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O. |editor4-last=Carver|editor4-first=Peggy L. |title=Essential Metals in Medicine:Therapeutic Use and Toxicity of Metal Ions in the Clinic |journal=Metal Ions in Life Sciences |volume=19 |publisher=de Gruyter GmbH|location=Berlin |isbn=978-3-11-052691-2 |pmid=30855105 |pages=87–122|chapter=Chapter 4. Ironing out the Brain |doi=10.1515/9783110527872-010 |date=2019}}</ref> Some of the NBIA disorders have also been associated with several genes in synapse and lipid metabolism related pathways.<ref>{{cite journal |vauthors=Bettencourt C, Forabosco P, Wiethoff S, Heidari M, Johnstone DM, Botía JA, Collingwood JF, Hardy J, Milward EA, Ryten M, Houlden H |title=Gene co-expression networks shed light into diseases of brain iron accumulation |journal=Neurobiology of Disease |volume=87 |pages=59–68 |pmid=26707700 |pmc=4731015 |department=primary |doi=10.1016/j.nbd.2015.12.004 |date=March 2016}}</ref> NBIA is not one disease but an entire group of disorders, characterized by an accumulation of brain iron, sometimes in the presence of [[axonal spheroid]]s in the [[central nervous system]].<ref name=Gregory2009>{{cite journal |vauthors=Gregory A, Polster BJ, Hayflick SJ |title=Clinical and genetic delineation of neurodegeneration with brain iron accumulation |journal=Journal of Medical Genetics |volume=46 |issue=2 |pages=73–80 |pmid=18981035 |pmc=2675558 |department=review |doi=10.1136/jmg.2008.061929 |date=February 2009}}</ref> Iron accumulation can occur anywhere in the brain, with accumulation typically occurring in [[globus pallidus]], [[substantia nigra]], pars reticula, [[striatum]] and cerebellar [[dentate nucleus|dentate nuclei]].<ref name=Dusek2012/> Symptoms can include various movement disorders, neuropsychiatric issues, seizures, visual disturbances, and cognitive decline, usually in different combinations.<ref name=Dusek2012/> Ten to fifteen genetic NBIA disorders involving various cell processes have been identified: iron metabolism, [[coenzyme A]] biosynthesis, [[phospholipid]] metabolism, [[ceramide]] metabolism, lysosomal disorders, as well as mutations in genes with unknown functions.<ref name=Spaull2021>{{cite journal |last1=Spaull |first1=Robert V. V. |last2=Soo |first2=Audrey K. S. |last3=Hogarth |first3=Penelope |last4=Hayflick |first4=Susan J. |last5=Kurian |first5=Manju A. |title=Towards Precision Therapies for Inherited Disorders of Neurodegeneration with Brain Iron Accumulation |journal=Tremor and Other Hyperkinetic Movements |volume=11 |issue=1 |pages=51 |doi-access=free |doi=10.5334/tohm.661 |date=24 November 2021|pmid=34909266 |pmc=8641530 }}</ref><ref name=Dusek2012/> Onset can occur at different ages, from early childhood to late adulthood.<ref name=Dusek2012>{{cite journal |vauthors=Dusek P, Schneider SA |title=Neurodegeneration with brain iron accumulation |journal=Current Opinion in Neurology |volume=25 |issue=4 |pages=499–506 |pmid=22691760 |department=review |doi=10.1097/wco.0b013e3283550cac |date=August 2012}}</ref> {{as of|2021}} there were no curative treatments for any of the NBIA disorders, though several medications have been subject to clinical trial including the iron [[chelation|chelator]] [[deferiprone]].<ref name=Spaull2021/> ==Variants== {| class="wikitable" |+Overview of monogenic NBIA disorders<ref name=Spaull2021/><ref>{{cite book |title=Neurodegeneration with Brain Iron Accumulation Disorders Overview |vauthors=Gregory A, Hayflick S |veditors=Adam MP, Ardinger HH, Pagon RA, Wallace SE, Bean LJ, Stephens K, Amemiya A |publisher=University of Washington, Seattle |series=GeneReviews [Internet] |location=Seattle (WA) |pmid=23447832 |date=28 February 2013 |url=https://www.ncbi.nlm.nih.gov/books/NBK121988/}}</ref><ref>{{cite journal |vauthors=Hogarth P |title=Neurodegeneration with brain iron accumulation: diagnosis and management |language=en |journal=Journal of Movement Disorders |volume=8 |issue=1 |pages=1–13 |pmid=25614780 |pmc=4298713 |doi=10.14802/jmd.14034 |date=January 2015}}</ref> |- ! NBIA variant !! [[Gene]] !! [[Heredity|Inheritance]] |- | [[Pantothenate kinase-associated neurodegeneration]] (PKAN)<ref>{{cite journal |vauthors=Gregory A, Hayflick SJ |veditors=Adam MP, Ardinger HH, Pagon RA, Wallace SE, Bean LJ, Stephens K, Amemiya A |title=Pantothenate Kinase-Associated Neurodegeneration |journal=GeneReviews [Internet] |year=2003 |pmid=20301663 |url=https://www.ncbi.nlm.nih.gov/books/NBK1490/}}</ref>|| ''[[PANK2 (gene)|PANK2]]'' || [[autosome|autosomal]] [[dominance (genetics)|recessive]] |- | [[PLA2G6-associated neurodegeneration|''PLA2G6''-associated neurodegeneration]] (PLAN)<ref>{{cite journal |vauthors=Gregory A, Kurian MA, Maher ER, Hogarth P, Hayflick SJ |veditors=Adam MP, Ardinger HH, Pagon RA, Wallace SE, Bean LJ, Stephens K, Amemiya A |title=PLA2G6-Associated Neurodegeneration |journal=GeneReviews [Internet] |year=2008 |pmid=20301718 |url=https://www.ncbi.nlm.nih.gov/books/NBK1675/}}</ref>|| ''[[PLA2G6]]'' || autosomal recessive |- | [[Mitochondrial membrane protein-associated neurodegeneration]] (MPAN)<ref>{{cite journal |vauthors=Gregory A, Hartig M, Prokisch H, Kmiec T, Hogarth P, Hayflick SJ |veditors=Adam MP, Ardinger HH, Pagon RA, Wallace SE, Bean LJ, Stephens K, Amemiya A |year=2014 |title=Mitochondrial Membrane Protein-Associated Neurodegeneration |journal=GeneReviews [Internet] |pmid=24575447 |url=https://www.ncbi.nlm.nih.gov/books/NBK185329/}}</ref> || ''C19orf12'' || autosomal [[dominance (genetics)|recessive or dominant]] |- | [[Beta-propeller protein-associated neurodegeneration]] (BPAN)<ref>{{cite journal |vauthors=Gregory A, Kurian MA, Haack T, Hayflick SJ, Hogarth P |veditors=Adam MP, Ardinger HH, Pagon RA, Wallace SE, Bean LJ, Stephens K, Amemiya A |title=Beta-Propeller Protein-Associated Neurodegeneration |journal=GeneReviews [Internet] |pmid=28211668 |date=16 Feb 2017 |url=https://www.ncbi.nlm.nih.gov/books/NBK424403/}}</ref> || ''[[WDR45]]'' || [[X-linked dominant inheritance|X-linked dominant]] (mostly [[de novo mutation]]s) |- | [[Fatty acid hydroxylase-associated neurodegeneration]] (FAHN)<ref>{{cite journal |vauthors=Kruer MC, Gregory A, Hayflick SJ |veditors=Adam MP, Ardinger HH, Pagon RA, Wallace SE, Bean LJ, Stephens K, Amemiya A |title=Fatty Acid Hydroxylase-Associated Neurodegeneration |journal=GeneReviews [Internet] |pmid=21735565 |date=28 Jun 2011 |url=https://www.ncbi.nlm.nih.gov/books/NBK56080/}}</ref> || ''[[FA2H]]'' || autosomal recessive |- | [[Kufor–Rakeb syndrome]] || ''[[ATP13A2]]'' || autosomal recessive |- | [[Neuroferritinopathy]] || ''[[Ferritin light chain|FTL]]'' || autosomal [[dominance (genetics)|dominant]] |- | [[Aceruloplasminemia]] || ''[[Ceruloplasmin|CP]]'' || autosomal recessive |- | [[Woodhouse–Sakati syndrome]] || ''[[DCAF17]]'' || autosomal recessive |- | [[COASY protein-associated neurodegeneration]] (CoPAN)|| ''[[COASY]]'' || autosomal recessive |- | NBIA7<ref name=Drecourt2018>{{cite journal |vauthors=Drecourt A, Babdor J, Dussiot M, Petit F, Goudin N, Garfa-Traoré M, Habarou F, Bole-Feysot C, Nitschké P, Ottolenghi C, Metodiev MD, Serre V, Desguerre I, Boddaert N, Hermine O, Munnich A, Rötig A |display-authors=6 |title=Impaired Transferrin Receptor Palmitoylation and Recycling in Neurodegeneration with Brain Iron Accumulation |journal=American Journal of Human Genetics |volume=102 |issue=2 |pages=266–277 |pmid=29395073 |pmc=5985451 |department=primary |doi=10.1016/j.ajhg.2018.01.003 |date=February 2018}}</ref> || ''[[REPS1]]'' || autosomal recessive |- | NBIA8<ref name=Drecourt2018/> || ''[[Carnitine O-acetyltransferase|CRAT]]'' || autosomal recessive |} ==Symptoms and signs== {{Empty section|date=October 2024}} ==Cause== {{Empty section|date=October 2024}} ==Diagnosis== [[DaT scan]]s, [[transcranial Doppler]] sonography (TCD), [[PET scan]]s, and, in some cases, [[magnetic resonance imaging]] (MRI) (type of scans depending on the symptoms)<ref>Brüggemann N. et al.: Recessively inherited parkinsonism: effect of ATP13A2 mutations on the clinical and neuroimaging phenotype. Arch Neurol. 