This article is a US Government work and, as such, is in the public domain in the United States of America.
Early inflammation and dementia: A 25-year follow-up of the Honolulu-Asia aging study†
Article first published online: 22 MAY 2002
Published 2002 Wiley-Liss, Inc.
Annals of Neurology
Volume 52, Issue 2, pages 168–174, August 2002
How to Cite
Schmidt, R., Schmidt, H., Curb, J. D., Masaki, K., White, L. R. and Launer, L. J. (2002), Early inflammation and dementia: A 25-year follow-up of the Honolulu-Asia aging study. Ann Neurol., 52: 168–174. doi: 10.1002/ana.10265
- Issue published online: 23 JUL 2002
- Article first published online: 22 MAY 2002
- Manuscript Accepted: 3 APR 2002
- Manuscript Received: 3 JAN 2002
- National Institutes of Health
- National Institute on Aging. Grant Number: N01-AG-4-2149
- National Heart, Lung, and Blood Institute. Grant Number: N01-HC-05102
Inflammatory responses are associated with cardiovascular disease and may be associated with dementing disease. We evaluated the long-term prospective association between dementia and high-sensitivity C-reactive protein, a nonspecific marker of inflammation. Data are from the cohort of Japanese American men who were seen in the second examination of the Honolulu Heart Program (1968–1970) and subsequently were reexamined 25 years later for dementia in the Honolulu-Asia Aging Study (1991–1996). In a random subsample of 1,050 Honolulu-Asia Aging Study cases and noncases, high-sensitivity C-reactive protein concentrations were measured from serum taken at the second examination; dementia was assessed in a clinical examination that included neuroimaging and neuropsychological testing and was evaluated using international criteria. Compared with men in the lowest quartile (<0.34mg/L) of high-sensitivity C-reactive protein, men in the upper three quartiles had a 3-fold significantly increased risk for all dementias combined, Alzheimer's disease, and vascular dementia. For vascular dementia, the risk increased with increasing quartile. These relations were independent of cardiovascular risk factors and disease. These data support the view that inflammatory markers may reflect not only peripheral disease, but also cerebral disease mechanisms related to dementia, and that these processes are measurable long before clinical symptoms appear.