ArticleFrontiers in neuroscience2023
Senolytic therapy is neuroprotective and improves functional outcome long-term after traumatic brain injury in mice.
Article in Frontiers in neuroscience, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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Who cites it
25 citing papers in PubMed, 31 citations in OpenAlex.
- Review
- KDM6A/MMP-3 epigenetic axis governs macrophage senescence after spinal cord injury for mediating the regenerative niche to promote neurological repair.Journal of advanced research · 2026Article
- Traumatic Brain Injury Induces Senescence in Brain Microvasculature.Biomolecules · 2026Article
- Cellular senescence and senolytic therapy in traumatic brain injury.Frontiers in neuroscience · 2026Review
- Immunosenescence and inflammaging in Parkinson's disease: mechanisms and therapeutic prospects.Frontiers in immunology · 2026Review
- Targeting microglia-mediated neuroinflammation in Alzheimer's disease: mechanisms and therapeutic approaches.Frontiers in immunology · 2026Review
- Natural Products as Anti-Senescence-Associated Secretory Phenotype (SASP) Agents.Current medicinal chemistry · 2026Review
- Dasatinib and Quercetin Alleviate Retinal Ganglion Cell Dendritic Shrinkage and Promote Axonal Regeneration in Mice with Optic Nerve Injury.International journal of molecular sciences · 2025Article
- Senolytics as Modulators of Critical Signaling Pathways: a Promising Strategy to Combat Brain Aging and Neurodegenerative Disorders.Molecular neurobiology · 2025Review
- Unleashing endogenous regeneration by senolytics.Journal of translational medicine · 2025Review
- Senolytic Treatment Attenuates Global Ischemic Brain Injury and Enhances Cognitive Recovery by Targeting Mitochondria.Cellular and molecular neurobiology · 2025Article
- The senolytic ABT-263 improves cognitive functions in middle-aged male, but not female, atherosclerotic LDLrGeroScience · 2025Article
- The Role of Glial Cell Senescence in Alzheimer's Disease.Journal of neurochemistry · 2025Review
- Inflammation and aging-related disease: A transdisciplinary inflammaging framework.GeroScience · 2025Review
- Contemporary insights into neuroimmune interactions across development and aging.Frontiers in neurology · 2025Review
- Astrocyte-mediated inflammatory responses in traumatic brain injury: mechanisms and potential interventions.Frontiers in immunology · 2025Review
- Experimental and clinical tests of FDA-approved kinase inhibitors for the treatment of neurological disorders (update 2024).Exploration of drug science · 2025Article
- Cellular senescence as a key contributor to secondary neurodegeneration in traumatic brain injury and stroke.Translational neurodegeneration · 2024Review
- Senolytic treatment diminishes microglia and decreases severity of experimental autoimmune encephalomyelitis.Journal of neuroinflammation · 2024Article
- Microglia and Astrocytes in Alzheimer's Disease: Significance and Summary of Recent Advances.Aging and disease · 2024Review
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Introduction: Chronic neuroinflammation can exist for months to years following traumatic brain injury (TBI), although the underlying mechanisms remain poorly understood. Methods: In the current study, we used a controlled cortical impact mouse model of TBI to examine whether proinflammatory senescent cells are present in the brain long-term (months) after TBI and whether ablation of these cells via administration of senolytic drugs can improve long-term functional outcome after TBI. The results revealed that astrocytes and microglia in the cerebral cortex, hippocampus, corpus callosum and lateral posterior thalamus colocalized the senescent cell markers, p16 Discussion: Taken as a whole, these findings indicate there is robust and widespread induction of senescent cells in the brain long-term after TBI, and that senolytic drug treatment begun 1-month after TBI can efficiently ablate the senescent cells, reduce expression of proinflammatory SASP factors, reduce neurodegeneration, and rescue defects in reference memory, recognition memory, and depressive behavior.
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