ArticleMolecular medicine (Cambridge, Mass.)2014
The molecular mechanisms affecting N-acetylaspartate homeostasis following experimental graded traumatic brain injury.
Article in Molecular medicine (Cambridge, Mass.), 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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Who cites it
26 citing papers in PubMed, 39 citations in OpenAlex.
- N-Acetylaspartate Synthesis as a Thermodynamic Relief Mechanism for Mitochondrial Aspartate Aminotransferase.bioRxiv : the preprint server for biology · 2026Article
- Cell-free DNA methylation profiling reveals injury types and severities in swine rotational and contusional models of traumatic brain injury.Acta neuropathologica communications · 2026Article
- Longitudinal Brain Structural, Neurochemical, and Behavioral Changes Following Traumatic Brain Injury in Immature Rat Brain with ALCAR Treatment.Neurochemical research · 2025Article
- The impact of the let-7 family on the pathophysiological mechanisms of traumatic brain injury: a systematic review.Frontiers in neurology · 2025Review
- Metabolic Diaschisis in Mild Traumatic Brain Injury.Journal of neurotrauma · 2024Article
- Tracing the path of disruption:CNS neuroscience & therapeutics · 2024Review
- ILBInternational journal of molecular sciences · 2022Article
- Traumatic brain injury induces region-specific glutamate metabolism changes as measured by multiple mass spectrometry methods.iScience · 2021Article
- Cerebral Energy Status and Altered Metabolism in Early Severe TBI: First Results of a ProspectiveNeurocritical care · 2021Article
- Neither Excessive Nitric Oxide Accumulation nor Acute Hyperglycemia Affects theInternational journal of molecular sciences · 2020Article
- Low Molecular Weight Dextran Sulfate (ILBAntioxidants (Basel, Switzerland) · 2020Article
- Pyruvate Dehydrogenase and Tricarboxylic Acid Cycle Enzymes Are Sensitive Targets of Traumatic Brain Injury Induced Metabolic Derangement.International journal of molecular sciences · 2019Article
- Dynamin and reverse-mode sodium calcium exchanger blockade confers neuroprotection from diffuse axonal injury.Cell death & disease · 2019Article
- Dynamics of in Vivo Metabolites Concentrations in Posttraumatic Period of Human Brain.Doklady. Biochemistry and biophysics · 2019Article
- Beneficial Effects of Kaempferol after Developmental Traumatic Brain Injury Is through Protection of Mitochondrial Function, Oxidative Metabolism, and Neural Viability.Journal of neurotrauma · 2019Article
- Water- and Fat-Soluble Antioxidants in Human Seminal Plasma and Serum of Fertile Males.Antioxidants (Basel, Switzerland) · 2019Article
- Longitudinal Changes in Magnetic Resonance Spectroscopy in Pediatric Concussion: A Pilot Study.Frontiers in neurology · 2019Article
- Neuroimaging and Neuropsychological Studies in Sports-Related Concussions in Adolescents: Current State and Future Directions.Frontiers in neurology · 2019Review
- MicroRNA Signature of Traumatic Brain Injury: From the Biomarker Discovery to the Point-of-Care.Frontiers in neurology · 2018Review
- Neurometabolic indicators of mitochondrial dysfunction in repetitive mild traumatic brain injury.Concussion (London, England) · 2017Review
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Authors and funding
9 authors at 5 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
To characterize the molecular mechanisms of N-acetylaspartate (NAA) metabolism following traumatic brain injury (TBI), we measured the NAA, adenosine triphosphate (ATP) and adenosine diphosphate (ADP) concentrations and calculated the ATP/ADP ratio at different times from impact, concomitantly evaluating the gene and protein expressions controlling NAA homeostasis (the NAA synthesizing and degrading enzymes N-acetyltransferase 8-like and aspartoacylase, respectively) in rats receiving either mild or severe TBI. The reversible changes in NAA induced by mild TBI were due to a combination of transient mitochondrial malfunctioning with energy crisis (decrease in ATP and in the ATP/ADP ratio) and modulation in the gene and protein levels of N-acetyltransferase 8-like and increase of aspartoacylase levels. The irreversible decrease in NAA following severe TBI, was instead characterized by profound mitochondrial malfunctioning (constant 65% decrease of the ATP/ADP indicating permanent impairment of the mitochondrial phosphorylating capacity), dramatic repression of the N-acetyltransferase 8-like gene and concomitant remarkable increase in the aspartoacylase gene and protein levels. The mechanisms underlying changes in NAA homeostasis following graded TBI might be of note for possible new therapeutic approaches and will help in understanding the effects of repeat concussions occurring during particular periods of the complex NAA recovery process, coincident with the so called window of brain vulnerability.
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