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From Taub Institute for Research on Alzheimer’s Disease and the Aging Brain, the Gertrude H. Sergievsky Center, and the Department of Neurology (Drs. Honig and Mayeux), Columbia University College of Physicians & Surgeons, New York, NY; National Alzheimer’s Coordinating Center (Dr. Kukull), Department of Epidemiology, School of Public Health & Community Medicine, University of Washington, Seattle; and Departments of Epidemiology/Public Health and Psychiatry (Dr. Mayeux), Columbia University, New York, NY.
Address correspondence and reprint requests to Dr. Lawrence S. Honig, Taub Institute and G. H. Sergievsky Center, Columbia University College of Physicians and Surgeons, 630 West 168th Street (P& S Unit 16), New York, NY 10032; e-mail: lh456{at}columbia.edu
Background: Epidemiologic studies have implicated cerebrovascular disease and its antecedents as risk factors for Alzheimer disease (AD). Cerebral atherosclerosis or strokes may increase the deposition of neuritic plaques or the formation of neurofibrillary tangles. Alternatively, they may simply hasten the age at onset of disease, or increase the severity of disease symptoms. This investigation examined the association between cerebrovascular disease and the pathologic manifestations of AD in an autopsy series.
Methods: This was a cross-sectional study using data from the United States National Alzheimer’s Coordinating Center database. The primary analysis included 1,054 individuals with clinical information and semiquantitative neuropathologic measurements: 921 had AD as the primary neuropathologic diagnosis and 133 were considered neuropathologically normal.
Results: Overall, 9% of the individuals had clinical history of stroke during life, but 33% had evidence of cerebral infarcts at postmortem. There was no association between neuritic plaques or neurofibrillary tangles, the primary neuropathologic manifestations of AD, with either clinical history of stroke or the presence of cerebral infarcts at postmortem. The authors did find a higher frequency of neuritic plaques and neurofibrillary tangles with increased amyloid angiopathy. Neither plaques nor tangles were associated with small vessel cerebrovascular disease, arteriosclerosis. However, the presence of large-vessel cerebrovascular disease, or atherosclerosis, was strongly associated with an increased frequency of neuritic plaques.
Conclusions: Atherosclerotic cerebrovascular disease may have a role in the pathogenesis of Alzheimer disease, because of a strong association with frequent neuritic plaques.
Additional material related to this article can be found on the Neurology Web site. Go to www.neurology.org and scroll down the Table of Contents for the February 8 issue to find the title link for this article.
L.S.H. and R.M. were supported by the US NIH-National Institute on Aging funded grant (P50-AG 08702; PI Michael Shelanski) entitled "Alzheimer’s Disease Research Center at Columbia University," as well as by the Charles S. Robertson Memorial Gift for AD Research from the Banbury Fund, and the Blanchette Hooker Rockefeller Foundation (both to R.M./Columbia University). L.S.H., W.K., and R.M. received support from the US NIH-National Institute on Aging funded grant (AG16976; PI Walter Kukull) entitled "National Alzheimer’s Disease Coordinating Center," and its associated cooperative agreement with Columbia University.
Received May 26, 2004. Accepted in final form October 13, 2004.
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