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Invited Commentary |

The Continuing Challenge of Turning Promising Observational Evidence About Risk for Dementia to Evidence Supporting Prevention

Carole Dufouil, PhD1; Carol Brayne, MD2
[+] Author Affiliations
1Institut National de la Santé et de la Recherche Médicale (INSERM) Centre U897 and Clinical Investigation Centre EC7, Institut de Santé Publique, d’Épidémiologie et de Développement, Bordeaux University, Centre Hospitalier Universitaire de Bordeaux (Pole de Sante Publique), INSERM, Bordeaux, France
2Department of Public Health and Primary Care, Cambridge Institute of Public Health, University of Cambridge, Cambridge, England
JAMA Intern Med. 2014;174(3):333-335. doi:10.1001/jamainternmed.2013.7674.
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As our society ages, we fear the onset of dementia and Alzheimer disease (AD) every time we forget the name of a person we are sure we once knew. Hard evidence for prevention and causation of dementia remains elusive.1 Models have shown that primary prevention of risks appears more effective for population outcomes than screening or treatment.2 Evidence from observational population-based studies3 suggests that vascular risk factors, including type 2 diabetes mellitus (T2DM), are associated with brain changes, and research on the causes of dementia remains a priority. Trials for prevention of vascular dementia and AD are challenging, requiring many years and many participants for interventions that need to start in middle-aged or younger populations with decades of follow-up. To try to obtain evidence more quickly, attention has focused on surrogate markers (eg, magnetic resonance imaging of the brain), evolution of cognitive tests, and β-amyloid biomarkers.

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