The genetic background of Alzheimer's disease (AD) encompasses both rare familial forms and more common late-onset forms. Familial Alzheimer's disease (FAD) represents a small percentage of Alzheimer's cases and is inherited in an autosomal dominant pattern, meaning that an affected individual has a 50% chance of passing the mutated gene to their offspring. Mutations in three genes have been identified as causative for FAD: (i) Amyloid precursor protein (APP): mutations in the APP gene, located on chromosome 21, tend to inhibit cleavage by α-secretase and facilitate preferential cleavage by β-secretase, which leads to increased production or altered processing of β-amyloid, resulting in the accumulation of amyloid plaques in the brain; (ii) Presenilin 1 (PSEN1): mutations in the PSEN1 gene, located on chromosome 14, are the most common cause of FAD. PSEN1 is a component of the γ-secretase complex involved in the cleavage of amyloid precursor protein (APP), and mutations in PSEN1 enhance cleavage by γ-secretase and lead to increased production of β-amyloid; (iii) Presenilin 2 (PSEN2): mutations in the PSEN2 gene, located on chromosome 1, are less common but can also cause FAD. Like PSEN1, PSEN2 is involved in the processing of APP, enhanced cleavage by γsecretase, and the production of β-amyloid. Late-onset Alzheimer's disease (LOAD) is the most common form of AD and typically occurs after age of 65. While LOAD has a strong genetic component, it is influenced by multiple genetic and environmental factors. The strongest genetic risk factor for LOAD is the apolipoprotein E (APOE) gene, located on chromosome 19. The APOE gene has three common alleles: ε2, ε3, and ε4. The ε4 allele of APOE is associated with an increased risk of developing AD and a younger age of onset. Individuals who inherit one copy of the APOE ε4 allele have an increased risk, while those who inherit two copies have an even higher risk. In addition to APOE, several other genetic variants have been identified as risk factors for LOAD through genome-wide association studies. These include genes involved in inflammation, cholesterol metabolism, immune response, and synaptic function. While these genetic risk factors increase susceptibility to AD, they do not guarantee that an individual will develop the condition. Environmental factors and gene-environment interactions also play a significant role in disease risk.