ArticleJournal of neurotrauma2010
Metabolic acetate therapy for the treatment of traumatic brain injury.
Article in Journal of neurotrauma, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers, 1 of them a synthesis that pooled it.
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
39 citing papers in PubMed, 1 synthesis or guideline pooled it, 70 citations in OpenAlex.
- The role of short-chain fatty acids in spinal cord injury: A systematic review of human and animal evidence.The journal of spinal cord medicine · 2026Pooled it
- The Case for Vinegar Ingestion.Nutrients · 2026Review
- Acetate enhances neuronal plasticity and reduces ischemic brain injury by promoting tau protein lactylation.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2026Article
- Administration of ketogenic intervention as a potential treatment during post-traumatic brain injury recovery: a scoping review.Frontiers in nutrition · 2026Review
- Multi-omic spatially resolved analysis of the neuroinflammatory response to intracortical microelectrode arrays.Biomaterials · 2026Article
- The role of mitochondrial uncoupling in the regulation of mitostasis after traumatic brain injury.Neurochemistry international · 2024Article
- Tracing the path of disruption:CNS neuroscience & therapeutics · 2024Review
- Mitochondria-Targeted Antioxidant Therapeutics for Traumatic Brain Injury.Antioxidants (Basel, Switzerland) · 2024Review
- Evaluation of microglia activation related markers following a clinical course of TBS: A non-human primate study.PloS one · 2024Article
- Article
- Short chain fatty acids: key regulators of the local and systemic immune response in inflammatory diseases and infections.Open biology · 2023Review
- Effects of Pyruvate Administration on Mitochondrial Enzymes, Neurological Behaviors, and Neurodegeneration after Traumatic Brain Injury.Aging and disease · 2021Article
- Acetyl-CoA Metabolism and Histone Acetylation in the Regulation of Aging and Lifespan.Antioxidants (Basel, Switzerland) · 2021Review
- Gut Microbiota Interaction with the Central Nervous System throughout Life.Journal of clinical medicine · 2021Review
- Acetate Revisited: A Key Biomolecule at the Nexus of Metabolism, Epigenetics, and Oncogenesis - Part 2: Acetate and ACSS2 in Health and Disease.Frontiers in physiology · 2020Review
- Intraperitoneal Injection of Acetate Protects Mice Against Lipopolysaccharide (LPS)‑Induced Acute Lung Injury Through Its Anti-Inflammatory and Anti-Oxidative Ability.Medical science monitor : international medical journal of experimental and clinical research · 2019Article
- Comprehensive Profile of Acute Mitochondrial Dysfunction in a Preclinical Model of Severe Penetrating TBI.Frontiers in neurology · 2019Article
- A translational perspective on histone acetylation modulators in psychiatric disorders.Psychopharmacology · 2018Review
- Acetate Attenuates Lipopolysaccharide-Induced Nitric Oxide Production Through an Anti-Oxidative Mechanism in Cultured Primary Rat Astrocytes.Neurochemical research · 2016Article
- Acetate supplementation as a means of inducing glioblastoma stem-like cell growth arrest.Journal of cellular physiology · 2015Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 2 institutions in 1 country.
Funding
Abstract
Patients suffering from traumatic brain injury (TBI) have decreased markers of energy metabolism, including N-acetylaspartate (NAA) and ATP. In the nervous system, NAA-derived acetate provides acetyl-CoA required for myelin lipid synthesis. Acetate can also be oxidized in mitochondria for the derivation of metabolic energy. In the current study, using the controlled cortical impact model of TBI in rats, we investigated the effects of the hydrophobic acetate precursor, glyceryltriacetate (GTA), as a method of delivering metabolizable acetate to the injured brain. We found that GTA administration significantly increased the levels of both NAA and ATP in the injured hemisphere 4 and 6 days after injury, and also resulted in significantly improved motor performance in rats 3 days after injury.
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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.