Alpha-synuclein spreading in Parkinson's disease.
Identifieur interne : 000440 ( PubMed/Curation ); précédent : 000439; suivant : 000441Alpha-synuclein spreading in Parkinson's disease.
Auteurs : Ariadna Recasens [Espagne] ; Benjamin Dehay [France]Source :
- Frontiers in neuroanatomy ; 2014.
Abstract
Formation and accumulation of misfolded protein aggregates are a central hallmark of several neurodegenerative diseases. In Parkinson's disease (PD), the aggregation-prone protein alpha-synuclein (α-syn) is the culprit. In the past few years, another piece of the puzzle has been added with data suggesting that α-syn may self-propagate, thereby contributing to the progression and extension of PD. Of particular importance, it was the seminal observation of Lewy bodies (LB), a histopathological signature of PD, in grafted fetal dopaminergic neurons in the striatum of PD patients. Consequently, these findings were a conceptual breakthrough, generating the "host to graft transmission" hypothesis, also called the "prion-like hypothesis." Several in vitro and in vivo studies suggest that α-syn can undergo a toxic templated conformational change, spread from cell to cell and from region to region, and initiate the formation of "LB-like aggregates," contributing to the PD pathogenesis. Here, we will review and discuss the current knowledge for such a putative mechanism on the prion-like nature of α-syn, and discuss about the proper use of the term prion-like.
DOI: 10.3389/fnana.2014.00159
PubMed: 25565982
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Here, we will review and discuss the current knowledge for such a putative mechanism on the prion-like nature of α-syn, and discuss about the proper use of the term prion-like.</div></front></TEI><pubmed><MedlineCitation Status="PubMed-not-MEDLINE" Owner="NLM"><PMID Version="1">25565982</PMID><DateCreated><Year>2015</Year><Month>01</Month><Day>08</Day></DateCreated><DateCompleted><Year>2015</Year><Month>01</Month><Day>08</Day></DateCompleted><DateRevised><Year>2015</Year><Month>01</Month><Day>13</Day></DateRevised><Article PubModel="Electronic-eCollection"><Journal><JournalIssue CitedMedium="Print"><Volume>8</Volume><PubDate><Year>2014</Year></PubDate></JournalIssue><Title>Frontiers in neuroanatomy</Title><ISOAbbreviation>Front Neuroanat</ISOAbbreviation></Journal><ArticleTitle>Alpha-synuclein spreading in Parkinson's disease.</ArticleTitle><Pagination><MedlinePgn>159</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.3389/fnana.2014.00159</ELocationID><Abstract><AbstractText>Formation and accumulation of misfolded protein aggregates are a central hallmark of several neurodegenerative diseases. In Parkinson's disease (PD), the aggregation-prone protein alpha-synuclein (α-syn) is the culprit. In the past few years, another piece of the puzzle has been added with data suggesting that α-syn may self-propagate, thereby contributing to the progression and extension of PD. Of particular importance, it was the seminal observation of Lewy bodies (LB), a histopathological signature of PD, in grafted fetal dopaminergic neurons in the striatum of PD patients. Consequently, these findings were a conceptual breakthrough, generating the "host to graft transmission" hypothesis, also called the "prion-like hypothesis." Several in vitro and in vivo studies suggest that α-syn can undergo a toxic templated conformational change, spread from cell to cell and from region to region, and initiate the formation of "LB-like aggregates," contributing to the PD pathogenesis. 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