A number of genetic risk factors have been identified, but only a small proportion of Alzheimer's disease (AD) cases can be explained by specific gene mutations. Several genetic risk factors have been linked to AD. Mutations in APP, PS1, and PS2 genes have consistently been associated with early-onset familial Alzheimer's disease (FAD). A majority of AD cases manifest as sporadic late onset form (LOAD) typically with onset above the age of 65 years. Most people who develop Alzheimer's are diagnosed after age 80. More recently a large number of genes have been implicated as a risk to LOAD, but only a few of these associations have been replicated such as the gene encoding for the APOE4 allele or loci in the clusterin (CLU), phosphatidylinositol binding clathrin assembly protein (PICALM), and complement receptor1 (CR1). Most diseases of aging are inşuenced by gene-environment interactions. AD has both genetic and environmental risk factors. The genetic susceptibility inşuenced by genes like ApoE4 are factors to be aware of, but perhaps more important are the environmental risk factors. Environmental risk factors can act as triggers in the expression of gene potential. Numerous studies indicate that ApoE4 carriers may be more vulnerable to environmental factors. Recent studies have shown that dietary factors, such as exposure to a Mediterranean diet, fish and high omega-3 diets, cigarette smoking, head trauma, infections, systemic inşammation, and metal exposure can significantly alter an individual's risk of developing AD. On the other hand psychosocial factors such as education, social network, leisure activities and physical activity, chronic stress, and depression also seem to be connected to the risk of developing AD. There are some somatic factors that are under the direct inşuence of environmental exposures, such as blood pressure, obesity, diabetes mellitus, cardio- and cerebrovascular diseases, and hyperlipidemia, have additionally been implicated in AD etiology.