Molecular chaperones, α-synuclein, and neurodegeneration

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

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.

Publication types

  • Research Support, N.I.H., Extramural
  • Review

MeSH terms

  • Animals
  • Cell Communication / physiology
  • Cell Death / physiology
  • Humans
  • Molecular Chaperones / chemistry*
  • Molecular Chaperones / metabolism
  • Molecular Chaperones / physiology*
  • Neurodegenerative Diseases / metabolism*
  • Neurodegenerative Diseases / pathology*
  • Neurotransmitter Agents / metabolism
  • Neurotransmitter Agents / physiology
  • alpha-Synuclein / chemistry*
  • alpha-Synuclein / physiology*

Substances

  • Molecular Chaperones
  • Neurotransmitter Agents
  • alpha-Synuclein