Neuronal apoptosis induced by neuroinflammation is recognized as the fate of neurodegenerative neurons during the development of AD, which exacerbates the resulting spatial and temporal deficits.38 Cleaved‐CASP3 has been identified as an apoptosis executioner in neuronal cells.39 Cleaved‐CASP3 activation can result in DNA condensation or fragmentation, which further contributes to mitochondrial dysfunction, and caspase cascade events, and ultimately leads to neuronal death. This evidence concerns the gene CASP3 and Alzheimer disease.