The study investigates the molecular mechanism of neurodegeneration in Alzheimer's disease (AD), focusing on the role of β-amyloid peptide (AβP). The authors report that synthetic AβPs induce degeneration of cultured neurons through an apoptotic pathway. Neurons treated with AβPs exhibit morphological and biochemical characteristics of apoptosis, including membrane blebbing, nuclear chromatin compaction, and internucleosomal DNA fragmentation. Aurintricarboxylic acid, an inhibitor of nucleases, prevents DNA fragmentation and delays cell death. These findings suggest that apoptosis may play a role in the neuronal loss associated with AD. The study also highlights the sequence and conformation specificity of AβP-induced apoptosis, as well as the potential for interruption of the apoptotic pathway to delay neurodegeneration in AD.The study investigates the molecular mechanism of neurodegeneration in Alzheimer's disease (AD), focusing on the role of β-amyloid peptide (AβP). The authors report that synthetic AβPs induce degeneration of cultured neurons through an apoptotic pathway. Neurons treated with AβPs exhibit morphological and biochemical characteristics of apoptosis, including membrane blebbing, nuclear chromatin compaction, and internucleosomal DNA fragmentation. Aurintricarboxylic acid, an inhibitor of nucleases, prevents DNA fragmentation and delays cell death. These findings suggest that apoptosis may play a role in the neuronal loss associated with AD. The study also highlights the sequence and conformation specificity of AβP-induced apoptosis, as well as the potential for interruption of the apoptotic pathway to delay neurodegeneration in AD.