The cellular pathways causing these anomalies are still being investigated, but oxidative stress [4], energy deprivation [5, 6], and neuroinflammation [7, 8] are thought to be critical processes that initiate and/or exacerbate the pathophysiological substrates of AD [9], which were originally defined as extracellular cortical plaques containing Aβ, and intraneuronal tangles containing aggregated tau protein [10]. Here, MAPT is linked to Alzheimer disease.