ArticleNeurobiology of aging2019
Old age increases microglial senescence, exacerbates secondary neuroinflammation, and worsens neurological outcomes after acute traumatic brain injury in mice.
Article in Neurobiology of aging, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 105 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
105 citing papers in PubMed, 152 citations in OpenAlex.
- Hypothalamic Inflammaging: A Central Driver of Type 2 Diabetes Mellitus and Metabolic Disease in Aging.Diabetes & metabolism journal · 2026Review
- Lifelong restriction of dietary valine has sex-specific benefits for health and lifespan in mice.Nature aging · 2026Article
- Aging reprograms microglia toward an inflammasome-linked response to traumatic brain injury.The Journal of clinical investigation · 2026Article
- Lipopolysaccharide-induced Neuroimmune Alteration and Memory Decline in Aging Mice: The Role of Augmented Cellular Senescence.Neurotoxicity research · 2026Article
- PU.1 restores microglial dysfunction caused by C9ORF72 repeat expansions in neural organoids.Brain : a journal of neurology · 2026Article
- Immunosenescence in Human Disease: Mechanistic Insights and Therapeutic Opportunities.Biomolecules & therapeutics · 2026Review
- Phagocytosis and neuroinflammation: orchestrating central nervous system homeostasis, repair, and the resolution of inflammation.Trends in neurosciences · 2026Review
- Traumatic Brain Injury Induces Senescence in Brain Microvasculature.Biomolecules · 2026Article
- The Dynamics of Neuroinflammation in Traumatic Brain Injury: Molecular Markers Useful for Establishing the Post-Traumatic Interval in Forensic Practice.International journal of molecular sciences · 2026Review
- Factors Affecting Recovery from Post-Traumatic Amnesia During Inpatient Brain Injury Rehabilitation: A Retrospective Cohort Study.Life (Basel, Switzerland) · 2026Article
- Cytokines and related signaling pathways in traumatic brain injury.Frontiers in immunology · 2026Review
- Cellular senescence and senolytic therapy in traumatic brain injury.Frontiers in neuroscience · 2026Review
- Senolytics as Modulators of Critical Signaling Pathways: a Promising Strategy to Combat Brain Aging and Neurodegenerative Disorders.Molecular neurobiology · 2025Review
- Microglia in Brain Aging and Age-Related Diseases: Friends or Foes?International journal of molecular sciences · 2025Review
- Ligustilide Ameliorates Traumatic Brain Injury in Aged Mice by Attenuating Microglia-Mediated Neuroinflammation.Neurochemical research · 2025Article
- Lifelong restriction of dietary valine has sex-specific benefits for health and lifespan in mice.bioRxiv : the preprint server for biology · 2025Article
- Advances and challenges in experimental models of posttraumatic epilepsy for therapeutic interventions.Pharmacological reviews · 2025Review
- Article
- Cathepsins in Neurological Diseases.International journal of molecular sciences · 2025Review
- Behavioral assessment and gene expression changes in a mouse model with dysfunctional STAT1 signaling.Cell communication and signaling : CCS · 2025Article
45 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
After traumatic brain injury (TBI), individuals aged over 65 years show increased mortality and worse functional outcomes compared with younger persons. As neuroinflammation is a key pathobiological mechanism of secondary injury after TBI, we examined how aging affects post-traumatic microglial responses and functional outcomes. Young (3-month-old) and aged (18-month-old) male C57Bl/6 mice were subjected to moderate-level controlled cortical impact or sham surgery, and neurological function was evaluated. At 72 hours after injury, brain, blood, and spleen leukocyte counts were assessed ex vivo using flow cytometry. Aged mice demonstrated more severe deficits in forelimb grip strength, balance and motor coordination, spontaneous locomotor activity, and anxiety-like behavior. These animals also exhibited more robust microglial proliferation and significantly higher numbers of brain-infiltrating leukocytes. Microglia in aged mice showed impairments in phagocytic activity and higher production of interleukin-1β (IL-1β). Infiltrating myeloid cells in aged TBI mice also had deficits in phagocytosis but showed diminished proinflammatory cytokine production and greater reactive oxygen species production. Expression of several senescence markers (Bcl-2, p16
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.