The DOI matches its Crossref record; 50 of the 50 references it cites were found in a registry or an index.
Traumatic Brain Injury and Risk of Neurodegenerative Disorder
Open accessAbstract
Traumatic brain injury (TBI), particularly of greater severity (i.e., moderate-to-severe), has been identified as a risk factor for all-cause dementia and Parkinson’s disease (PD), with risk for specific dementia sub-types being more variable. Among the limited studies involving neuropathological (post-mortem) confirmation, the association between TBI and risk for neurodegenerative disease increases in complexity, with polypathology often reported on examination. The heterogeneous clinical and neuropathological outcomes associated with TBI are likely reflective of the multifaceted post-injury acute and chronic processes that may contribute to neurodegeneration. Acutely in TBI, axonal injury and disrupted transport influences molecular mechanisms fundamental to the formation of pathological proteins, such as amyloid (A) β peptide and hyperphosphorylated tau (pTau). These protein deposits may develop into Aβ plaques, pTau positive neurofibrillary tangles and dystrophic neurites. These and other characteristic neurodegenerative diseases pathologies may then spread across brain regions. The acute immune and neuroinflammatory response involves alteration of microglia, astrocytes, oligodendrocytes, and endothelial cells, release of downstream pro- and anti-inflammatory cytokines and chemokines, and recruitment of peripheral immune cells. Though thought to be neuroprotective and reparative initially, prolongation of these processes may promote neurodegeneration. We review the evidence for TBI as a risk factor for neurodegenerative disorders, including Alzheimer’s dementia and PD, in clinical and neuropathological studies. Further, we describe the dynamic interactions between acute response to injury and chronic processes that may be involved in TBI-related pathogenesis and progression of neurodegeneration.
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Cites
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Clinicopathological evaluation of chronic traumatic encephalopathy in players of American football
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Inflammation after trauma: Microglial activation and traumatic brain injury
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Traumatic brain injury: progress and challenges in prevention, clinical care, and research
Maas, A. I. R., Menon, D. K., Manley, G. T., Abrams, M., Åkerlund, C., Andelic, N., Aries, M., Bashford, T., Bell, M. J., Bodien, Y. G., et al. (2022) · The Lancet Neurology · doi:10.1016/s1474-4422(22)00309-x · Cited by 1,520
Self-citationMental Health Consequences of Traumatic Brain Injury
Howlett, J. R., Nelson, L. D., & Stein, M. B. (2022) · Biological Psychiatry · doi:10.1016/j.biopsych.2021.09.024 · Cited by 389
Recent Research Trends in Neuroinflammatory and Neurodegenerative Disorders
Cohen, J., Mathew, A., Dourvetakis, K. D., Sanchez-Guerrero, E., Pangeni, R. P., Gurusamy, N., Aenlle, K. K., Ravindran, G., Twahir, A., Isler, D., et al. (2024) · Cells · doi:10.3390/cells13060511 · Cited by 103
Hering, C., & Shetty, A. K. (2023) · Stem Cells Translational Medicine · doi:10.1093/stcltm/szad004 · Cited by 50
Metadata
- Authors
- Brett, B. L., Gardner, R. C., Godbout, J., Dams-O’Connor, K., & Keene, C. D.
- Venue
- Biological Psychiatry
- Publisher
- Elsevier BV
- Published
- 2022-03
- Volume
- 91
- Issue
- 5
- Pages
- 498-507
- ISSN
- 0006-3223 (ISSN-L)
- OpenAlex
- W3170885926
- Cited by
- 430
- References
- 50
- FWCI
- 31.86
- Type
- journal article
- Language
- en
- Open access
- bronze
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Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
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