The pathology of AD begins before overt cognitive symptoms and includes the accumulation of amyloid β peptide (Aβ) as extracellular plaques, hyper‐phosphorylated tau as intracellular neurofibrillary tangles (NFTs), and chronic neuroinflammation, followed by the loss of neuronal cells mainly in the cerebral cortex and hippocampus (Braak & Braak, 1991; Hyman et al, 2012). This evidence concerns the gene MAPT and Alzheimer disease.