ReviewFrontiers in aging neuroscience2022
Microglia and Neuroinflammation: Crucial Pathological Mechanisms in Traumatic Brain Injury-Induced Neurodegeneration.
Review in Frontiers in aging neuroscience, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 138 papers, 1 of them a synthesis that pooled it.
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Who cites it
138 citing papers in PubMed, 1 synthesis or guideline pooled it, 221 citations in OpenAlex.
- The Role of Neuroinflammation in Shaping Neuroplasticity and Recovery Outcomes Following Traumatic Brain Injury: A Systematic Review.International journal of molecular sciences · 2024Pooled it
- Neurometabolite abnormalities and associations with epilepsy duration and cognition in patients with idiopathic generalized epilepsies.Epilepsia open · 2026Article
- Mild and repetitive mild traumatic brain injury: Changes in microglial cells and synapses.Neural regeneration research · 2026Article
- Spatiotemporal disarray of inflammatory microenvironment following spinal cord injury.Neural regeneration research · 2026Article
- Apigenin as a Potential Modulator of Neuroinflammation in Multiple Sclerosis: A Review.Biology · 2026Review
- Neuroprotective Effects of Cistanoside A against Cadmium-induced Neurotoxicity via Keap1/Nrf2/NF-kB Signaling: In Vivo and In Silico approaches.Molecular neurobiology · 2026Article
- The Gut-Brain Axis in Neurodegeneration: Mechanistic Links Between Dysbiosis and Neuropathology.Iranian journal of pathology · 2026Review
- Intranasal CRISPR lipid nanoparticles targeting MAPK9 attenuate neuroinflammation after traumatic brain injury.Biomedical microdevices · 2026Article
- Chemical Constituents ofACS omega · 2026Article
- Polygala oligosaccharide esters improve memory disorder by restoring gut microbiota homeostasis through the regulation of the "gut-brain" axis.Chinese medicine · 2026Article
- Targeting mGluR1-Mediated Microglial ER Stress Mitigates Copper-Induced TBI Neuroinflammation.Molecular neurobiology · 2026Article
- Repeated head impacts establish a senescent cranial bone marrow niche that impairs brain metabolism.Journal of neuroinflammation · 2026Article
- Mesenchymal stromal cells and neuroinflammation: a multimodal approach to neuroprotection and future therapeutic horizons.Translational neurodegeneration · 2026Review
- Intranasal CRISPR- lipid nanoparticles targeting MAPK9 reduce neuroinflammation after traumatic brain injury.Research square · 2026Article
- Extracellular vesicles released from blood-brain barrier endothelial cells mediate brain iron accumulation during LPS-induced brain inflammation.The Journal of biological chemistry · 2026Article
- Intranasal CRISPR-lipid nanoparticles targeting MAPK9 reduce neuroinflammation after traumatic brain injury.bioRxiv : the preprint server for biology · 2026Article
- Telomerase mRNA-Lipid nanoparticles attenuate neuroinflammation after traumatic brain injury in mice.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2026Article
- Review: Systemic inflammation after stroke. Therapy and perspective.GeroScience · 2026Review
- Psilocybin mitigates chronic behavioral and neurobiological alterations in a rat model of recurrent intimate partner violence-related brain injury.Molecular psychiatry · 2026Article
- Time of day alters olfactory bulb immune state with ramifications for intranasal inflammatory challenge.Cell reports · 2026Article
78 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
5 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Traumatic brain injury (TBI) is one of the most common diseases in the central nervous system (CNS) with high mortality and morbidity. Patients with TBI usually suffer many sequelae in the life time post injury, including neurodegenerative disorders such as Alzheimer's disease (AD) and Parkinson's disease (PD). However, the pathological mechanisms connecting these two processes have not yet been fully elucidated. It is important to further investigate the pathophysiological mechanisms underlying TBI and TBI-induced neurodegeneration, which will promote the development of precise treatment target for these notorious neurodegenerative consequences after TBI. A growing body of evidence shows that neuroinflammation is a pivotal pathological process underlying chronic neurodegeneration following TBI. Microglia, as the immune cells in the CNS, play crucial roles in neuroinflammation and many other CNS diseases. Of interest, microglial activation and functional alteration has been proposed as key mediators in the evolution of chronic neurodegenerative pathology following TBI. Here, we review the updated studies involving phenotypical and functional alterations of microglia in neurodegeneration after injury, survey key molecules regulating the activities and functional responses of microglia in TBI pathology, and explore their potential implications to chronic neurodegeneration after injury. The work will give us a comprehensive understanding of mechanisms driving TBI-related neurodegeneration and offer novel ideas of developing corresponding prevention and treatment strategies for this disease.
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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.