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.
No takes yet. Share an insight, caveat, or question.
Ma et al. (2011) studied this question.
Synapse has enriched 4 closely related papers on similar clinical questions. Consider them for comparative context: