In the past few decades research in AD focused mainly on the deposition in the brain of the protein fragment beta-amyloid (Aβ) into extracellular plaques followed by the accumulation of an abnormal, hyperphosphorylated form of the protein tau (p-tau), as the main driving factors in the AD pathology, leading to extended neuronal damage and synaptic dysfunction. This evidence concerns the gene MAPT and Alzheimer disease.