On a molecular level, extracellular deposits of amyloid beta and the resulting neuritic plaques along with the intracellular accumulation of hyperphosphorylated tau protein into paired helical filaments (PHFs) and neurofibrillary tangles (NFTs) contribute to neuronal loss and the pathological hallmarks seen in AD brains (De Strooper and Karran, 2016). This evidence concerns the gene MAPT and Alzheimer disease.