Involvement of 'stress-response' kinase pathways in Alzheimer's disease progression

Curr Opin Neurobiol. 2014 Aug;27:110-7. doi: 10.1016/j.conb.2014.03.011. Epub 2014 Apr 5.

Abstract

Alzheimer's disease (AD) is the most prevalent cause of dementia, affecting more than 25 million people worldwide. Current models of the pathophysiological mechanisms of AD suggest that the accumulation of soluble oligomeric forms of amyloid-β (Aβ) peptides causes early loss of excitatory synapses and impairs synaptic plasticity. The signaling pathways mediating Aβ oligomer-induced impairment of synaptic plasticity and loss of excitatory synapses are only beginning to be unraveled. Here, we review recent evidence supporting the critical contribution of conserved 'stress-response' kinase pathways in AD progression.

Publication types

  • Review

MeSH terms

  • AMP-Activated Protein Kinases / genetics
  • AMP-Activated Protein Kinases / metabolism
  • Alzheimer Disease / metabolism*
  • Amyloid beta-Peptides / metabolism
  • Animals
  • Calcium-Calmodulin-Dependent Protein Kinase Kinase / genetics
  • Calcium-Calmodulin-Dependent Protein Kinase Kinase / metabolism*
  • Disease Progression
  • Endoplasmic Reticulum Stress / physiology*
  • Humans
  • Signal Transduction / physiology*
  • TOR Serine-Threonine Kinases / genetics
  • TOR Serine-Threonine Kinases / metabolism

Substances

  • Amyloid beta-Peptides
  • TOR Serine-Threonine Kinases
  • CAMKK2 protein, human
  • Calcium-Calmodulin-Dependent Protein Kinase Kinase
  • AMP-Activated Protein Kinases