ArticleJournal of neuroinflammation2022
TREM2 activation alleviates neural damage via Akt/CREB/BDNF signalling after traumatic brain injury in mice.
Article in Journal of neuroinflammation, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 68 papers, 1 of them a synthesis that pooled it.
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Who cites it
68 citing papers in PubMed, 1 synthesis or guideline pooled it, 123 citations in OpenAlex.
- Cortical Neuroprotective Mechanisms of Exercise Training in Post-Traumatic Brain Injury: A Systematic Review.International journal of molecular sciences · 2025Pooled it
- Post-Translational Modifications in Traumatic Brain Injury: Decoding the Proteomic Landscape and Molecular Mechanisms of Secondary Injury.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026Review
- Sunflower oil-loaded lycopene protects intestinal barrier integrity following traumatic brain injury.Journal of molecular histology · 2026Article
- Traumatic Brain Injury and the Road to Alzheimer's Disease.Biomedicines · 2026Review
- ACP5-positive macrophages contribute to cerebral oedema and neuroinflammation after traumatic brain injury.Clinical and translational medicine · 2026Article
- PDCD1 Signaling in Microglia Can Reduce Neuroinflammation and Apoptosis Induced by Traumatic Brain Injury by Regulating PI3K/Akt Signaling Pathway, Thereby Alleviating Neurological Dysfunction.Molecular neurobiology · 2026Article
- Upregulation of CREB1 by Mycobacterium Tuberculosis Transcriptionally Activates TREM2 to Promote Macrophage M2 Polarization.Cell biochemistry and function · 2026Article
- Eerdun Wurile, a Mongolian medicine, alleviates neuronal damage and improves neurological dysfunction after cerebral hemorrhage by activating the PI3K/AKT signaling pathway.Chinese medicine · 2026Article
- Synthetic Sweeteners and Human Health: An Overview of Health Risks, Vulnerable Populations, and Effects on Key Biological Systems.Medicina (Kaunas, Lithuania) · 2026Review
- Inflammatory-neurodegenerative crosstalk in pediatric severe traumatic brain injury: a multi-domain plasma proteomic study.Molecular medicine (Cambridge, Mass.) · 2026Article
- Co-Delivery of Ferrostatin-1 and M2 Macrophage-Derived Exosomal Signals via Engineered Hybrid Nanovesicles Enables Synergistic Neuroprotection in Traumatic Brain Injury.ACS applied materials & interfaces · 2026Article
- Targeting neuroinflammation and PVNMaterials today. Bio · 2026Article
- Parkinson's disease: spatiotemporal regulation and therapeutic prospects of TREM2-mediated microglial responses.NPJ Parkinson's disease · 2026Review
- Investigating associations between serum inflammatory cytokines at the time of second mild traumatic brain injury with acute neurological signs, axonal injury and behavioural outcomes in male Sprague-Dawley rats.Brain communications · 2026Article
- TREM2 as a central hub of neuroimmune-metabolic crosstalk in central nervous system disorders: from microglial biology to therapeutic targeting.Frontiers in immunology · 2026Review
- TREM2: A Potential Target for the Targeted Therapy of Metabolic Diseases.Mediators of inflammation · 2026Review
- MFSD2A: a molecular nexus linking blood-brain barrier, lipid metabolism, and ischemia-reperfusion injury.Cellular & molecular biology letters · 2025Review
- Role of TREM2 in neuroinflammation regulation: mechanisms, disease associations, and therapeutic translation advances.Journal of translational medicine · 2025Review
- The Role of TREM2 After Stroke: From Mechanisms to Therapeutic Potential.Molecular neurobiology · 2025Review
- Exploring potential targets and molecular mechanisms of traumatic brain injury exacerbated by Benzo(a)pyrene via network toxicology and molecular dynamics simulation.Cell biology and toxicology · 2025Article
8 more citing papers are in PubMed but not listed here.
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Authors and funding
9 authors at 4 institutions in 1 country.
Funding
Abstract
backgroundNeuroinflammation is one of the most important processes in secondary injury after traumatic brain injury (TBI). Triggering receptor expressed on myeloid cells 2 (TREM2) has been proven to exert neuroprotective effects in neurodegenerative diseases and stroke by modulating neuroinflammation, and promoting phagocytosis and cell survival. However, the role of TREM2 in TBI has not yet been elucidated. In this study, we are the first to use COG1410, an agonist of TREM2, to assess the effects of TREM2 activation in a murine TBI model.
methodsAdult male wild-type (WT) C57BL/6 mice and adult male TREM2 KO mice were subjected to different treatments. TBI was established by the controlled cortical impact (CCI) method. COG1410 was delivered 1 h after CCI via tail vein injection. Western blot analysis, immunofluorescence, laser speckle contrast imaging (LSCI), neurological behaviour tests, brain electrophysiological monitoring, Evans blue assays, magnetic resonance imaging (MRI), and brain water content measurement were performed in this study.
resultsThe expression of endogenous TREM2 peaked at 3 d after CCI, and it was mainly expressed on microglia and neurons. We found that COG1410 improved neurological functions within 3 d, as well as neurological functions and brain electrophysiological activity at 2 weeks after CCI. COG1410 exerted neuroprotective effects by inhibiting neutrophil infiltration and microglial activation, and suppressing neuroinflammation after CCI. In addition, COG1410 treatment alleviated blood brain barrier (BBB) disruption and brain oedema; furthermore, COG1410 promoted cerebral blood flow (CBF) recovery at traumatic injury sites after CCI. In addition, COG1410 suppressed neural apoptosis at 3 d after CCI. TREM2 activation upregulated p-Akt, p-CREB, BDNF, and Bcl-2 and suppressed TNF-α, IL-1β, Bax, and cleaved caspase-3 at 3 d after CCI. Moreover, TREM2 knockout abolished the effects of COG1410 on vascular phenotypes and microglial states. Finally, the neuroprotective effects of COG1410 were suppressed by TREM2 depletion.
conclusionsAltogether, we are the first to demonstrate that TREM2 activation by COG1410 alleviated neural damage through activation of Akt/CREB/BDNF signalling axis in microglia after CCI. Finally, COG1410 treatment improved neurological behaviour and brain electrophysiological activity after CCI.
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