ArticleJournal of cellular and molecular medicine2017
Severity of experimental traumatic brain injury modulates changes in concentrations of cerebral free amino acids.
Article in Journal of cellular and molecular medicine, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 papers, 1 of them a synthesis that pooled it.
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Who cites it
51 citing papers in PubMed, 1 synthesis or guideline pooled it, 87 citations in OpenAlex.
- Biomarkers of hypoxic-ischemic encephalopathy: a systematic review.World journal of pediatrics : WJP · 2023Pooled it
- Metabolic changes and plasma glycine predict the risk of acute cellular rejection in heart transplantation.JTCVS open · 2026Article
- Electroactive biomaterials modulating ion channels in nervous system regeneration.Regenerative biomaterials · 2026Review
- Targeted metabolomic evaluation of peripheral blood mononucleated cells from patients with PMM2-CDG.Scientific reports · 2025Article
- Photobiomodulation improves functional recovery after mild traumatic brain injury.Bioengineering & translational medicine · 2025Article
- Vibrational fiber photometry: label-free and reporter-free minimally invasive Raman spectroscopy deep in the mouse brain.Nature methods · 2025Article
- Mitochondria: the hidden engines of traumatic brain injury-driven neurodegeneration.Frontiers in cellular neuroscience · 2025Review
- Annexin-A1 tripeptide enhances functional recovery and mitigates brain damage in traumatic brain injury by inhibiting neuroinflammation and preventing ANXA1 nuclear translocation in mice.Metabolic brain disease · 2024Article
- Mapping small metabolite changes after traumatic brain injury using AP-MALDI MSI.Analytical and bioanalytical chemistry · 2024Article
- Exploring cerebral structural and functional abnormalities in a mouse model of post-traumatic headache induced by mild traumatic brain injury.Zoological research · 2024Article
- Plasma Amino Acid Profiles and Clinical Outcome in Patients with Traumatic Brain Injury: A Study Protocol.Galen medical journal · 2024Article
- Reactive gliosis in traumatic brain injury: a comprehensive review.Frontiers in cellular neuroscience · 2024Review
- Using metabolomics to predict severe traumatic brain injury outcome (GOSE) at 3 and 12 months.Critical care (London, England) · 2023Article
- Extracellular tau oligomers affect extracellular glutamate handling by astrocytes through downregulation of GLT-1 expression and impairment of NKA1A2 function.Neuropathology and applied neurobiology · 2022Article
- ILBInternational journal of molecular sciences · 2022Article
- The role of L-arginine metabolism in neurocritical care patients.Neural regeneration research · 2022Review
- Biochemical Discrimination of the Down Syndrome-Related Metabolic and Oxidative/Nitrosative Stress Alterations from the Physiologic Age-Related Changes through the Targeted Metabolomic Analysis of Serum.Antioxidants (Basel, Switzerland) · 2022Article
- Effects of Traumatic Brain Injury on the Gut Microbiota Composition and Serum Amino Acid Profile in Rats.Cells · 2022Article
- Branched-Chain Amino Acids Are Neuroprotective Against Traumatic Brain Injury and Enhance Rate of Recovery: Prophylactic Role for Contact Sports and Emergent Use.Neurotrauma reports · 2022Article
- Glutamate, Glutamine, GABA and Oxidative Products in the Pons Following Cortical Injury and Their Role in Motor Functional Recovery.Neurochemical research · 2021Article
Corrections and comments
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Authors and funding
7 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
In this study, concentrations of free amino acids (FAA) and amino group containing compounds (AGCC) following graded diffuse traumatic brain injury (mild TBI, mTBI; severe TBI, sTBI) were evaluated. After 6, 12, 24, 48 and 120 hr aspartate (Asp), glutamate (Glu), asparagine (Asn), serine (Ser), glutamine (Gln), histidine (His), glycine (Gly), threonine (Thr), citrulline (Cit), arginine (Arg), alanine (Ala), taurine (Tau), γ-aminobutyrate (GABA), tyrosine (Tyr), S-adenosylhomocysteine (SAH), l-cystathionine (l-Cystat), valine (Val), methionine (Met), tryptophane (Trp), phenylalanine (Phe), isoleucine (Ile), leucine (Leu), ornithine (Orn), lysine (Lys), plus N-acetylaspartate (NAA) were determined in whole brain extracts (n = 6 rats at each time for both TBI levels). Sham-operated animals (n = 6) were used as controls. Results demonstrated that mTBI caused modest, transient changes in NAA, Asp, GABA, Gly, Arg. Following sTBI, animals showed profound, long-lasting modifications of Glu, Gln, NAA, Asp, GABA, Ser, Gly, Ala, Arg, Citr, Tau, Met, SAH, l-Cystat, Tyr and Phe. Increase in Glu and Gln, depletion of NAA and Asp increase, suggested a link between NAA hydrolysis and excitotoxicity after sTBI. Additionally, sTBI rats showed net imbalances of the Glu-Gln/GABA cycle between neurons and astrocytes, and of the methyl-cycle (demonstrated by decrease in Met, and increase in SAH and l-Cystat), throughout the post-injury period. Besides evidencing new potential targets for novel pharmacological treatments, these results suggest that the force acting on the brain tissue at the time of the impact is the main determinant of the reactions ignited and involving amino acid metabolism.
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