4.6 Article

Inflammatory Biomarkers and Cognitive Decline: The Ginkgo Evaluation of Memory Study

Journal

JOURNAL OF THE AMERICAN GERIATRICS SOCIETY
Volume 64, Issue 6, Pages 1171-1177

Publisher

WILEY-BLACKWELL
DOI: 10.1111/jgs.14140

Keywords

cognition; dementia; inflammation; biomarkers; Alzheimer's; 3MSE

Funding

  1. National Center for Complementary and Integrative Health (NCCIH) [R01 AT006668-01, 5 U01 AT000162]
  2. National Institute on Aging (NIA)
  3. National Heart, Lung, and Blood Institute
  4. University of Pittsburgh Alzheimer's Disease Research Center [P50AG05133]
  5. Roena Kulynych Center for Memory and Cognition Research
  6. National Institute of Neurological Disorders and Stroke
  7. NIA [U24 AG21886]

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OBJECTIVES: To examine the association between inflammatory biomarkers and global cognitive function. DESIGN: Case-cohort. SETTING: Ginkgo Evaluation of Memory Study. PARTICIPANTS: Individuals aged 75 and older free of neurological or neurodegenerative conditions recruited from 2000 to 2002 (N = 1,315). MEASUREMENTS: Outcome was cognitive function assessed using the modified Mini-Mental State Examination (3MSE) every 6 months for up to 7 years. Exposures were 10 biomarkers measured at baseline: interleukin-2, -6, and -10 (general systemic inflammation); pentraxin 3 (PTX3) and serum amyloid P (SAP) (vascular inflammation); plasminogen activator inhibitor-1, adiponectin, and resistin (metabolic function); receptor for advanced glycation endproduct (oxidative stress); and endothelin-1 (endothelial function). Associations between biomarkers and 3MSE scores (stratified according to mild cognitive impairment (MCI) at baseline) were analyzed using Cox regression (outcome: 3MSE decline of >= 5 points) and mixed-model regression. Bonferroni correction was used to determine significance threshold (P<.0025). RESULTS: In individuals with baseline MCI, PTX3 was associated with a 20% greater hazard of cognitive decline (95% confidence interval = 1.07-1.35), although this association was no longer statistically significant after adjustment for apolipoprotein (APO)E epsilon 4 allele. Adiponectin was associated with faster rate of 3MSE decline in individuals without baseline MCI in mixed-model regression, but the association was similarly attenuated after adjustment for APOE-epsilon 4. CONCLUSION: This study did not find strong evidence of the utility of the biomarkers evaluated for identifying individuals at risk of cognitive decline. Future studies investigating the association between PTX3, SAP, and adiponectin and 3MSE scores may be useful.

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