Stroke is one of the three most common causes of death, is a major cause of adult chronic disability,1 and represents an important cause of age-related cognitive decline and dementia. Conventional risk factors explain only a small proportion of all stroke risk.2 Evidence from studies of twins and family history suggests that genetic predisposition is important.3 In common with many other complex diseases, in which environmental risk factors are thought to interact with multiple genes, the identification of the underlying molecular mechanisms contributing to stroke risk has been a challenge. Candidate gene studies have produced few replicable associations.4 More recently, the genome-wide association study (GWAS) approach has transformed the genetics of other complex diseases and is just beginning to affect the study of stroke.5, 6
