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Hemostatic factor levels and cognitive decline in older adults: The Cardiovascular Health Study
Laura B Harrington1,2,3, Alexa N Ehlert4, Evan L Thacker5
1Kaiser Permanente Washington Health Research Institute, Seattle, WA, USA.
Insights
Certain hemostatic factors, including plasmin-α2-antiplasmin complex (PAP) and tissue factor pathway inhibitor (TFPI), are linked to cognitive decline in older adults. Lower levels of factor X (FXc) also correlated with faster cognitive decline.
Area of Science:
- Gerontology
- Neuroscience
- Hematology
Background:
- Hemostasis plays a critical role in cerebrovascular disease.
- The relationship between hemostatic factors and cognitive decline remains incompletely understood.
Purpose of the Study:
- To prospectively investigate the association between 20 hemostatic factor levels and cognitive changes over 8 years in older adults.
- To analyze cognitive changes using the Modified Mini-Mental State Examination (3MSE) and Digit Symbol Substitution Tests within the Cardiovascular Health Study (CHS).
Main Methods:
- Utilized data from 400 CHS participants with hemostatic factors measured between 1989-1990.
- Employed mixed-effects linear regression models to assess cognitive change, adjusting for covariates and APOE genotype.
- Applied principal component analysis to explore interrelationships among hemostatic factors.
Main Results:
- Higher levels of plasmin-α2-antiplasmin complex (PAP) and tissue factor pathway inhibitor (TFPI) were associated with faster cognitive decline.
- Lower levels of factor X (FXc) were also linked to accelerated cognitive decline.
- A principal component including D-dimer, prothrombin fragment 1.2 (F1.2), and PAP significantly correlated with cognitive change.
Conclusions:
- Specific hemostatic factors (PAP, TFPI, FXc) and a composite factor (PAP, D-dimer, F1.2) are associated with cognitive decline.
- Further research is needed to determine the clinical utility of these findings for dementia prevention and prediction.
Background:
Hemostasis is a key factor in cerebrovascular disease, but the association of hemostatic factors with cognitive decline is unclear.
Objective:
To prospectively evaluate associations of 20 hemostatic factor levels with changes in cognition during ≥8 years of follow-up in the Cardiovascular Health Study (CHS) of older adults.
Methods:
We included participants of an existing CHS cross-sectional substudy (n = 400) with hemostatic factors measured in 1989-1990. Between 1989-1990 and 1998-1999, cognitive function was measured using the Modified Mini-Mental State Examination (3MSE) and Digit Symbol Substitution Tests. Mixed-effects linear regression models estimated change in cognitive function over time, adjusting for sociodemographic and clinical factors and APOE genotype, using Bonferroni adjustment. We also derived principal components to account for the interrelationship among factors.
Results:
Of 20 factors evaluated individually, only higher levels of plasmin-α2 -antiplasmin complex (PAP), tissue factor pathway inhibitor (TFPI), and lower factor X (FXc) levels were associated with faster cognitive decline, estimated by annual change in 3MSE points (1 standard deviation PAP β = -0.65, 95% confidence interval [CI]: -1.08 to -0.21; TFPI β = -0.55, 95% CI: -0.90 to -0.19; FXc β = 0.52, 95% CI: 0.21-0.84). One of four principal components, loading positively on D-dimer, prothrombin fragment 1.2 (F1.2), and PAP was significantly associated with change in 3MSE.
Conclusions:
Levels of PAP, TPFI, and FXc and a combination of factors driven by PAP, D-dimer, and F1.2 were associated with cognitive decline. Whether these findings can be used to improve dementia prevention or prediction requires further study.
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