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From the Department of Neurology and Clinical Trials Unit (A.V.), Massachusetts General Hospital and Harvard Medical School, Boston; Division of Epidemiology (W.A.R.), Department of Health Sciences Research and Department of Neurology, College of Medicine, Mayo Clinic, Rochester, MN; INSERM (C.T.), Unit 708 Neuroepidemiology, Paris; UPMC Univ Paris6 (C.T.); and Department of Neurology (C.T.), Hôpital Lariboisière, Paris, France.
Address correspondence and reprint requests to Dr. Christophe Tzourio, INSERM, Unit 708, Hôpital de la Salpêtrière, 47, boulevard de l'Hopital, 75651 Paris Cedex 13, France tzourio{at}chups.jussieu.fr or Dr. Anand Viswanathan, Stroke Service and Memory Disorders Unit, Neurology Clinical Trial Unit, 175 Cambridge Street, Suite 300, Boston, MA 02114 aviswanathan1{at}partners.org.
In recent years, accumulating evidence has suggested that vascular risk factors contribute to Alzheimer disease (AD). Vascular dementia had been traditionally considered secondary to stroke and vascular disease. It has been traditionally distinguished from AD, considered to be a purely neurodegenerative form of dementia. However, in light of this more recent literature, it appears that there is a spectrum: ranging from patients with pure vascular dementia to patients with pure AD and including a large majority of patients with contributions from both Alzheimer and vascular pathologies. In this article, we discuss the impact of vascular risk factors on AD and its consequences at the individual level and at the population level by highlighting the concept of attributable risk. We then discuss the key questions and next steps involved in designing a therapeutic trial to control vascular risk factors for the prevention of dementia.
Abbreviations: AD = Alzheimer disease; VaD = vascular dementia; WMH = white matter hyperintensities.
Supported by ARNEVA (Association de Recherche en Neurologie Vasculaire), Hôpital Lariboisière, Paris, France.
Disclosure: The authors report no disclosures.
Received July 1, 2008. Accepted in final form October 13, 2008.
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