ReviewMolecular neurobiology2025
The Gut-Brain Axis and Neuroinflammation in Traumatic Brain Injury.
Review in Molecular neurobiology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers, 1 of them a synthesis that pooled it.
What it found
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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.
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Who cites it
10 citing papers in PubMed, 1 synthesis or guideline pooled it.
- The Role of Genetics in Stroke Risk and Outcome: A Review of Current Evidence.Brain and behavior · 2025Pooled it
- Stable serum peptidoglycan fragment levels do not support leaky gut in the acute phase or at one month following "mild" traumatic brain injury: A preliminary study.Brain, behavior, & immunity - health · 2026Article
- Severity-stratified gut microbiome dysbiosis and systemic neuroinflammation in acute traumatic brain injury: a metagenomic and cytokine profiling study.Frontiers in microbiology · 2026Article
- Th17 cells and IL-17A in traumatic brain injury: mechanisms and therapeutic perspectives.Frontiers in immunology · 2026Review
- Bidirectional Communication of Estrogen in Gut-Brain Axis: Evidence from Preclinical and Clinical Studies.Current drug targets · 2026Review
- How gut microbiota contribute to neuropsychiatric disorders: evidence from neuroimaging studies.Frontiers in microbiology · 2026Review
- Article
- Microbial modulators of the mind: probiotic interventions in hippocampal neurogenesis and cognitive flexibility.Antonie van Leeuwenhoek · 2025Review
- Concussion and the Autonomic, Immune, and Endocrine Systems: An Introduction to the Field and a Treatment Framework for Persisting Symptoms.Journal of personalized medicine · 2025Review
- Unveiling Role of Gut Microbiota in Alzheimer's Disease: Mechanisms, Challenges and Future Perspectives.Current Alzheimer research · 2025Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Traumatic brain injury (TBI) is a major global disability and mortality cause, with the gut-brain axis playing a crucial role in its pathophysiology. Neuroinflammation, triggered by microglia and astrocytes, contributes to neuronal damage and cognitive impairment. This paper aims to explore the relationship between the gut-brain axis and neuroinflammation in TBI and its potential implications for therapeutic interventions. A comprehensive review of the literature was conducted using PubMed, MEDLINE, and Google Scholar databases. Studies investigating the gut-brain axis, neuroinflammation, and TBI were included. Evidence suggests that TBI disrupts the gut-brain axis, leading to alterations in gut microbiota composition, intestinal permeability, and immune responses. These gut-related changes promote the activation of microglia and astrocytes in the central nervous system, contributing to neuroinflammation and neuronal damage. Conversely, interventions that modulate gut microbiota or reduce intestinal permeability have been shown to attenuate neuroinflammation and improve cognitive outcomes in TBI models. The gut-brain axis plays a significant role in the pathogenesis of neuroinflammation following TBI. Targeting the gut-brain axis through interventions that restore gut homeostasis and reduce intestinal permeability holds promise as a novel therapeutic strategy for mitigating neuroinflammation and improving cognitive function in TBI patients. Further research is needed to elucidate the specific mechanisms involved and to develop effective therapies based on this understanding.
Indexed as
Identifiers
39466574What 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.