Starting decades prior to the onset of the clinical symptoms [22], neuroinflammation and the accumulation of extracellular amyloid plaques and intraneuronal neurofibrillary tangles (NFTs) containing hyperphosphorylated tau protein (p-tau) are the central neuropathological hallmarks of AD, leading to synaptic dysfunction and, ultimately, to neurodegeneration with consequential brain atrophy and cognitive decline [21]. The gene discussed is MAPT; the disease is Mental deterioration.