Amyloid and tau accumulation as an etiology of AD has been proposed as well as other etiologies including cerebral insulin resistance and glucose hypometabolism (De La Monte, 2016; Mullins et al., 2017; Neth and Craft, 2017), and synaptic dysfunction and the role of mitochondrial dysfunction with alterations in intracerebral adenosine triphosphate (ATP) levels (De La Monte, 2016; Cenini and Voos, 2019). This evidence concerns the gene MAPT and Alzheimer disease.