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Controlling Vascular Disease May Be Key to Reducing Prevalence of Alzheimer’s Disease

International Experts Review the Latest Thinking in a Special Issue of Journal of Alzheimer’s Disease

November 6, 2012
Over the last 15 years, researchers have found a significant association between vascular diseases such as hypertension, atherosclerosis, diabetes type 2, hyperlipidemia, and heart disease and an increased risk of Alzheimer’s disease. In a special issue of the Journal of Alzheimer’s Disease, leading experts provide a comprehensive overview of the pathological, biochemical, and physiological processes that contribute to Alzheimer’s disease risk and ways that may delay or reverse these age-related abnormalities.

“Vascular risk factors to Alzheimer’s disease offer the possibility of markedly reducing incident dementia by early identification and appropriate medical management of these likely precursors of cognitive deterioration and dementia,” says Guest Editor Jack C. de la Torre, MD, PhD, of the University of Texas, Austin.  “Improved understanding coupled with preventive strategies could be a monumental step forward in reducing worldwide prevalence of Alzheimer’s disease, which is doubling every 20 years.”

The issue explores how vascular disease can affect cerebral blood flow and impair signaling, contributing to Alzheimer’s disease (AD).  The diagnostics of cardiovascular risk factors in AD are addressed, as are potential therapeutic approaches.

Paradoxically, the presence of vascular risk factors in middle age is associated with the development of AD more strongly than late-life vascular disease.  In fact, some research suggests that vascular symptoms later in life may have a protective effect against the development of the disease.  The physiopathological mechanisms that may underlie this phenomenon are discussed.

To date, trials that target major cardiovascular risk factors in the prevention of AD remain inconclusive but have become an important focus of international research as described by contributors of this special volume in their overviews. The multifactorial nature of AD and the need to identify the proper time window for intervention when designing possible interventions, and methodological issues that will have to be addressed to achieve an optimal design of new randomized controlled trials, are discussed.  Promising avenues for treatment, such as the potential of low-level light therapy to increase the rate of oxygen consumption in the brain and enhance cortical metabolic capacity, and the possibility that some antihypertensive drug classes reduce the risk and progression of AD more than others, are discussed.

Dr. de la Torre notes that the presence of vascular risk factors is not an absolute pathway to dementia, and it may be as important to study how or why individuals who are cognitively normal but have vascular risk are able to avoid dementia.  “Reducing Alzheimer’s disease prevalence by focusing right now on vascular risk factors to Alzheimer’s disease, even with our limited technology, is not a simple or easy task.  But the task must begin somewhere and without delay because time is running out for millions of people whose destiny with dementia may start sooner rather than later,” he concludes.


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“Physiopathology of Vascular Risk Factors in Alzheimer’s Disease,” Guest Edited by Jack C. de la Torre. Journal of Alzheimer’s Disease, Volume 32, Issue 3 (October 2012). Published by IOS Press.

Full text of the articles in this special issue is available to credentialed journalists upon request. Contact Esther Mateike, IOS Press, at +31 20 688 3355, to obtain a copy or to request an interview with the authors.

Table of Contents:

Preface, J.C. de la Torre

A Review of the Major Vascular Risk Factors Related to Alzheimer’s Disease, M.C. Polidori, L. Pientka, P. Mecocci

Midlife Vascular Risk Factors and Alzheimer’s Disease:  Evidenece from Epidemiological Studies, A-M. Tolppanen, A. Solomon, H. Soininen, M. Kivipelto

Arterial Stiffness: Detection and Consequences in Cognitive Impairment and Dementia of the Elderly, S.W. Rabkin


Cerebral Hemodynamics and Vascular Risk Factors:  Setting the Stage for Alzheimer’s Disease, J.C. de la Torre

Cerebral Blood Flow Regulation by Nitric Oxide in Alzheimer’s Disease, N. Toda, T. Okamura

Association of Lower Hemoglobin Level and Neuropathology in Community-Dwelling Older Persons, R.C. Shah, J.A. Schneider, S. Leurgans, D.A. Bennett

p38 MAPK:  A Mediator of Hypoxia-Induced Cerebrovascular Inflammation, A. Sanchez, D. Tripathy, X. Yin, et al.

