To think or not to think: synaptic activity and Abeta release

Neuron. 2005 Dec 22;48(6):873-5. doi: 10.1016/j.neuron.2005.12.005.

Abstract

Accumulation of beta-amyloid protein (Abeta) in the extracellular space of the brain has been hypothesized to be a culprit in the pathogenesis of Alzheimer's disease. In this issue of Neuron, Cirrito et al. describe a series of experiments demonstrating that extracellular Abeta levels are directly modulated by neuronal and synaptic activity.

Publication types

  • Review
  • Comment

MeSH terms

  • Alzheimer Disease / metabolism*
  • Alzheimer Disease / physiopathology
  • Amyloid Precursor Protein Secretases
  • Amyloid beta-Peptides / metabolism*
  • Animals
  • Aspartic Acid Endopeptidases
  • Brain / metabolism*
  • Brain / physiopathology
  • Endopeptidases / metabolism
  • Extracellular Fluid / metabolism
  • Humans
  • Plaque, Amyloid / metabolism
  • Presynaptic Terminals / metabolism*
  • Synaptic Transmission / physiology*
  • Synaptic Vesicles / metabolism

Substances

  • Amyloid beta-Peptides
  • Amyloid Precursor Protein Secretases
  • Endopeptidases
  • Aspartic Acid Endopeptidases
  • BACE1 protein, human