At 8 months of age, intensive Aβ plaques surrounded by diffuse amyloid deposits cover almost the entire neocortex.32 Our previous studies found that 12‐month‐old APP/PS1 mice displayed robust Aβ plaque formation throughout the hippocampus and cortex as well as obvious cognitive deficits.33 Because the development of neuropathological changes in the hippocampal regions lags behind that in the cortex, our study focused on whether BAI could reduce neural apoptosis resulting from neuroinflammation in the hippocampus, which is the key region responsible for memory formation. The gene discussed is APP; the disease is amyloidosis.