ArticleGeroScience2022
Functional and transcriptional profiling of microglial activation during the chronic phase of TBI identifies an age-related driver of poor outcome in old mice.
Article in GeroScience, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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Who cites it
26 citing papers in PubMed, 48 citations in OpenAlex.
- Aging reprograms microglia toward an inflammasome-linked response to traumatic brain injury.The Journal of clinical investigation · 2026Article
- Multiorgan transcriptomics and circulating extracellular vesicle profiling reveal age-dependent systemic vulnerability to isoflurane anesthesia and surgery.GeroScience · 2026Article
- Ganoderic Acid a Promotes Functional Recovery After Traumatic Brain Injury By Protecting Blood-brain Barrier Integrity and Modulating Microglial Polarization.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2026Article
- Ligustilide Ameliorates Traumatic Brain Injury in Aged Mice by Attenuating Microglia-Mediated Neuroinflammation.Neurochemical research · 2025Article
- Immunosenescence and cancer: molecular hallmarks, tumor microenvironment remodeling, and age-specific immunotherapy challenges.Journal of hematology & oncology · 2025Review
- Adolescent mice exposed to TBI developed PD-like pathology in middle age.Translational psychiatry · 2025Article
- TREM2 affects DAM-like cell transformation in the acute phase of TBI in mice by regulating microglial glycolysis.Journal of neuroinflammation · 2025Article
- Trehalose Inhibits ferroptosis Through Activating SIRT3/SOD2 Signaling Axis and Alleviates Brain Injury After Traumatic Brain Injury.Neurochemical research · 2025Article
- Article
- Old age alters inflammation and autophagy signaling in the brain, leading to exacerbated neurological outcomes after spinal cord injury in male mice.Brain, behavior, and immunity · 2024Article
- International consensus guidelines for the definition, detection, and interpretation of autophagy-dependent ferroptosis.Autophagy · 2024Review
- Article
- Bi-directional neuro-immune dysfunction after chronic experimental brain injury.Journal of neuroinflammation · 2024Article
- Ablation of the integrin CD11b mac-1 limits deleterious responses to traumatic spinal cord injury and improves functional recovery in mice.Research square · 2024Article
- Old Age Exacerbates White Matter Neuroinflammation and Cognitive Deficits Following Closed-Head Injury, Particularly in Female Mice.Neurotrauma reports · 2024Article
- Age at Injury as a Modifier of Preclinical TBI Behavioral, Neuropathological, and Inflammatory Outcomes.Advances in neurobiology · 2024Review
- The Role of Methionine-Rich Diet in Unhealthy Cerebrovascular and Brain Aging: Mechanisms and Implications for Cognitive Impairment.Nutrients · 2023Review
- Traumatic brain injury-induced inflammatory changes in the olfactory bulb disrupt neuronal networks leading to olfactory dysfunction.Brain, behavior, and immunity · 2023Article
- Iron overload induces cerebral endothelial senescence in aged mice and in primary culture in a sex-dependent manner.Aging cell · 2023Article
- Microglia moonlighting after traumatic brain injury: aging and interferons influence chronic microglia reactivity.Trends in neurosciences · 2023Review
Corrections and comments
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Authors and funding
12 authors at 1 institution in 1 country.
Funding
Abstract
Elderly patients with traumatic brain injury (TBI) have greater mortality and poorer outcomes than younger individuals. The extent to which old age alters long-term recovery and chronic microglial activation after TBI is unknown, and evidence for therapeutic efficacy in aged mice is sorely lacking. The present study sought to identify potential inflammatory mechanisms underlying age-related outcomes late after TBI. Controlled cortical impact was used to induce moderate TBI in young and old male C57BL/6 mice. At 12 weeks post-injury, aged mice exhibited higher mortality, poorer functional outcomes, larger lesion volumes, and increased microglial activation. Transcriptomic analysis identified age- and TBI-specific gene changes consistent with a disease-associated microglial signature in the chronically injured brain, including those involved with complement, phagocytosis, and autophagy pathways. Dysregulation of phagocytic and autophagic function in microglia was accompanied by increased neuroinflammation in old mice. As proof-of-principle that these pathways have functional importance, we administered an autophagic enhancer, trehalose, in drinking water continuously for 8 weeks after TBI. Old mice treated with trehalose showed enhanced functional recovery and reduced microglial activation late after TBI compared to the sucrose control group. Our data indicate that microglia undergo chronic changes in autophagic regulation with both normal aging and TBI that are associated with poorer functional outcome. Enhancing autophagy may therefore be a promising clinical therapeutic strategy for TBI, especially in older patients.
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