Chaperoning the SNAREs: a role in preventing neurodegeneration?

Nat Cell Biol. 2011 Jan;13(1):8-9. doi: 10.1038/ncb0111-8.

Abstract

Despite their potential importance as therapeutic targets, the initial events in neurodegenerative diseases are poorly understood. Emerging evidence suggests that presynaptic dysfunction might be an early event in these pathologies, and three papers now link dysregulation of SNAREprotein levels and function caused by the absence of synuclein or cysteine string protein (CSP) to activity-dependent neurodegeneration.

Publication types

  • Comment
  • News

MeSH terms

  • Animals
  • Cells, Cultured
  • HSP40 Heat-Shock Proteins / genetics
  • HSP40 Heat-Shock Proteins / metabolism
  • HSP40 Heat-Shock Proteins / physiology*
  • Membrane Proteins / genetics
  • Membrane Proteins / metabolism
  • Membrane Proteins / physiology*
  • Mice
  • Mice, Knockout
  • Mice, Transgenic
  • Models, Neurological
  • Neurodegenerative Diseases / genetics
  • Neurodegenerative Diseases / metabolism
  • Neurodegenerative Diseases / physiopathology
  • Neurons / cytology
  • Neurons / metabolism
  • Neurons / physiology
  • Protein Binding
  • SNARE Proteins / genetics
  • SNARE Proteins / metabolism*
  • Synaptic Transmission / physiology*
  • Synaptic Vesicles / metabolism
  • Synaptosomal-Associated Protein 25 / genetics
  • Synaptosomal-Associated Protein 25 / metabolism*
  • alpha-Synuclein / genetics
  • alpha-Synuclein / metabolism
  • alpha-Synuclein / physiology

Substances

  • HSP40 Heat-Shock Proteins
  • Membrane Proteins
  • SNARE Proteins
  • Snap25 protein, mouse
  • Synaptosomal-Associated Protein 25
  • alpha-Synuclein
  • cysteine string protein