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The heritability of stroke risk is supported by family-based analyses and concordance analyses focusing on monozygotic twins.1,2 While mutations in certain genes, such as notch3 causing cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy, predispose to cerebral ischemic events, the genetic underpinnings in nonsyndromic stroke remain largely unknown. In most stroke patients without a genetic syndrome, ischemic stroke is likely multifactorial, resulting from complex interactions among multiple genetic and environmental risk factors. Unlike the approach to monogenetic diseases, where genetic risk is dichotomous (i.e., an abnormal gene causes disease but disease does not occur when the gene is normal), the complex disease model holds that a collection of haplotypes confers disease risk in a graded manner with variable penetrance and unpredictable interactions among polygenic traits.3
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See page 678
- © 2014 American Academy of Neurology
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