Alzheimer’s disease is characterized by extracellular amyloid beta (Aβ) (~40 amino acid long peptide cleaved from the amyloid-β precursor protein (APP)) accumulation forming amyloid plaques, hyperphosphorylation and aggregation of tau forming intracellular neurofibrillary tangles (NFTs), and neuroinflammation. This evidence concerns the gene APP and early-onset autosomal dominant Alzheimer disease.