By: Ariyannur Arun, P; Moffett, J; Xing, G; Hamilton, K; Grunberg, N; John Ives; Namboodiri, A
Publication Name: J Neurotrauma
Year: 2010
Patients suffering from brain injury 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 brain injury 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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