| Literature DB >> 19803785 |
Peethambaran Arun1, Prasanth S Ariyannur, John R Moffett, Guoqiang Xing, Kristen Hamilton, Neil E Grunberg, John A Ives, Aryan M A Namboodiri.
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.Entities:
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Year: 2010 PMID: 19803785 PMCID: PMC2824219 DOI: 10.1089/neu.2009.0994
Source DB: PubMed Journal: J Neurotrauma ISSN: 0897-7151 Impact factor: 5.269