Alzheimer’s disease (AD) is one of the neurodegenerative disorders, characterized by gradual loss of memory, decline in other cognitive functions and decrease in functional capacity. Increasing age and a positive family history of dementia are the defi nite risk factors of the disease. Molecular analysis of families with early onset of AD (EOAD) has made it possible to identify dominantly acting mutations in genes such as amyloid precursor protein precursor protein and presenilin 1 and 2 (PSEN 1 & PSEN 2). However, the etiology of the late onset of AD (LOAD) is less straightforward than EOAD. The availability of novel genetic tools such as high throughput methods for single nucleotide polymorphism (SNP) genotyping, which simultaneously genotype hundreds of thousands of SNPs using a single SNP array, may facilitate the discovery of genetic infl uences in the disease. These genome-wide association studies have great potential to revolutionize our ability to identify additional genes that contribute to the risk of sporadic AD. It is hoped that the identifi cation of individuals with a high genetic risk of AD will help to develop more rational, cost effective and novel prevention strategies and therapeutic approaches.