S. Lippa, J. Gill, T. Brickell, Vivian A. Guedes, L. French, R. Lange
{"title":"Blood Biomarkers Predict Future Cognitive Decline after Military-Related Traumatic Brain Injury.","authors":"S. Lippa, J. Gill, T. Brickell, Vivian A. Guedes, L. French, R. Lange","doi":"10.2174/1567205019666220330144432","DOIUrl":null,"url":null,"abstract":"BACKGROUND\nTraumatic brain injury (TBI) has been associated with increased likelihood of late-life dementia; however, the mechanisms driving this relationship are elusive. Blood-based biomarkers may provide insight into these mechanisms and serve as useful prognostic indicators of cognitive recovery or decline following a TBI.\n\n\nOBJECTIVE\nThe aim of this study was to examine blood biomarkers within one year of TBI and explore their relationship with cognitive decline.\n\n\nMETHODS\nService members and veterans (n=224) without injury (n=77), or with history of bodily injury (n=37), uncomplicated mild TBI (n=55), or more severe TBI (n=55), underwent a blood draw and neuropsychological assessment within one year of their injury as part of a case-control study. A subsample (n=87) completed follow-up cognitive assessment.\n\n\nRESULTS\nIn the more severe TBI group, baseline glial fibrillary acidic protein (p=.008) and ubiquitin C-terminal hydrolase-L1 (p=.026) were associated with processing speed at baseline, and baseline ubiquitin C-terminal hydrolase-L1 predicted change in immediate (R2Δ=.244, p=.005) and delayed memory (R2Δ=.390, p=.003) over time. In the mild TBI group, higher baseline tau predicted greater negative change in perceptual reasoning (R2Δ=.188, p=.033) and executive functioning (R2Δ=.298, p=.007); higher baseline neurofilament light predicted greater negative change in perceptual reasoning (R2Δ=.211, p=.012).\n\n\nCONCLUSION\nBaseline ubiquitin C-terminal hydrolase-L1 strongly predicted memory decline in the more severe TBI group, while tau and neurofilament light strongly predicted decline in the mild TBI group. A panel including these biomarkers could be particularly helpful in identifying those at risk for future cognitive decline following TBI.","PeriodicalId":10810,"journal":{"name":"Current Alzheimer research","volume":null,"pages":null},"PeriodicalIF":1.8000,"publicationDate":"2022-03-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"1","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Current Alzheimer research","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.2174/1567205019666220330144432","RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q3","JCRName":"CLINICAL NEUROLOGY","Score":null,"Total":0}
引用次数: 1
Abstract
BACKGROUND
Traumatic brain injury (TBI) has been associated with increased likelihood of late-life dementia; however, the mechanisms driving this relationship are elusive. Blood-based biomarkers may provide insight into these mechanisms and serve as useful prognostic indicators of cognitive recovery or decline following a TBI.
OBJECTIVE
The aim of this study was to examine blood biomarkers within one year of TBI and explore their relationship with cognitive decline.
METHODS
Service members and veterans (n=224) without injury (n=77), or with history of bodily injury (n=37), uncomplicated mild TBI (n=55), or more severe TBI (n=55), underwent a blood draw and neuropsychological assessment within one year of their injury as part of a case-control study. A subsample (n=87) completed follow-up cognitive assessment.
RESULTS
In the more severe TBI group, baseline glial fibrillary acidic protein (p=.008) and ubiquitin C-terminal hydrolase-L1 (p=.026) were associated with processing speed at baseline, and baseline ubiquitin C-terminal hydrolase-L1 predicted change in immediate (R2Δ=.244, p=.005) and delayed memory (R2Δ=.390, p=.003) over time. In the mild TBI group, higher baseline tau predicted greater negative change in perceptual reasoning (R2Δ=.188, p=.033) and executive functioning (R2Δ=.298, p=.007); higher baseline neurofilament light predicted greater negative change in perceptual reasoning (R2Δ=.211, p=.012).
CONCLUSION
Baseline ubiquitin C-terminal hydrolase-L1 strongly predicted memory decline in the more severe TBI group, while tau and neurofilament light strongly predicted decline in the mild TBI group. A panel including these biomarkers could be particularly helpful in identifying those at risk for future cognitive decline following TBI.
期刊介绍:
Current Alzheimer Research publishes peer-reviewed frontier review, research, drug clinical trial studies and letter articles on all areas of Alzheimer’s disease. This multidisciplinary journal will help in understanding the neurobiology, genetics, pathogenesis, and treatment strategies of Alzheimer’s disease. The journal publishes objective reviews written by experts and leaders actively engaged in research using cellular, molecular, and animal models. The journal also covers original articles on recent research in fast emerging areas of molecular diagnostics, brain imaging, drug development and discovery, and clinical aspects of Alzheimer’s disease. Manuscripts are encouraged that relate to the synergistic mechanism of Alzheimer''s disease with other dementia and neurodegenerative disorders. Book reviews, meeting reports and letters-to-the-editor are also published. The journal is essential reading for researchers, educators and physicians with interest in age-related dementia and Alzheimer’s disease. Current Alzheimer Research provides a comprehensive ''bird''s-eye view'' of the current state of Alzheimer''s research for neuroscientists, clinicians, health science planners, granting, caregivers and families of this devastating disease.