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Mol Neurobiol. 2013 Apr;47(2):552-60. doi: 10.1007/s12035-012-8325-2. Epub 2012 Aug 25.

Molecular chaperones, α-synuclein, and neurodegeneration.

Author information

1
Department of Biochemistry and Molecular Biology, Louisiana State University Health Sciences Center at Shreveport, Shreveport, LA, USA. switt1@lsuhsc.edu

Abstract

Parkinson's disease (PD) is a devastating neurological condition that affects about 1 % of people older than 65 years of age. In PD, dopaminergic neurons in the mid-brain slowly accumulate cytoplasmic inclusions (Lewy bodies, LBs) of the protein alpha-synuclein (α-syn) and then gradually lose function and die off. Cell death is thought to be causally linked to the aggregation/fibrillization of α-syn. This review focuses on new findings about the structure of α-syn, about how α-syn cooperates with Hsp70 and Hsp40 chaperones to promote neurotransmitter release, and about cell-to-cell transfer of pathogenic forms of α-syn and how Hsp70 might protect against this disease process.

PMID:
22923346
PMCID:
PMC3537861
DOI:
10.1007/s12035-012-8325-2
[Indexed for MEDLINE]
Free PMC Article
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