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(Stroke. 2004;35:2615.)
© 2004 American Heart Association, Inc.

Articles

Vascular Cognitive Impairment

Introduction

From the Department of Neurology, University of Western Ontario (V.H.), London, Ontario, Canada; and the Division of Neurobiology (C.I.), Weill Medical College of Cornell University and Neuroscience, New York, NY.

Correspondence to Dr Vladimir Hachinski, Editor-in-Chief, Stroke, UWO Research Park, 100 Collip Circle, Suite 116, London, Ontario, Canada, N6G 4X8. E-mail stroke@lhsc.on.ca

An extract of the first 250 words of the full text is provided, because this article has no abstract.

One of the greatest advances in the understanding of cognitive disorders comes from the realization that Alzheimer disease (AD) and vascular cognitive impairment share common risk factors. This opens the door to a common approach to both and promises that if vascular risk factors are controlled, then not only strokes but also cognitive impairment could be prevented. It also has become evident that AD pathology and vascular lesions often coexist in the brains of the elderly. Less certain is whether the effects are additive or multiplicative.

Gorelick¹ reviews and categorizes systematically the different risk factors as demographic, atherosclerotic, genetic, and stroke-related. As our knowledge grows, perhaps another relevant category will be identified, namely protective factors. Not all brains are created equal, varying both in their capacity and in their resistance to injury. Moreover, the brain is molded by experience and environment. We are just beginning to glimpse what strengthens and weakens the brain’s natural resilience.

Amyloid angiopathy has long been recognized in association with cognitive impairment, especially AD. What was not realized is that amyloidal deposition is strongly associated with white matter changes and a host of vascular alterations. Greenberg et al² emphasize that microcirculatory changes long precede the familiar catastrophic hemorrhage, sometimes heralded by small warning leaks. Understanding the mechanisms of amyloid deposition and clearance may hold the key to successful interventions.

Deave et al³ describe the important and interactive roles of the receptor for advanced glycation end products and low-density lipoprotein receptor-related protein-1 in the trafficking of ß-amyloid . . . [Full Text of this Article]

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