Fibrinogen and Altered Hemostasis in Alzheimer’s Disease, M. Cortes-Canteli, D. Zamolodchikov, H.J.Ahn, et al.

Walking the Cognitive “Minefield” between High and Low Blood Pressure, S. Kennelly, O. Collins

Hypertension is Related to the Microstructure of the Corpus Callosum:  The RUN DMC Study, R.A.R. Gons, L.J.B. van Oudheusden, K.F. de Laat, et al.

Effects of Altered Cerebral Hemodynamics on Cognitive Function, R.S. Marshall

Microvascular Burden and Alzheimer-Type Lesions Across the Age Spectrum, A. Costanza, A. Xekardaki, E. Kövari, et al.

Modifiable Vascular Markers for Cognitive Decline and Dementia:  The Importance of Arterial Aging and Hemodynamic Factors, M.P. Pase


Cognitive Function in Small Vessel Disease:  The Additional Value of Diffusion Tensor Imaging to Conventional Magnetic Resonance Imaging:  The RUN DMC Study, A.G.W. van Norden, I.W.M van Ulden, K.F. de Laat, et al.

Microvascular Perfusion Based on Arterial Spin Labeled Perfusion MRI as a Measure of Vascular Risk in Alzheimer’s Disease, Q. Zhang, R.B. Stafford, Z. Wang, et al.

Cerebrovascular Assessment for the Risk Prediction of Alzheimer’s Disease, M. Silvestrini, G. Viticchi, C. Altamura, et al.

The Imbalance of Vascular Molecules in Alzheimer’s Disease, R.D. Bell

Are Vascular Factors Linked to the Development of Hippocampal Atrophy in Alzheimer’s Disease?  V. Dhikav, K.S. Anand


Preventing Alzheimer’s Disease by Targeting Vascular Risk Factors:  Hope and Gap, C. Qui

Vascular Risk Factors as Treatment Target to Prevent Cognitive Decline, E. Richard, E.P. Moll van Charante, W.A. van Gool

Low-Level Light Therapy Improves Cortical Metabolic Capacity and Memory Retention, J.C. Rojas, A.K. Bruchey, F. Gonzalez-Lima

Association between Chronic Blood Pressure Changes and Development of Alzheimer’s Disease, C.A. Feldstein

Can the Treatment of Vascular Risk Factors Slow Cognitive Decline in Alzheimer’s Disease Patients?  F. Richard, F. Pasquier

Neuroangiogenesis:  A Vascular Basis for Alzheimer’s Disease and Cognitive Decline During Aging, C.T. Ambrose


The Journal of Alzheimer’s Disease ( is an international multidisciplinary journal to facilitate progress in understanding the etiology, pathogenesis, epidemiology, genetics, behavior, treatment and psychology of Alzheimer’s disease. Groundbreaking research that has appeared in the journal includes novel therapeutic targets, mechanisms of disease and clinical trial outcomes. The Journal of Alzheimer’s Disease has an Impact Factor of 3.745 according to Thomson Reuters’ 2011 Journal Citation Reports, 2012. It is ranked #22 on the Index Copernicus Top 100 Journal List. The journal is published by IOS Press.


Commencing its publishing activities in 1987, IOS Press ( serves the information needs of scientific and medical communities worldwide. IOS Press now (co-)publishes over 100 international journals and about 120 book titles each year on subjects ranging from computer sciences and mathematics to medicine and the natural sciences.

All journals are available electronically and an ebook platform was launched in 2005.

Headquartered in Amsterdam with satellite offices in the USA, Germany, India and China, IOS Press has established several strategic co-publishing initiatives. Notable acquisitions included Delft University Press in 2005 and Millpress Science Publishers in 2008.


George Perry, PhD
Editor-in-Chief, Journal of Alzheimer’s Disease
Dean and Professor of Biology, The University of Texas at San Antonio
Tel: +1 210 458 4450
Fax: +1 210 458 4445

Esther Mateike
IOS Press
Tel: +31 20 688 3355
Fax: +31 20 687 0019