Imaging studies show that APOE-ɛ4 carriers present with more severely atrophied temporal areas (Filippini et al., 2009a; Filippini et al., 2009b; Juottonen et al., 1998), and have elevated levels in temporo-parietal areas of the two main harmful brain deposits seen in AD: the tau protein (Ossenkoppele et al., 2016), causing neurofibrillary tangles, and amyloid-β (Drzezga et al., 2009), the peptide accumulating in the pathognomonic intercellular plaques. The gene discussed is APOE; the disease is Alzheimer disease.