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Iron toxicity has been established in the pathogenesis of Parkinson\u2019s disease; however, its contribution to multiple system atrophy (MSA) remains elusive. MSA is characterized by cytoplasmic inclusions of misfolded \u03b1-synuclein (\u03b1-SYN) in oligodendrocytes referred to as glial cytoplasmic inclusions (GCIs). Remarkably, the oligodendrocytes possess high amounts of iron, which together with GCI pathology make a contribution toward MSA pathogenesis likely. Consistent with this observation, the GCI density is associated with neurodegeneration in central autonomic networks as well as olivopontocerebellar and striatonigral pathways. Iron converts native \u03b1-SYN into a \u03b2-sheet conformation and promotes its aggregation either directly or via increasing levels of oxidative stress. Interestingly, \u03b1-SYN possesses ferrireductase activity and \u03b1-SYN expression underlies iron mediated translational control via RNA stem loop structures. Despite a correlation between progressive putaminal atrophy and iron accumulation as well as clinical decline, it remains unclear whether pathologic iron accumulation in MSA is a secondary event in the cascade of neuronal degeneration rather than a primary cause. This review summarizes the current knowledge of iron in MSA and gives evidence for perturbed iron homeostasis as a potential pathogenic factor in MSA-associated neurodegeneration.<\/jats:p>","DOI":"10.3233\/jad-170601","type":"journal-article","created":{"date-parts":[[2018,1,23]],"date-time":"2018-01-23T11:31:41Z","timestamp":1516707101000},"page":"1253-1273","update-policy":"https:\/\/doi.org\/10.1177\/sage-journals-update-policy","source":"Crossref","is-referenced-by-count":68,"title":["The Relevance of Iron in the Pathogenesis of Multiple System Atrophy: A Viewpoint"],"prefix":"10.1177","volume":"61","author":[{"given":"Christine","family":"Kaindlstorfer","sequence":"first","affiliation":[{"name":"Department of Neurology, Medical University of Innsbruck, Innsbruck, Austria"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Kurt A.","family":"Jellinger","sequence":"additional","affiliation":[{"name":"Institute of Clinical Neurobiology, Vienna, 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