Peripheral levels of fibrinogen, C-reactive protein, and plasma viscosity predict future cognitive decline in individuals without dementia.
OBJECTIVE
To determine whether circulating levels of the biomarkers C-reactive protein (CRP), fibrinogen, plasma viscosity, and hematocrit were associated with cognitive decline in middle-aged to elderly people.


METHODS
Subjects consisted of 2312 men and women aged 50 to 80 years participating in the Aspirin for Asymptomatic Atherosclerosis Trial, all of whom were free of symptomatic cardiovascular disease at baseline. Biomarker levels and cognitive ability were measured at baseline with cognition assessed in all subjects using the Mill Hill Vocabulary Scale and in a subgroup of 504 persons using tests of memory, nonverbal reasoning, information processing speed, executive function, and mental flexibility. After 5 years, the five-test battery was administered to all participants and scores were used to derive a general cognitive ability factor.


RESULTS
Baseline CRP and fibrinogen levels were associated negatively with age and sex-adjusted follow-up scores on the majority of the cognitive tests, and the general cognitive ability factor (correlations = -0.054 to 0.105, p < .05). In analyses adjusting for baseline cognitive scores, asymptomatic atherosclerotic disease, and cardiovascular risk factors, both markers predicted decline in several cognitive domains (excluding memory). Baseline plasma viscosity, but not hematocrit, was associated negatively with follow-up test scores for general cognitive ability, information processing speed, and mental flexibility (correlations = -0.050 to -0.098, p < .05) and with decline across the same domains (p < .05).


CONCLUSIONS
Increased circulating levels of CRP, fibrinogen, and elevated plasma viscosity predicted poorer subsequent cognitive ability and were associated with age-related cognitive decline in several domains, including general ability.
Marioni
Riccardo E
RE
Centre for Population Health Sciences, Public Health Sciences Section, University of Edinburgh, Edinburgh, EH8 9AG, Scotland, UK. R.E.Marioni@sms.ed.ac.uk
Stewart
Marlene C
MC
Murray
Gordon D
GD
Deary
Ian J
IJ
Fowkes
F Gerry R
FG
Lowe
Gordon D O
GD
Rumley
Ann
A
Price
Jackie F
JF
D001241:Aspirin / Q000627:therapeutic use; D050197:Atherosclerosis / Q000188:drug therapy / Q000517:prevention & control; D015415:Biomarkers / Q000097:blood; D001809:Blood Viscosity / Q000502:physiology*; D002097:C-Reactive Protein / Q000032:analysis*; D003072:Cognition Disorders / Q000097:blood* / Q000175:diagnosis; D056344:Executive Function / Q000502:physiology; D005260:Female; D005340:Fibrinogen / Q000032:analysis*; D005500:Follow-Up Studies; D006400:Hematocrit / Q000706:statistics & numerical data; D006801:Humans; D007249:Inflammation / Q000097:blood; D018836:Inflammation Mediators / Q000097:blood; D008297:Male; D008875:Middle Aged; D009483:Neuropsychological Tests; D010949:Plasma / Q000502:physiology; D012307:Risk Factors; D012720:Severity of Illness Index
D015415:Biomarkers; D018836:Inflammation Mediators; D005340:Fibrinogen; D002097:C-Reactive Protein; D001241:Aspirin