The pathological cascade of AD is initiated by extracellular amyloid-β42 (Aβ42) plaques deposition and Tau hyper-phosphorylation, which forms intracellular neurofibrillary tangles (NFTs), leading to oxidative stress, mitochondrial dysfunction, neuroinflammation, as well as, excitotoxicity, and insulin signaling impairment, resulting in neuronal apoptosis (Alhazmi and Albratty 2022). This evidence concerns the gene INS and Alzheimer disease.