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Keywords:

  • amyloid β;
  • glycogen synthase kinase-3;
  • long-term potentiation;
  • mammalian target of rapamycin;
  • NMDA receptors;
  • reactive oxygen species

J. Neurochem. (2012) 120 (Suppl. 1), 140–148.

Abstract

Mounting evidence suggests that amyloid beta-induced impairments in synaptic plasticity that is accompanied by cognitive decline and dementia represent key pathogenic steps of Alzheimer’s disease. In this study, we review recent advances in the study of the molecular and cellular mechanisms underlying Alzheimer’s disease-associated synaptic dysfunction and memory deficits, and how these mechanisms could provide novel avenues for therapeutic intervention to treat this devastating neurodegenerative disease.