Elevated blood pressure is a major modifiable risk factor for mortality worldwide and can lead to the development of cerebrovascular disease and dementia. Observational and prospective studies, as well as randomized clinical trials of antihypertensive drugs, have shown that hypertension may be causally related to cognitive impairment. At the same time, elevated blood pressure causes long-term changes in specific brain structures. While the links between blood pressure and cognitive function may be mediated by changes in brain structures, the causal nature and exact mechanisms of these links have been difficult to study in the past. Therefore, the identification of specific brain areas mediating blood pressure-dependent cognitive changes is of paramount clinical importance.
Whole-genome studies of the human genome (known as GWAS) enable the identification of genetic tools causally related to a trait, which can be used to accurately study brain regions and cognitive functions, since they are, at least in part, heritable. While randomized clinical trials remain the gold standard for inferring a causal relationship between different clinical traits, approaches to causal inference using genetic tools through Mendelian randomization (MR) are at the intersection of experimental/clinical and observational studies. At the same time, a growing number of comprehensive human genome studies with high statistical power are facilitating the identification of genetic proxies for complex phenotypes, such as blood pressure and cognitive function, which can be used for MR analysis both as causal variables and as effects of the process under study. Importantly, they can provide unique tools to pinpoint specific brain structures a...
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