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From the Departments of Psychiatry (Dr. Yaffe), Neurology (Dr. Yaffe), Epidemiology (Dr. Yaffe), and Geriatrics (K. Lindquist) and Prevention Sciences Group (Dr. Yaffe, S. Rubin), University of California, San Francisco; Sticht Center on Aging (Drs. Penninx and Pahor), Wake Forest University School of Medicine, Winston–Salem, NC; Intramural Research Program (Dr. Simonsick), National Institute on Aging, and Laboratory of Epidemiology, Demography, and Biometry (Drs. Launer and Harris), National Institute on Aging, Bethesda, MD; Department of Preventive Medicine (Dr. Kritchevsky), University of Tennessee at Memphis; and Department of Epidemiology (Dr. Kuller), Graduate School of Public Health, University of Pittsburgh School of Medicine, PA.
Address correspondence and reprint requests to Dr. K. Yaffe, University of California, San Francisco, 4150 Clement St., Box 111G, San Francisco, CA 94121; e-mail: kyaffe{at}itsa.ucsf.edu
Background: Several lines of evidence suggest that inflammatory mechanisms contribute to AD.
Objective: To examine whether several markers of inflammation are associated with cognitive decline in African-American and white well-functioning elders.
Methods: The authors studied 3,031 African-American and white men and women (mean age 74 years) enrolled in the Health, Aging, and Body Composition Study. Serum levels of interleukin-6 (IL-6) and C-reactive protein (CRP) and plasma levels of tumor necrosis factor-
(TNF) were measured at baseline; cognition was assessed with the Modified Mini-Mental State Examination (3MS) at baseline and at follow-up. Cognitive decline was defined as a decline of >5 points.
Results: In age-adjusted analyses, participants in the highest tertile of IL-6 or CRP performed nearly 2 points lower (worse) on baseline and follow-up 3MS (p < 0.001 for all) and declined by almost 1 point over the >2 years (p = 0.01 for IL-6 and p = 0.04 for CRP) compared with those in the lowest tertile. After multivariate adjustment, 3MS scores among participants in the highest tertile of IL-6 and CRP were similar at baseline but remained significantly lower at follow-up (p 
0.05 for both). Those in the highest inflammatory marker tertile were also more likely to have cognitive decline compared with the lowest tertile for IL-6 (26 vs 20%; age-adjusted odds ratio [OR] = 1.34; 95% CI 1.06 to 1.69) and for CRP (24 vs 19%; OR = 1.41; 95% CI 1.10 to 1.79) but not for TNF (23 vs 21%; OR = 1.12; 95% CI 0.88 to 1.43). There was no significant interaction between race and inflammatory marker or between nonsteroidal anti-inflammatory drug use and inflammatory marker on cognition.
Conclusions: Serum markers of inflammation, especially IL-6 and CRP, are prospectively associated with cognitive decline in well-functioning elders. These findings support the hypothesis that inflammation contributes to cognitive decline in the elderly.
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