publication Trend on <b>“<a href="https://mutation.blog/publication-trends/index/neurodegenerative diseases" target="_blank" title="neurodegenerative diseases - yearwise publication trends">neurodegenerative diseases</a>”</b></h2> </div> </div><div class="results-container"><div class="chart-block" style="padding:15px;"> <div class="left"> <div id="results" class="results"></div> </div> <div class="right"> <div class="chart-container"><canvas id="publicationChart"></canvas></div> </div> <div class="keywordsdiv"> <div style="text-align:center;"><b>Find publication trends on relevant topics</b> </div> <span class="gp-icon icon-tags"><svg viewBox="0 0 512 512" aria-hidden="true" xmlns="http://www.w3.org/2000/svg" width="1em" height="1em"><path d="M20 39.5c-8.836 0-16 7.163-16 16v176c0 4.243 1.686 8.313 4.687 11.314l224 224c6.248 6.248 16.378 6.248 22.626 0l176-176c6.244-6.244 6.25-16.364.013-22.615l-223.5-224A15.999 15.999 0 00196.5 39.5H20zm56 96c0-13.255 10.745-24 24-24s24 10.745 24 24-10.745 24-24 24-24-10.745-24-24z"></path><path d="M259.515 43.015c4.686-4.687 12.284-4.687 16.97 0l228 228c4.686 4.686 4.686 12.284 0 16.97l-180 180c-4.686 4.687-12.284 4.687-16.97 0-4.686-4.686-4.686-12.284 0-16.97L479.029 279.5 259.515 59.985c-4.686-4.686-4.686-12.284 0-16.97z"></path></svg></span> <span id="keyword-stats"></span> </div> </div></div></div><div class="inside-article"><style> table { margin: 0 0 1.5em; 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Genetics may very well play a role in predispositions that are passed down, but the exact origins remain obscure and veiled in mystery. It will likely be the case that both our intrinsic biology and our encounters in the molding of who we become will interact in very complex ways to initiate whether the devastating decay takes root or not. Intriguing new research associates subtle differences in the mitochondrial genome and maternally inherited ancestry patterns with increased susceptibility, particularly variations that perturb cellular energy production, our lifeline at a microscopic level. Other research explores possible connections between head injuries incurred in youth or metabolic disorders like midlife diabetes and increased risk later in life. While the causes are intricate, grasping how lifestyle and inheritance come into collision could tell strategies for its prevention, possibly helping to spare succeeding generations from the all-too-common devastation of this condition.</span></p> <p><span style="font-weight: 400;">For instance, damage to mitochondrial DNA structure and copy number, known as DPM, hinders oxidative phosphorylation and ATP generation while promoting harmful reactive oxygen species. This oxidative stress damages neurons, exacerbating Alzheimer’s hallmark amyloid plaques and tau tangles. Furthermore, mitochondrial DNA mutations may reduce crucial enzyme activity in processes key to neuronal function. As neurons require immense energy, mitochondrial dysfunction means cellular death, severing more and more neural connections over time. Some mitochondrial DNA types associate positively with Alzheimer’s in certain patients, indicating a genetic predisposition that could aid in future prevention or early detection efforts.</span></p> <h3><b>Parkinson’s Disease</b></h3> <p><span style="font-weight: 400;">Parkinson’s disease affects the central nervous system, impacting movement control. Patients often display tremors, muscle stiffness, and slow motions. A core symptom relates to degenerating dopamine-producing neurons in the substantia nigra region governing motion. Prior discussions highlighted impaired mitochondrial function linked to Parkinson’s pathogenesis. Additionally, mutations in mitochondrial DNA contribute to the condition’s development. Such mutations may disrupt Complex I in the mitochondrial electron transport chain critical to ATP production. This reduces neural energy supplies and triggers oxidative stress, ultimately killing neurons. However, certain mitochondrial DNA haplogroups are associated with risk or protective factors. For example, the J and T haplogroups may increase or decrease Parkinson’s probability, respectively. Consequently, individuals carrying the J or T haplogroups vary in their Parkinson’s predisposition owing to underlying mitochondrial divergences.