Amyloid β: linking synaptic plasticity failure to memory disruption in Alzheimer’s disease
Version of Record online: 28 NOV 2011
© 2011 The Authors. Journal of Neurochemistry © 2011 International Society for Neurochemistry
Journal of Neurochemistry
Special Issue: Alzheimer’s Disease
Volume 120, Issue Supplement s1, pages 140–148, January 2012
How to Cite
Ma, T. and Klann, E. (2012), Amyloid β: linking synaptic plasticity failure to memory disruption in Alzheimer’s disease. Journal of Neurochemistry, 120: 140–148. doi: 10.1111/j.1471-4159.2011.07506.x
- Issue online: 23 DEC 2011
- Version of Record online: 28 NOV 2011
- Received July 1, 2011; revised manuscript received September 8, 2011; accepted September 20, 2011.
- 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.
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.