Commentary: “Treatment of hypertension and prevention of dementia” by Oliver Hanon and Françoise Forette

s m f s S d w n p m f n t r i o Treating hypertension: It’s not just for stroke reducion—Sometime in the not too distant past, dementia reearchers (this writer, at least) thought of vascular dementia, o the extent they thought about it at all, as being quite istinct from Alzheimer’s disease (AD). Then, in the last ecade or so, evidence began to mount that has steadily rought down the walls between AD and the cognitive onsequences of cerebrovascular disease. Observations in representative populations confirm that he combination of cerebrovascular pathology and AD is ommon [1–3]. Clinical–neuropathologic studies have hown that cerebrovascular pathology and AD pathology dditively affect cognitive function [4–6]. Therefore, it is a istake to ignore cerebrovascular disease (either clinically r pathologically) even if it appears that AD is present in ufficient intensity to account for the dementia. It may not e possible in the neuropathologic setting to determine what he relative contributions are of AD and cerebrovascular athology, but the key point is that both are important. By he same line of reasoning, risk factors that are linked to erebrovascular disease should be scrutinized for their links o AD. The observations from epidemiologic surveys on the ssociation between hypertension and AD are a case in oint (See Hanon and Forette [7] for references). The assoiation between diabetes mellitus [8–10] and AD is another xample. These findings have been confirmed repeatedly. In oth conditions, there are associations with change in cogitive function over time. There is also evidence for assoiations between hypertension [11] (and diabetes [12]) and tructural changes in the brain. In the case of hypertension, t is clear that the disorder has an impact on brain structure