</span></p> <p><span style="font-weight: 400;">More so, mutations directly carried on the mtDNA can influence the genes responsible for the right regulation of mitochondrial fission and fusion, both of which are critical in the right functioning of mitochondria. This means that the failure to direct them will result in the accumulation of defective mitochondria and subsequently add fuel to neuronal death progression in PD.</span></p> <h3><b>Leigh Syndrome</b></h3> <p><span style="font-weight: 400;">Leigh syndrome is a severe neurodegenerative disease that has a common onset in infancy or early childhood. This results from mutations in the nuclear and mitochondrial genes encoding the components of oxidative phosphorylation and leads to energy depletion in the brain and other vital organs. Most of the LS instances have a genetic connection with mtDNA abnormalities that affect the functionality of RCs, complex I, and complex IV.</span></p> <p><span style="font-weight: 400;">These mutations can lead to the buildup of lactate in the brain, leading to lesions in the basal ganglia, brain stem, and other essential areas for motor and cognitive functions. The nature of this affliction is progressive, and sufferers commonly experience extensive neurological damage, dying young. As an effect of the genetic character of the disease, mtDNA mutations are one of the most critical tendencies for diagnosis as well as possible treatment methodologies. Present research in mitochondrial replacement therapy and gene editing shows potential in the treatment of Leigh syndrome, but the methods are currently experimental.</span></p> <p></div></div> <div style="background: #f7f7f7;border: 1px solid rgba(0, 0, 0, 0.07);"> <div style="padding: 30px;"><div class="Adblock-main"> <div class="Adblock-head"> <h2>Recent Publications on <b>“<a href="https://mutation.blog/recent-publications/index/neurodegenerative diseases" target="_blank" rel="noopener" title="neurodegenerative diseases - yearwise publication list">neurodegenerative diseases</a>”</b></h2> </div> </div> <div class="pb-main"><div class="article-scroll"><div id="results_recent" class="results"></div></div><div class="keywordsdiv" style="margin: 0px 15px;margin-top:20px;"> <div style="text-align:center;"><b>Find publications on relevant topics</b> </div> <span class="gp-icon icon-tags"><svg viewBox="0 0 512 512" aria-hidden="true" xmlns="http://www.w3.org/2000/svg" width="1em" height="1em"><path d="M20 39.5c-8.836 0-16 7.163-16 16v176c0 4.243 1.686 8.313 4.687 11.314l224 224c6.248 6.248 16.378 6.248 22.626 0l176-176c6.244-6.244 6.25-16.364.013-22.615l-223.5-224A15.999 15.999 0 00196.5 39.5H20zm56 96c0-13.255 10.745-24 24-24s24 10.745 24 24-10.745 24-24 24-24-10.745-24-24z"></path><path d="M259.515 43.015c4.686-4.687 12.284-4.687 16.97 0l228 228c4.686 4.686 4.686 12.284 0 16.97l-180 180c-4.686 4.687-12.284 4.687-16.97 0-4.686-4.686-4.686-12.284 0-16.97L479.029 279.5 259.515 59.985c-4.686-4.686-4.686-12.284 0-16.97z"></path></svg></span> <span id="keyword-papers"></span> </div></div></div><div class="inside-article"> <style> .pb-main{ border: solid 1px #ccc; 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Alzheimer\\\\\\'s disease is Type 3 Diabetes: Evidences from Bench to Bedside.", "url": "https:\/\/pubmed.ncbi.nlm.nih.gov\/38955264", "publishedDate": "2024" }, { "title": "No causal relationship between serum urate and neurodegenerative diseases: A Mendelian randomization