Ap-lnduced Toxicity Mediated by Caspase Cleavage of the Amyloid Precursor Protein (APP)

摘要

Synapse and neuron losses are characteristic features of Alzheimer's disease (AD) and are believed to underlie the cognitive impairments seen in this disorder. Amyloid beta-protein (Abeta) is hypothesized to play a pivotal role in initiating AD pafhogenesis, but the precise mechanisms of Abeta-induced damage remain unclear. Caspases, a family of proteases best known for their role in programmed cell death, may play a role in neurodegeneration. This review will focus on recent findings implicating a role for caspase cleavage of the amyloid precursor protein (APP) in synaptic and neuronal injury in AD and how this pathway may be initiated by the interaction of Abeta with APP.