The intricate interplay between aging and AD involves various biological mechanisms, including the accumulation of amyloid-beta plaques due to the abnormal processing of amyloid precursor proteins, formation of neurofibrillary tangles from hyperphosphorylated tau proteins, mitochondrial dysfunction leading to oxidative stress, and chronic inflammation propelled by activated macrophages and microglia [2, 3]. The gene discussed is MAPT; the disease is Alzheimer disease.