study.", "url": "https:\/\/pubmed.ncbi.nlm.nih.gov\/38955238", "publishedDate": "2024" }, { "title": "The lipid side of unfolded protein response.", "url": "https:\/\/pubmed.ncbi.nlm.nih.gov\/38844203", "publishedDate": "2024" }, { "title": "Aerobic Exercise Ameliorates Cognitive Disorder and Declined Oxidative Stress via Modulating the Nrf2 Signaling Pathway in D-galactose Induced Aging Mouse Model.", "url": "https:\/\/pubmed.ncbi.nlm.nih.gov\/38839706", "publishedDate": "2024" }, { "title": "CSF neurosecretory proteins VGF and neuroserpin in patients with Alzheimer\\\\\\'s and Lewy body diseases.", "url": "https:\/\/pubmed.ncbi.nlm.nih.gov\/38850771", "publishedDate": "2024" }, { "title": "No trend to rising rates: A review of Parkinson\\\\\\'s prevalence studies in the United Kingdom.", "url": "https:\/\/pubmed.ncbi.nlm.nih.gov\/38876845", "publishedDate": "2024" }, { "title": "Unveiling brain disorders using liquid biopsy and Raman spectroscopy.", "url": "https:\/\/pubmed.ncbi.nlm.nih.gov\/38845582", "publishedDate": "2024" } ]; var keywordsArray = ["Mitochondrial DNA","Neurodegenerative Diseases","Alzheimer’s Disease","Parkinson’s Disease","Leigh Syndrome","Mitochondrial Dysfunction","Genetic Bottleneck","Heteroplasmy","Oxidative Stress","Mitochondrial Replacement Therapy"]; displayResults_recent(recent_papers); displayKeywordPapers(keywordsArray); // function stripslashes(str) { // if (typeof str === 'string') { // return str.replace(/\/g, ''); // } // } </script></p> <h4><b>The Genetic Bottleneck and Its Implications</b></h4> <p><span style="font-weight: 400;">One of the most interesting aspects of mtDNA inheritance has to do with the genetic bottleneck phenomenon, whereby there is a sharp decrease in the number of mtDNA molecules passed from mother to offspring during oogenesis. This bottleneck may further result in a drastic shifting of proportions between normal and mutated mtDNA in the next generation and thus will modify the onset and severity of mtDNA-related diseases. The bottleneck may determine if a child will inherit high or low levels of mutated mtDNA; therefore, their risk for conditions like Alzheimer’s, Parkinson’s, or Leigh syndrome.</span></p> <p><span style="font-weight: 400;">It also presents a challenge to genetic counseling and the prediction of disease outcomes. The likelihood of a child having an extreme mutation load and thus a severe phenotype is still quite high, even from a mother harboring a low percentage of mutated mtDNA. Unraveling the mechanisms responsible for the bottleneck will thus have an impact not only on the prevention strategies designed to reduce the transmission of harmful mtDNA mutations but also on designing targeted therapies that could mitigate the consequences of such events.</span></p> <h4><b>Conclusion</b></h4> <p><span style="font-weight: 400;">Mitochondrial DNA acts at the core level in the development of neurodegenerative illnesses and impacts energy generation through oxidative stress and cellular demise. Characteristics unique to mtDNA, for example, maternal inheritance and a high somatic mutation rate coupled with heteroplasmy, designate this genome as a prime player in disorders such as Alzheimer’s disease, Parkinson’s disease, and Leigh syndrome. Exploration into these intricate relationships continues to reveal new opportunities for diagnosis, avoidance, and therapies for these neurodegenerative conditions. In these devastating disorders, targeting the mitochondrial dysfunctions centrally could result in effective treatments and an improved quality of life for patients. Some sentences in the revised text are longer to capture intricate details, while others are shorter to vary the structure.</span></p> <p></p> <h4><b>References</b></h4> <ol> <li>Annis, S., Fleischmann, Z., Khrapko, M., Franco, M., Wasko, K., Woods, D., Kunz, W.S., Ellis, P. and Khrapko, K., 2019. <a href="https://www.pnas.org/doi/abs/10.1073/pnas.1821436116">Quasi-Mendelian paternal inheritance of mitochondrial DNA: A notorious artifact, or anticipated behavior?. </a><i>Proceedings of the National Academy of Sciences</i>, <i>116</i>(30), pp.14797-14798.