Inflammatory markers and cognition in well-functioning African-American and white elders

• Published in: Neurology Vol. 61; no. 1; p. 76
• Main Authors: Yaffe, K, Lindquist, K, Penninx, B W, Simonsick, E M, Pahor, M, Kritchevsky, S, Launer, L, Kuller, L, Rubin, S, Harris, T
• Format: Journal Article
• Language: English
• Published: United States 08.07.2003
• Subjects: African Americans - statistics & numerical data; Age Factors; Aged; Aging - physiology; Biomarkers - analysis; C-Reactive Protein - analysis; Cognition - physiology; Cohort Studies; European Continental Ancestry Group - statistics & numerical data; Female; Follow-Up Studies; Humans; Interleukin-6 - blood; Likelihood Functions; Male; Multivariate Analysis; Neuropsychological Tests - statistics & numerical data; Odds Ratio; Prospective Studies; Tumor Necrosis Factor-alpha - analysis
• ISSN: 1526-632X
• DOI: 10.1212/01.wnl.0000073620.42047.d7

Several lines of evidence suggest that inflammatory mechanisms contribute to AD. To examine whether several markers of inflammation are associated with cognitive decline in African-American and white well-functioning elders. 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-alpha (TNFalpha) 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. 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 < or = 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 TNFalpha (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. 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.