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Traumatic brain injury in aged animals increases lesion size and chronically alters microglial/macrophage classical and alternative activation states
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Traumatic brain injury (TBI) causes chronic microglial activation that contributes to subsequent neurodegeneration, with clinical outcomes declining as a function of aging. Microglia/macrophages (MG/Mɸ) have multiple phenotypes, including a classically activated, proinflammatory (M1) state that might contribute to neurotoxicity, and an alternatively activated (M2) state that might promote repair. In this study we used gene expression, immunohistochemical, and stereological analyses to show that TBI in aged versus young mice caused larger lesions associated with an M1/M2 balance switch and increased numbers of reactive (bushy and hypertrophic) MG/Mɸ in the cortex, hippocampus, and thalamus. Chitinase3-like 3 (Ym1), an M2 phenotype marker, displayed heterogeneous expression after TBI with amoeboid-like Ym1-positive MG/Mɸ at the contusion site and ramified Ym1-positive MG/Mɸ at distant sites; this distribution was age-related. Aged-injured mice also showed increased MG/Mɸ expression of major histocompatibility complex II and NADPH oxidase, and reduced antioxidant enzyme expression which was associated with lesion size and neurodegeneration. Thus, altered relative M1/M2 activation and an nicotinamide adenine dinucleotide phosphate oxidase (NADPH oxidase)-mediated shift in redox state might contribute to worse outcomes observed in older TBI animals by creating a more proinflammatory M1 MG/Mɸ activation state.
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“The mode of activation following TBI is somewhat age-dependent and may be less neuroprotective and more toxic in older animals [109].”
From Untangling senescent and damage‐associated microglia in the aging and diseased brain (2023) · cites this paper as [109]
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“Elderly individuals are at greater risk to suffer significant cognitive impairment and early morbidity following TBI, potentially due to an already present dysfunction in the microglial compartment [109,122,123].”
From Untangling senescent and damage‐associated microglia in the aging and diseased brain (2023) · cites this paper as [109]
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Metadata
- Authors
- Kumar, A., Stoica, B. A., Sabirzhanov, B., Burns, M. P., Faden, A. I., & Loane, D. J.
- Affiliations
- University of Maryland, Baltimore (US)
- Georgetown University Medical Center (US)
- Corresponding author
- Loane, David J.
- Venue
- Neurobiology of Aging
- Publisher
- Elsevier BV
- Published
- 2013-05
- Volume
- 34
- Issue
- 5
- Pages
- 1397-1411
- ISSN
- 0197-4580 (ISSN-L)
- PMC
- PMC3572914
- OpenAlex
- W2043020388
- Cited by
- 244
- References
- 69
- Citations by year
- 2026: 7 · 2025: 8 · 2024: 13 · 2023: 10 · 2022: 14 · 2021: 16 · 2020: 21 · 2019: 15 · 2018: 21 · 2017: 24 · 2016: 33 · 2015: 27 · 2014: 25 · 2013: 10
- FWCI
- 12.91
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Neurobiology of Aging (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Capital Area Rehabilitation Research Network (R24HD050845)
- Topics
- Health Sciences › Medicine › Clinical Neurology › Traumatic Brain Injury and Neurovascular Disturbances
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Health Sciences › Medicine › Clinical Neurology › Traumatic Brain Injury Research
- Keywords
- traumatic brain injury, aging, microglial activation, macrophages, macrophage polarization, Ym1, NADPH oxidase, MHC class II, antioxidant enzymes, neurodegeneration, lesion size, reactive microglia, redox state, proinflammation
- MeSH terms
- Aging, Animals, Brain, Brain Injuries, Cells, Cultured, Chronic Disease, Macrophage Activation, Macrophages, Male, Mice, Inbred C57BL, Microglia, Mice
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