OCA2 and Alzheimer disease: The prevailing AD pathogenesis hypothesis suggests that AD is mainly due to the accumulation of insoluble amyloid‐β (Aβ) deposits and neurofibrillary tangles induced by highly phosphorylated tau (p‐τ) proteins in the neocortex, hippocampus, and amygdala, accompanied by massive loss of neurons and synapses leading to brain atrophy (Duyckaerts et al., 2009; Markesbery, 1997; Mirra et al., 1991).