The main theoretical concept in Alzheimer’s disease (AD) is the amyloid cascade hypothesis, postulating that amyloid-β (Aβ) deposition in the brain is a primary driver of AD pathogenesis, impairing synaptic efficacy, and causes calcium dyshomeostasis, inflammation, oxidative stress, as well as tau hyperphosphorylation and the formation of neurofibrillary tangles (NFTs) at specific brain regions [1]. The gene discussed is MAPT; the disease is early-onset autosomal dominant Alzheimer disease.