Alzheimers disease (AD) is a common neurodegenerative disorder characterized clinically by progress decline in memory and thinking and pathologically by the presence of senile plaques and neurofibrillary tangles. The strongest risk factors for AD are age family history. Early genetic studies of AD focused on families where the disease exhibited an autosomal dominant pattern of inheritance. Genetic studies in these families identified mutations in three genes that generally cause an early onset form of the disease. These genes pointed to the amyloid peptide, which is the primary component of the senile plaques as central to disease pathogenesis. Subsequent studies in the late onset form of the disease using genome-wide approaches to study both common and rare genetic variation have identified evidence for many more genes that can influence risk for AD. These studies have uncovered other pathways including innate immunity and lipid metabolism that also play key roles in disease risk and point to potential therapeutic targets for treatment of disease.