</li> <li>Wei, W., Tuna, S., Keogh, M.J., Smith, K.R., Aitman, T.J., Beales, P.L., Bennett, D.L., Gale, D.P., Bitner-Glindzicz, M.A., Black, G.C. and Brennan, P., 2019. <a href="https://www.science.org/doi/abs/10.1126/science.aau6520">Germline selection shapes human mitochondrial DNA diversity.</a> <i>Science</i>, <i>364</i>(6442), p.eaau6520.</li> <li>Chinnery, P.F. and Gomez-Duran, A., 2018. <a href="https://www.frontiersin.org/journals/neuroscience/articles/10.3389/fnins.2018.00682/full">Oldies but goldies mtDNA population variants and neurodegenerative diseases.</a> <i>Frontiers in neuroscience</i>, <i>12</i>, p.682.</li> <li>Zhang, H., Burr, S.P. and Chinnery, P.F., 2018. <a href="https://portlandpress.com/essaysbiochem/article-abstract/62/3/225/78534/The-mitochondrial-DNA-genetic-bottleneck">The mitochondrial DNA genetic bottleneck: inheritance and beyond.</a> <i>Essays in biochemistry</i>, <i>62</i>(3), pp.225-234.</li> <li>Otten, A.B., Sallevelt, S.C., Carling, P.J., Dreesen, J.C., Drüsedau, M., Spierts, S., Paulussen, A.D., de Die-Smulders, C.E., Herbert, M., Chinnery, P.F. and Samuels, D.C., 2018. <a href="https://academic.oup.com/humrep/article/33/7/1331/5025586">Mutation-specific effects in germline transmission of pathogenic mtDNA variants.</a> <i>Human Reproduction</i>, <i>33</i>(7), pp.1331-1341.</li> <li>Wilson, I.J., Carling, P.J., Alston, C.L., Floros, V.I., Pyle, A., Hudson, G., Sallevelt, S.C., Lamperti, C., Carelli, V., Bindoff, L.A. and Samuels, D.C., 2016. <a href="https://academic.oup.com/hmg/article/25/5/1031/2384671">Mitochondrial DNA sequence characteristics modulate the size of the genetic bottleneck.</a> <i>Human molecular genetics</i>, <i>25</i>(5), pp.1031-1041.</li> <li>Chinnery, P.F., Craven, L., Mitalipov, S., Stewart, J.B., Herbert, M. and Turnbull, D.M., 2014. <a href="https://journals.plos.org/plosgenetics/article?id=10.1371/journal.pgen.1004315">The challenges of mitochondrial replacement.</a> <i>PLoS genetics</i>, <i>10</i>(4), p.e1004315.</li> </ol> <p></div></div> <div style="background: #f7f7f7;border: 1px solid rgba(0, 0, 0, 0.07);"> <div style="padding: 30px;"><div class="Adblock-main"> <div class="Adblock-head"> <h2>Top Experts on “<b style="color:#000;font-size:22px;">neurodegenerative diseases</b>“</h2> </div> </div><div class="author-main"><div id="results_author"></div><div style="text-align: center;"><a class="register-button" href="https://mutation.blog/expert-search" target="_blank" rel="noopener">Find experts on any field</a></div></div><div class="inside-article" style="background: none;border: none;box-shadow: none;margin-top: -70px;"> <style> .author-block { padding: 15px; 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", "email": "tasano@hiroshima-u.ac.jp", "slug_tail": "t-asano" } }; //console.log(authors_data); displayResults_author(authors_data); var keywordsArray = ["Mitochondrial DNA","Neurodegenerative Diseases","Alzheimer’s Disease","Parkinson’s Disease","Leigh Syndrome","Mitochondrial Dysfunction","Genetic Bottleneck","Heteroplasmy","Oxidative Stress","Mitochondrial Replacement Therapy"]; displayKeywordAuthors(keywordsArray); </script></p> </div> <footer class="entry-meta" aria-label="Entry meta"> <span class="cat-links"><span class="gp-icon icon-categories"><svg viewBox="0 0 512 512" aria-hidden="true" xmlns="http://www.w3.org/2000/svg" width="1em" height="1em"><path d="M0 112c0-26.51 21.49-48 48-48h110.014a48 48 0 0143.592 27.907l12.349 26.791A16 16 0 00228.486 128H464c26.51 0 48 21.49 48 48v224c0 26.51-21.49 48-48 48H48c-26.51 0-48-21.49-48-48V112z" /></svg></span><span class="screen-reader-text">Categories </span><a 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