Alzheimer’s disease (AD) is characterized by intraneuronal and extracellular accumulation of amyloid-β peptide (Aβ), intracellular neurofibrillary tangles (NFTs), the major component of which is hyperphosphorylated tau protein (p-tau), disruption of both excitatory amino acid and cholinergic neurotransmission, and loss of vulnerable neurons, notably forebrain cholinergic neurons that project to the cerebral cortex and hippocampus. This evidence concerns the gene MAPT and early-onset autosomal dominant Alzheimer disease.