AD is marked by the presence of neuronal fibrillary tangles and senile plaques, with hyperphosphorylated tau protein forming the tangles inside neurons and extracellular amyloid-beta (Aβ) peptides contributing to senile plaques (Martin et al., 2019).The production of Aβ involves cleavage of amyloid precursor protein (APP) by α-, β-, and γ-secretases, with P2X7R potentially influencing this process (Allinson et al., 2003). The gene discussed is MAPT; the disease is Alzheimer disease.