Cell Rep: In Alzheimer's disease, apoptosis protein caspase is associated with abeta-induced synaptic loss

Studies have shown that the toxic effects of amyloid beta protein (A-beta) may play a pioneering role in the pathogenesis of Alzheimer's disease (AD)Until now, however, we have not yet been able to understand how A-beta causes synaptic dysfunction and synaptic lossresearchers speculated that one of the mechanisms by which A-beta induces synaptic damage was associated with amyloid beta precursor protein (APP) being cut by caspase at the D664 thio, releasing C31 peptides that may be cytotoxica significant reduction in A-beta-induced synaptic damage in two A-beta toxicity models in mouse organ-type cultures from the knockout app gene mutation (APP D664A) to inhibit caspase-cutIn mice treated with caspase inhibitors, the loss of synapses was also reducedimportant, the loss of time-dependent synapses is associated with local activation of caspase-3, but does not exist in APP D664A culturestherefore, the researchers suggest that the APP cytoplasmic region plays a crucial role in local caspase-activated medial damage pathways in A-beta-induced synaptic damage