Alzheimer’s Disease is classified by age of onset: early-onset (EOAD) before 60-65 years, comprising 5-10% of cases, and late-onset (LOAD) after 60-65 years, accounting for 95%. Familial AD, resulting from single gene mutations, represents a small percentage, with most cases being sporadic and multifactorial. Advancements in Next-Generation Sequencing (NGS) have enabled the identification of numerous genetic variants associated with AD. Early discoveries identified genes such as amyloid precursor protein (APP), presenilin-1 (PSEN1), and presenilin-2 (PSEN2) as monogenic causes of EOAD. Pathogenic variants in these genes are found in about 10-15% of EOAD cases, with PSEN1 variants being the most common. The APOE gene, particularly the ε4 allele, is the strongest genetic risk factor for sporadic LOAD. Individuals with one or two copies of the ε4 allele have a significantly increased risk of developing AD, with a higher risk and earlier onset in homozygotes. Other susceptibility genes identified through genome-wide association studies (GWAS) and whole genome sequencing (WGS) include TREM2, SORL1, ABCA7, and ADAM10.