Matthew J Lennon1,2, Rebecca Koncz2,3,4, Perminder S Sachdev1,2,5. 1. Faculty of Medicine, University of New South Wales. 2. Centre for Healthy Brain Aging, University of New South Wales, Sydney. 3. Discipline of Psychiatry, Concord Clinical School, The University of Sydney, Sydney. 4. Sydney Local Health District, Concord, New South Wales, Australia. 5. Department of Neuropsychiatry, Prince of Wales Hospital, Randwick.
Abstract
PURPOSE OF REVIEW: The relationship between hypertension and Alzheimer's disease (AD) is complex and varies across the lifespan. Studies have suggested that midlife hypertension is a risk factor for AD, although studies of late life hypertension have suggested that it either has no effect or a weak protective effect. RECENT FINDINGS: Animal models of induced and spontaneous hypertension have found that AD pathological change (β-amyloid plaques and tau tangles) occurs within weeks of a hypertensive insult. Human imaging and autopsy studies indicate that midlife and late life hypertension are associated with increased AD pathological change. Meta-analyses of longitudinal studies indicate that midlife rather than late life hypertension is a risk factor for AD. New areas of research have suggested that rather than mean blood pressure (BP), it is the negative BP trajectories or the variability of BP that contributes to AD. In a number of meta-analyses of antihypertensive medications and their effect on AD, there were weak associations between improved AD outcomes and treatment. SUMMARY: The combined analysis of animal, human clinical/pathological, epidemiological and drug trial data indicates that hypertension increases the risk of AD and treatment of hypertension may be an appropriate preventive measure.
PURPOSE OF REVIEW: The relationship between hypertension and Alzheimer's disease (AD) is complex and varies across the lifespan. Studies have suggested that midlife hypertension is a risk factor for AD, although studies of late life hypertension have suggested that it either has no effect or a weak protective effect. RECENT FINDINGS: Animal models of induced and spontaneous hypertension have found that AD pathological change (β-amyloid plaques and tau tangles) occurs within weeks of a hypertensive insult. Human imaging and autopsy studies indicate that midlife and late life hypertension are associated with increased AD pathological change. Meta-analyses of longitudinal studies indicate that midlife rather than late life hypertension is a risk factor for AD. New areas of research have suggested that rather than mean blood pressure (BP), it is the negative BP trajectories or the variability of BP that contributes to AD. In a number of meta-analyses of antihypertensive medications and their effect on AD, there were weak associations between improved AD outcomes and treatment. SUMMARY: The combined analysis of animal, human clinical/pathological, epidemiological and drug trial data indicates that hypertension increases the risk of AD and treatment of hypertension may be an appropriate preventive measure.