The pathology of AD is complex and varied, with neuronal loss, synaptic deficits (e.g., synaptic loss and prominent plasticity defects), extracellular amyloid beta (Aβ) deposits forming amyloid plaques, and abnormally phosphorylated Tau proteins forming intracellular neurofibrillary tangles, all of which are prevalent in patients with AD (Scheltens et al., 2016; Bondi et al., 2017). This evidence concerns the gene MAPT and Alzheimer disease.