Determining the mechanism of Aβ-induced NMDA receptor dysfunction
Beta amyloid (Aβ) triggers elimination of excitatory synaptic connections in the central nervous system, an early manifestation of Alzheimer’s disease. Oligomeric assemblies of Aβ peptide associate with excitatory synapses resulting in synapse elimination through a process that requires NMDA-type glutamate receptor activation. Where Aβ binds, whether Aβ directly impacts synaptic NMDA receptor function, whether Aβ acts locally at synapses to which it has bound and whether synaptic activity influences Aβ synaptic binding and synaptotoxicity have remained fundamental questions. In order to understand ...
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