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(Arteriosclerosis, Thrombosis, and Vascular Biology. 2003;23:1951.)
© 2003 American Heart Association, Inc.

Editorials

Atherosclerosis and Neurodegeneration

Unexpected Conspirators in Alzheimer’s Dementia

Costantino Iadecola

From the Division of Neurobiology, Department of Neurology and Neuroscience, New York, New York.

Correspondence to Costantino Iadecola, MD, Division of Neurobiology, Department of Neurology and Neuroscience, 411 East 69th St, New York, NY 10021. E-mail coi2001@mail.med.cornell.edu

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

Neurodegeneration, a process of neuronal dysfunction and death independent of vascular factors, has long been considered the main pathogenic process underlying Alzheimer’s disease (AD), the most common form of dementia in the elderly. At the other end of the spectrum, "vascular dementia" was attributed exclusively to vascular alterations resulting in cerebral blood flow (CBF) reductions. In this issue of Atherosclerosis, Thrombosis and Vascular Biology, Roher et al¹ provide new and provocative data indicating that cerebrovascular alterations are a prominent feature of AD neuropathology. These authors examined consecutive autopsy cases in which a diagnosis of AD was made according to well established neuropathological criteria. By comparing AD brains to a group of carefully matched controls, they found that the incidence of vascular narrowing due to atherosclerosis of the circle of Willis is greater in AD than in nondemented controls. Not only was the number of stenoses greater, but also the vascular narrowing was more severe in AD than in controls. The data provide quantitative evidence that atherosclerotic lesions of cerebral blood vessels constitute a major feature of AD neuropathology, perhaps, as prominent as amyloid plaques or neurofibrillary tangles, the traditional pathological hallmarks of the disease.

See page 2055

It has long been suggested that cerebrovascular factors contribute to AD. Alterations in the morphology of cerebral capillaries, smooth muscle cells, blood-brain barrier, and CBF have been reported in AD for several decades (see Kalaria² and de la Torre³ for a review). Furthermore, white matter lesions resembling ischemic lesions have been well . . . [Full Text of this Article]

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