Mutations in the dominant genes including Amyloid Precursor Protein (APP), Presenilin-1 (PSEN-1), Presenilin-2 (PSEN-2), apolipoprotein E (ApoE), and others, are associated with AD. From thirty discovered mutations in the APP gene, twentyfive have been found related to AD and causing accumulation of Aβ. 132, 133 PSEN1 and PSEN2 genes are also the autosomal dominant form of early-onset AD. Mutation in PSEN1 gene is more frequent, with more than 200 mutations, while in the PSEN2 gene only a rare form with less than 40 mutations was identified. Apolipoprotein E (ApoE), especially ApoEε4 plays an important role in Aβ deposition as a senile plaque. It has been found to cause cerebral amyloid angiopathy, known as a marker for AD. ApoEε4 is also related to vascular damage in the brain, leading to AD pathogenesis. Adenosine triphosphate (ATP)-binding cassette transporter A1 (ABCA1) is known to regulate the stability of ApoE lipidation. Mutation in the ABCA1 gene has been reported to result accumulation of cholesterol in tissues, and AD pathogenesis. In contrast to PSEN1, PSEN2, and APP mutations, Clusterin (CLU) and Bridging Integrator 1 (BIN1) genes are risk factors for late-onset AD. According to CAS Content Collection, the largest number of documents associate APP, ApoE, PSEN-1, and CLU genes with AD pathogenesis (Figure , lower panel). ABCA1, CLU, BIN1, and ApoE are the risk factors exhibiting the fastest growth in the number of documents in the last five years (2019-2023) (Figure , upper panel).