(i) The main components implicated in the pathogenesis of AD include amyloid-beta and p-tau, as well as amyloidogenic proteases and other proteins that bind to amyloid-beta or tau, such as the receptor for advanced glycation endproducts (RAGE); (ii) The elements that are linked to pathology and are anticipated to play a role in the manifestation of symptoms include neuroinflammation, oxidative stress, and mitochondrial dysfunction; and (iii) Pharmaceutical interventions targeting cognitive and behavioral symptoms of AD encompass neuronal function modulators and neurotransmitters. This evidence concerns the gene MAPT and Alzheimer disease.