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Modifiable risk factors like obesity, hypertension, smoking, physical inactivity or atrial fibrillation account for a significant proportion of the risk for ischaemic stroke, but genetic variation is also believed to contribute to the risk, although few genetic risk variants were identified to date. Common clinical subtypes of stroke are caused by cardiac embolism, large artery atherosclerosis and small cerebral vessel disease. Each of these underlying pathologies may have a specific genetic architecture.  Previous genome-wide association studies (GWAS) showed association of variants near  PITX2  and  ZFHX3  with atrial fibrillation and stroke.  ANRIL  (antisense Non-coding RNA in the  INK4  Locus (harboring the  CDKN2A/B  genes)) variants were related to a variety of vascular diseases (myocardial infarction, aortic and intracranial aneurysm), including ischaemic stroke. Now a recent GWAS published in  Nature Genetics  confirmed these previous associations, analyzed the specificity of the previous associations with particular stroke subtypes and identified a new association between  HDAC9  and large vessel stroke. The findings suggest that well-recognized clinical stroke subtypes correspond to distinct aetiological entities. However, the molecular pathways that are affected by the identified genetic variants are not yet pinpointed, and the observed associations apply only for some, but not all victims of a specific stroke aetiology.

Commentary on a GWAS: HDAC9 and the risk for ischaemic stroke