In neurons of AD patients, tau becomes hyperphosphorylated, causing it to disassociate from the microtubule and form pathological aggregates that spread in a characteristic pattern, originating in the entorhinal cortex and locus coeruleus and progressing to the neocortex (Grundke-Iqbal et al., 1986; Braak and Braak, 1991; Hyman, 1997; Franzmeier et al., 2020). This evidence concerns the gene MAPT and Alzheimer disease.