Acute reduction of microglia does not alter axonal injury in a mouse model of repetitive concussive traumatic brain injury
Open accessAbstract
The pathological processes that lead to long-term consequences of multiple concussions are unclear. Primary mechanical damage to axons during concussion is likely to contribute to dysfunction. Secondary damage has been hypothesized to be induced or exacerbated by inflammation. The main inflammatory cells in the brain are microglia, a type of macrophage. This research sought to determine the contribution of microglia to axon degeneration after repetitive closed-skull traumatic brain injury (rcTBI) using CD11b-TK (thymidine kinase) mice, a valganciclovir-inducible model of macrophage depletion. Low-dose (1 mg/mL) valganciclovir was found to reduce the microglial population in the corpus callosum and external capsule by 35% after rcTBI in CD11b-TK mice. At both acute (7 days) and subacute (21 days) time points after rcTBI, reduction of the microglial population did not alter the extent of axon injury as visualized by silver staining. Further reduction of the microglial population by 56%, using an intermediate dose (10 mg/mL), also did not alter the extent of silver staining, amyloid precursor protein accumulation, neurofilament labeling, or axon injury evident by electron microscopy at 7 days postinjury. Longer treatment of CD11b-TK mice with intermediate dose and treatment for 14 days with high-dose (50 mg/mL) valganciclovir were both found to be toxic in this injury model. Altogether, these data are most consistent with the idea that microglia do not contribute to acute axon degeneration after multiple concussive injuries. The possibility of longer-term effects on axon structure or function cannot be ruled out. Nonetheless, alternative strategies directly targeting injury to axons may be a more beneficial approach to concussion treatment than targeting secondary processes of microglial-driven inflammation.
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Low and moderate doses of valganciclovir reduced CD11b cell populations with no effect on axonal injury, silver staining, or APP accumulation at sub-acute post-injury time points.
“In these experiments, low and moderate doses of valganciclovir reduced CD11b cell populations with no effect on axonal injury, silver staining, or APP accumulation at sub-acute post-injury time points (241).”
From The Inflammatory Continuum of Traumatic Brain Injury and Alzheimer’s Disease (2018) · cites this paper as [241]
In the subacute-effects section (21 days; page unavailable), low-dose valganciclovir reduced microglial cells, with no difference in silver staining. The paper reports unchanged APP staining and axonal injury for intermediate-dose treatment at 7 days, not 21 days. At 21 days, intermediate-dose treatment caused tissue loss, and silver staining was not quantified, so the claim extends the no-effect finding beyond the reported results. (LLM, conf=0.89)
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- Authors
- Bennett, R. E., & Brody, D. L.
- Affiliations
- Washington University in St. Louis (US)
- Corresponding author
- Brody, David L.
- Venue
- Journal of Neurotrauma
- Publisher
- SAGE Publications
- Published
- 2014-10
- Volume
- 31
- Issue
- 19
- Pages
- 1647-1663
- ISSN
- 0897-7151 (ISSN-L)
- 1557-9042
- PMC
- PMC4170981
- OpenAlex
- W1971969390
- Cited by
- 64
- References
- 55
- Citations by year
- 2025: 5 · 2024: 2 · 2023: 3 · 2022: 6 · 2021: 9 · 2020: 7 · 2019: 4 · 2018: 6 · 2017: 5 · 2016: 8 · 2015: 9
- FWCI
- 4.78
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Journal of Neurotrauma (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Digital Commons@Becker (Washington University School of Medicine) (submittedVersion)
- Funders
- National Institutes of Health (NIH-R01)
- National Institute of Neurological Disorders and Stroke (F31NS076047, R01NS065069)
- Topics
- Health Sciences › Medicine › Neurology › Traumatic Brain Injury and Neurovascular Disturbances
- Health Sciences › Medicine › Epidemiology › Traumatic Brain Injury Research
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Keywords
- microglia, axonal injury, axonal degeneration, macrophage depletion, valganciclovir, corpus callosum, external capsule, amyloid precursor protein, neurofilaments, secondary injury, microglial inflammation
- MeSH terms
- Animals, Brain Injuries, Disease Models, Animal, Mice, Inbred C57BL, Mice, Mutant Strains, Microglia, Diffuse Axonal Injury, Microscopy, Electron, Transmission, Mice, Real-Time Polymerase Chain Reaction
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