The immunology of traumatic brain injury: a prime target for Alzheimer’s disease prevention
Open accessAbstract
A global health problem, traumatic brain injury (TBI) is especially prevalent in the current era of ongoing world military conflicts. Its pathological hallmark is one or more primary injury foci, followed by a spread to initially normal brain areas via cascades of inflammatory cytokines and chemokines resulting in an amplification of the original tissue injury by microglia and other central nervous system immune cells. In some cases this may predispose individuals to later development of Alzheimer's disease (AD). The inflammatory-based progression of TBI has been shown to be active in humans for up to 17 years post TBI. Unfortunately, all neuroprotective drug trials have failed, and specific treatments remain less than efficacious. These poor results might be explained by too much of a scientific focus on neurons without addressing the functions of microglia in the brain, which are at the center of proinflammatory cytokine generation. To address this issue, we provide a survey of the TBI-related brain immunological mechanisms that may promote progression to AD. We discuss these immune and microglia-based inflammatory mechanisms involved in the progression of post-trauma brain damage to AD. Flavonoid-based strategies to oppose the antigen-presenting cell-like inflammatory phenotype of microglia will also be reviewed. The goal is to provide a rationale for investigations of inflammatory response following TBI which may represent a pathological link to AD. In the end, a better understanding of neuroinflammation could open therapeutic avenues for abrogation of secondary cell death and behavioral symptoms that may mediate the progression of TBI to later AD.
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Neuroinflammation may be a significant contributor to secondary cell death immediately following moderate to severe TBI, and inflammatory effects persist up to 17 years post-injury.
“Neuroinflammation may be a significant contributor to secondary cell death immediately following moderate to severe TBI and inflammatory effects have been shown to persist up to 17 years post-injury [97, 98].”
From Glial contributions to neurodegeneration in tauopathies (2017) · cites this paper as [97]
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- Authors
- Giunta, B., Obregon, D., Velisetty, R., Sanberg, P. R., Borlongan, C. V., & Tan, J.
- Affiliations
- James A. Haley Veterans' Hospital (US)
- University of South Florida (US)
- Corresponding author
- Giunta, Brian
- Venue
- Journal of Neuroinflammation
- Published
- 2012-08-01
- Volume
- 9
- Issue
- 1
- Pages
- 185-185
- ISSN
- 1742-2094 (ISSN-L)
- PMC
- PMC3458981
- OpenAlex
- W2097143517
- Cited by
- 112
- References
- 98
- Citations by year
- 2026: 2 · 2025: 3 · 2024: 3 · 2023: 8 · 2022: 8 · 2021: 8 · 2020: 7 · 2019: 11 · 2018: 7 · 2017: 11 · 2016: 11 · 2015: 14 · 2014: 10 · 2013: 7 · 2012: 2
- FWCI
- 0.98
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Locations
- Journal of Neuroinflammation (publishedVersion, cc-by)
- Europe PMC (PubMed Central) (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion)
- Funders
- National Institute of Mental Health (R01MH098737)
- Topics
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Health Sciences › Medicine › Neurology › Traumatic Brain Injury and Neurovascular Disturbances
- Health Sciences › Medicine › Epidemiology › Traumatic Brain Injury Research
- Keywords
- traumatic brain injury, Alzheimer's disease, neuroinflammation, microglia, inflammatory cytokines, chemokines, secondary injury, flavonoids, neuroprotection, armed conflict
- MeSH terms
- Alzheimer Disease, Animals, Brain, Brain Injuries, Humans, Disease Progression, Inflammation Mediators
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