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. 2022 Apr 16;S0889-1591(22)00114-3.
doi: 10.1016/j.bbi.2022.04.014.
Online ahead of print.
Affiliations
Affiliations
- 1 Department of Psychology, University of Illinois at Chicago, Chicago, IL 60607 USA; Rush Alzheimer’s Disease Center, Rush University Medical Center, Chicago, IL 60612 USA.
- 2 Department of Anesthesiology, University of Illinois at Chicago, Chicago, IL 60612 USA; Jesse Brown VA Medical Center, Chicago, IL 60612 USA.
- 3 Rush Alzheimer’s Disease Center, Rush University Medical Center, Chicago, IL 60612 USA; Department of Psychiatry and Behavioral Sciences, Rush University Medical Center, Chicago, IL 60612 USA.
- 4 Department of Psychiatry, University of North Carolina at Chapel Hill School of Medicine, Chapel Hill NC 27516 USA.
- 5 Rush Alzheimer’s Disease Center, Rush University Medical Center, Chicago, IL 60612 USA; Department of Psychiatry and Behavioral Sciences, Rush University Medical Center, Chicago, IL 60612 USA; Department of Neurological Sciences, Rush University Medical Center, Chicago, IL 60612 USA.
- 6 Rush Alzheimer’s Disease Center, Rush University Medical Center, Chicago, IL 60612 USA; Department of Psychiatry and Behavioral Sciences, Rush University Medical Center, Chicago, IL 60612 USA. Electronic address: eboots2@uic.edu.
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Elizabeth A Boots et al.
Brain Behav Immun.
.
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. 2022 Apr 16;S0889-1591(22)00114-3.
doi: 10.1016/j.bbi.2022.04.014.
Online ahead of print.
Affiliations
- 1 Department of Psychology, University of Illinois at Chicago, Chicago, IL 60607 USA; Rush Alzheimer’s Disease Center, Rush University Medical Center, Chicago, IL 60612 USA.
- 2 Department of Anesthesiology, University of Illinois at Chicago, Chicago, IL 60612 USA; Jesse Brown VA Medical Center, Chicago, IL 60612 USA.
- 3 Rush Alzheimer’s Disease Center, Rush University Medical Center, Chicago, IL 60612 USA; Department of Psychiatry and Behavioral Sciences, Rush University Medical Center, Chicago, IL 60612 USA.
- 4 Department of Psychiatry, University of North Carolina at Chapel Hill School of Medicine, Chapel Hill NC 27516 USA.
- 5 Rush Alzheimer’s Disease Center, Rush University Medical Center, Chicago, IL 60612 USA; Department of Psychiatry and Behavioral Sciences, Rush University Medical Center, Chicago, IL 60612 USA; Department of Neurological Sciences, Rush University Medical Center, Chicago, IL 60612 USA.
- 6 Rush Alzheimer’s Disease Center, Rush University Medical Center, Chicago, IL 60612 USA; Department of Psychiatry and Behavioral Sciences, Rush University Medical Center, Chicago, IL 60612 USA. Electronic address: eboots2@uic.edu.
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Abstract
Peripheral inflammation is elevated in older Black adults, an elevation which prior work has suggested may be due to chronic stress associated with systemic racism and related adverse cardiovascular health conditions. Inflammation is also involved in the pathogenic processes of dementia; however, limited (and mixed) results exist concerning inflammation and cognitive decline in Black adults. We characterized patterns of inflammation and their role in cognitive decline in 280 older Black adults (age=72.99±6.00 years; 69.6% female) from the Minority Aging Research Study (MARS) who were without dementia at baseline and followed between 2 and 15 years (mean=9 years). Participants completed a blood draw at baseline and annual cognitive evaluations. Serum was assayed for 9 peripheral inflammatory markers; 19 neuropsychological test scores were used to create indices of global cognition and five cognitive domains. Principal component analysis with varimax rotation characterized patterns of inflammation with factor loadings >0.6 per component contributing to two composite scores representing acute/upstream and chronic/downstream inflammation. These composites were used as separate predictors in linear mixed regression models to determine associations with level and change in cognition adjusting for relevant covariates. Higher baseline upstream/acute inflammation associated with lower baseline semantic memory (p=.040) and perceptual speed (p=.046); it was not related to cognitive decline. By contrast, higher baseline downstream/chronic inflammation associated with faster declines in global cognition (p=.010), episodic (p=.027) and working memory (p=.006); it was not related to baseline cognition. For older Black adults, chronic, but not acute, inflammation may be a risk factor for changes in cognition.
Keywords:
African American/Black adults; aging; cognition; inflammation.
Copyright © 2022. Published by Elsevier Inc.
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