2010 Nov;67(11):1357-63. doi: 10.1001/archneurol.2010.281.</ref> are used to distinguish between the different forms of NBIA due to the accumulation of iron in different areas of the brain.<ref name=Hayflick2006>{{cite journal |vauthors=Hayflick SJ, Hartman M, Coryell J, Gitschier J, Rowley H |title=Brain MRI in neurodegeneration with brain iron accumulation with and without PANK2 mutations |journal=[[American Journal of Neuroradiology]] |volume=27 |issue=6 |pages=1230–3 |pmid=16775270 |pmc=2099458 |department=primary |date=2006-06-01 |url=https://www.ajnr.org/content/27/6/1230}}</ref> Patients typically fall into two different categories: (1) early onset, rapid progression or (2) late onset, slow progression.<ref name=Hayflick2006/> The first type is considered to be the classic presentation, while the second type is thought to be a more atypical presentation. Phenotypes of the different disorders appear to be dependent on age, i.e. amount of iron accumulation and cognitive abilities.<ref name=Schneider2012>{{cite journal |vauthors=Schneider SA, Bhatia KP |title=Syndromes of neurodegeneration with brain iron accumulation |journal=Seminars in Pediatric Neurology |volume=19 |issue=2 |pages=57–66 |pmid=22704258 |department=review |doi=10.1016/j.spen.2012.03.005 |date=June 2012}}</ref> ==Treatments== Effective disease-modifying treatments have not yet been found for any of the NBIA disorders.<ref name=Spaull2021/> Treatment is supportive and focused on improving symptoms: [[Dystonia]] is a common debilitating symptom and can be managed with oral medications, and sometimes with [[deep brain stimulation|deep-brain electrical stimulation]], therapy support for walking, eating, and manual tasks is essential. Later, in many of the diseases, slowing and stopping of movement (known as parkinsonism) can become common. Removal of iron, using medications known as iron [[chelation|chelators]], has been tested in clinical trial but was not definitively shown to be effective.<ref name=Klopstock2019>{{cite journal |last1=Klopstock |first1=Thomas |last2=Tricta |first2=Fernando |last3=Neumayr |first3=Lynne |last4=Karin |first4=Ivan |last5=Zorzi |first5=Giovanna |last6=Fradette |first6=Caroline |last7=Kmieć |first7=Tomasz |last8=Büchner |first8=Boriana |last9=Steele |first9=Hannah E |last10=Horvath |first10=Rita |last11=Chinnery |first11=Patrick F |last12=Basu |first12=Anna |last13=Küpper |first13=Clemens |last14=Neuhofer |first14=Christiane |last15=Kálmán |first15=Bernadette |last16=Dušek |first16=Petr |last17=Yapici |first17=Zuhal |last18=Wilson |first18=Ian |last19=Zhao |first19=Feng |last20=Zibordi |first20=Federica |last21=Nardocci |first21=Nardo |last22=Aguilar |first22=Christine |last23=Hayflick |first23=Susan J |last24=Spino |first24=Michael |last25=Blamire |first25=Andrew M |last26=Hogarth |first26=Penelope |last27=Vichinsky |first27=Elliott |title=Safety and efficacy of deferiprone for pantothenate kinase-associated neurodegeneration: a randomised, double-blind, controlled trial and an open-label extension study |journal=The Lancet Neurology |volume=18 |issue=7 |pages=631–642 |display-authors=5 |doi=10.1016/S1474-4422(19)30142-5 |date=July 2019|pmid=31202468 |s2cid=186245765 }}</ref> ==References== {{Reflist}} ==External links== {{Medical resources | ICD11 =  | ICD10 = {{ICD10|G23.0}} | ICD10CM =  | ICD9 =  | ICDO = | OMIM = | MeshID = C538421  | DiseasesDB = 35160  | SNOMED CT =  | Curlie = | MedlinePlus = 001225  | eMedicineSubj = | eMedicineTopic = | PatientUK = | NCI = | GeneReviewsNBK = NBK121988 | GeneReviewsName = Neurodegeneration with Brain Iron Accumulation Disorders Overview | NORD =  | GARDNum = 11899 | GARDName = Neurodegeneration with brain iron accumulation | RP = neurodegeneration-with-brain-iron-accumulation | AO = | WO = | OrthoInfo = | Orphanet = 385 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