Format

Send to

Choose Destination
See comment in PubMed Commons below
Neuron. 2013 Sep 18;79(6):1044-66. doi: 10.1016/j.neuron.2013.09.004.

The function of α-synuclein.

Author information

1
Departments of Neurology and Physiology, Graduate Programs in Biomedical Sciences, Cell Biology and Neuroscience, UCSF School of Medicine, San Francisco, CA 94158-2517, USA.

Abstract

Human genetics has indicated a causal role for the protein α-synuclein in the pathogenesis of familial Parkinson's disease (PD), and the aggregation of synuclein in essentially all patients with PD suggests a central role for this protein in the sporadic disorder. Indeed, the accumulation of misfolded α-synuclein now defines multiple forms of neural degeneration. Like many of the proteins that accumulate in other neurodegenerative disorders, however, the normal function of synuclein remains poorly understood. In this article, we review the role of synuclein at the nerve terminal and in membrane remodeling. We also consider the prion-like propagation of misfolded synuclein as a mechanism for the spread of degeneration through the neuraxis.

PMID:
24050397
PMCID:
PMC3866954
DOI:
10.1016/j.neuron.2013.09.004
[Indexed for MEDLINE]
Free PMC Article
PubMed Commons home

PubMed Commons

0 comments
How to join PubMed Commons

    Supplemental Content

    Full text links

    Icon for Elsevier Science Icon for PubMed Central
    Loading ...
    Support Center