The amyloid -peptide (A) is significantly linked to the pathogenesis of Alzheimer's disease by genetics. Early-onset familial Alzheimer's disease (FAD) is brought on by dominant missense mutations in the presenilin and the APP. γ-secretase inhibitors can reduce brain Aβ levels when taken orally, according to research in both genetic and non-genetic animal studies of AD. Drug development efforts have found substances that modify γ-secretase's ability to produce Aβ without disrupting Notch proteolysis or signaling, and these substances are under development at various phases of the process. Semagacestat (LY450139), which inhibits Aβ, greatly reduced CNS Aβ production in a dose-dependent manner. Lecanemab, however, failed to achieve the 12-month primary goal. However, our 18-month Bayesian evaluations revealed a fall in brain amyloid associated with a constant decline in clinical status across a number of clinical and biomarker endpoints.