{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Alegre-Abarrategui J"],"funding":["NIA NIH HHS","Medical Research Council","Network of Centres of excellence in Neurodegeneration","NIHR Imperial Biomedical Research Centre","Parkinson’s UK","Jean Shanks Foundation","National Institute on Aging","Michael J. Fox Foundation for Parkinson's Research","Parkinson's UK"],"pagination":["681-704"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC6800835"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["138(5)"],"pubmed_abstract":["Parkinson's disease, dementia with Lewy bodies, and multiple system atrophy are neurodegenerative disorders resulting in progressive motor/cognitive deficits among other symptoms. They are characterised by stereotypical brain cell loss accompanied by the formation of proteinaceous aggregations of the protein α-synuclein (α-syn), being, therefore, termed α-synucleinopathies. Although the presence of α-syn inclusions is a common hallmark of these disorders, the exact nature of the deposited protein is specific to each disease. Different neuroanatomical regions and cellular populations manifest a differential vulnerability to the appearance of protein deposits, cell dysfunction, and cell death, leading to phenotypic diversity. The present review describes the multiple factors that contribute "],"journal":["Acta neuropathologica"],"pubmed_title":["Selective vulnerability in α-synucleinopathies."],"pmcid":["PMC6800835"],"funding_grant_id":["P01 AG012411","J-0901","MR/P007058/1","J-1403","NIA AG12411","J-1402"],"pubmed_authors":["Brimblecombe KR","Roberts RF","Tilley BS","Bengoa-Vergniory N","Alegre-Abarrategui J","Proukakis C","Velentza-Almpani E"],"additional_accession":[]},"is_claimable":false,"name":"Selective vulnerability in α-synucleinopathies.","description":"Parkinson's disease, dementia with Lewy bodies, and multiple system atrophy are neurodegenerative disorders resulting in progressive motor/cognitive deficits among other symptoms. They are characterised by stereotypical brain cell loss accompanied by the formation of proteinaceous aggregations of the protein α-synuclein (α-syn), being, therefore, termed α-synucleinopathies. Although the presence of α-syn inclusions is a common hallmark of these disorders, the exact nature of the deposited protein is specific to each disease. Different neuroanatomical regions and cellular populations manifest a differential vulnerability to the appearance of protein deposits, cell dysfunction, and cell death, leading to phenotypic diversity. The present review describes the multiple factors that contribute ","dates":{"release":"2019-01-01T00:00:00Z","publication":"2019 Nov","modification":"2025-04-05T13:18:41.121Z","creation":"2019-11-09T08:00:50Z"},"accession":"S-EPMC6800835","cross_references":{"pubmed":["31006067"],"doi":["10.1007/s00401-019-02010-2"]}}