Cited by 500Traumatic Brain Injury and Neurovascular DisturbancesTraumatic Brain Injury ResearchNeuroinflammation and Neurodegeneration Mechanisms

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Progressive Neurodegeneration After Experimental Brain Trauma: Association With Chronic Microglial Activation

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Loane, David J., Kumar, Alok, Stoica, Bogdan A., Cabatbat, Rainier, Faden, Alan I.·2014·Journal of Neuropathology & Experimental Neurology

DOI 10.1097/nen.0000000000000021PMC PMC4267248

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Abstract

Recent clinical studies indicate that traumatic brain injury (TBI) produces chronic and progressive neurodegenerative changes leading to late neurologic dysfunction, but little is known about the mechanisms underlying such changes. Microglial-mediated neuroinflammationis an important secondary injury mechanism after TBI. In human studies, microglial activation has been found to persist for many years after the initial brain trauma, particularly after moderate to severe TBI. In the present study, adult C57Bl/6 mice were subjected to single moderate-level controlled cortical impact and were followed up by longitudinal T2-weighted magnetic resonance imaging in combination with stereologic histologic assessment of lesion volume expansion, neuronal loss, and microglial activation for up to 1 year after TBI. Persistent microglial activation was observed in the injured cortex through 1 year after injury and was associated with progressive lesion expansion, hippocampal neurodegeneration, and loss of myelin. Notably, highly activated microglia that expressed major histocompatibility complex class II (CR3/43), CD68, and NADPH oxidase (NOX2) were detected at the margins of the expanding lesion at 1 year after injury; biochemical markers of neuroinflammation and oxidative stress were significantly elevated at this time point. These data support emerging clinical TBI findings and provide a mechanistic link between TBI-induced chronic microglial activation and progressive neurodegeneration.

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Authors: Loane, D. J., Kumar, A., Stoica, B. A., Cabatbat, R., & Faden, A. I.
Affiliations: University of Maryland, Baltimore (US)
Corresponding author: Loane, David J.
ORCID: Loane, David J.
Kumar, Alok
Stoica, Bogdan A.
Faden, Alan I.
Venue: Journal of Neuropathology & Experimental Neurology
Publisher: Oxford University Press (OUP)
Published: 2014-01
Volume: 73
Issue: 1
Pages: 14-29
ISSN: 0022-3069 (ISSN-L)
DOI: 10.1097/nen.0000000000000021
PMC: PMC4267248
OpenAlex: W2067451082
Cited by: 498
References: 49
Citations by year: 2026: 35 · 2025: 28 · 2024: 42 · 2023: 39 · 2022: 39 · 2021: 68 · 2020: 56 · 2019: 42 · 2018: 36 · 2017: 41 · 2016: 31 · 2015: 24 · 2014: 17
FWCI: 15.23
Type: journal article
Language: en
Open access: bronze
doi.org
Locations: Journal of Neuropathology & Experimental Neurology (publishedVersion)
PubMed (publishedVersion)
PubMed Central (acceptedVersion)
Funders: National Institutes of Health
National Institute of Neurological Disorders and Stroke (R01NS037313, R01NS052568, R01NS082308)
Topics: Health Sciences › Medicine › Clinical Neurology › Traumatic Brain Injury and Neurovascular Disturbances
Health Sciences › Medicine › Clinical Neurology › Traumatic Brain Injury Research
Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
Keywords: traumatic brain injury, progressive neurodegeneration, microglial activation, neuroinflammation, controlled cortical impact, lesion expansion, hippocampal neurodegeneration, demyelination, oxidative stress, NADPH oxidase, CD68
MeSH terms: Animals, Brain Injuries, Disease Models, Animal, Male, Mice, Inbred C57BL, Time Factors, Microglia, Disease Progression, Neurodegenerative Diseases, Mice

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Progressive Neurodegeneration After Experimental Brain Trauma: Association With Chronic Microglial Activation

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