N-Acetylaspartate (NAA) is almost exclusively localized in neurons in the adult brain and is present in high concentration in the CNS. It can be measured by proton magnetic resonance spectroscopy and is seen as a marker of neuronal damage and death. NMR spectroscopy and animal models have shown NAA depletion to occur in various types of chronic and acute brain injury. We investigated 19 patients with traumatic brain injury (TBI). Microdialysis was utilized to recover NAA, lactate, pyruvate, glycerol and glutamate, at 12-h intervals. These markers were correlated with survival and a 6-month Glasgow Outcome Score. Eleven patients died and eight survived. A linear mixed model analysis showed a significant effect of outcome and of the interaction between time of injury and outcome on NAA levels (p = 0.009 and p = 0.004, respectively). Overall, extracellular NAA was 34% lower in non-survivors. A significant non-recoverable fall was observed in this group from day 4 onwards, with a concomitant rise in lactate-pyruvate ratio and glycerol. These results suggest that mitochondrial dysfunction is a significant contributor to poor outcome following TBI and propose extracellular NAA as a potential marker for monitoring interventions aimed at preserving mitochondrial function.

Belli A., S.J. (2006). Extracellular N-acetylaspartate depletion in traumatic brain injury. JOURNAL OF NEUROCHEMISTRY, 96(3), 861-869 [10.1111/j.1471-4159.2005.03602.x].

Extracellular N-acetylaspartate depletion in traumatic brain injury

VAGNOZZI, ROBERTO;
2006

Abstract

N-Acetylaspartate (NAA) is almost exclusively localized in neurons in the adult brain and is present in high concentration in the CNS. It can be measured by proton magnetic resonance spectroscopy and is seen as a marker of neuronal damage and death. NMR spectroscopy and animal models have shown NAA depletion to occur in various types of chronic and acute brain injury. We investigated 19 patients with traumatic brain injury (TBI). Microdialysis was utilized to recover NAA, lactate, pyruvate, glycerol and glutamate, at 12-h intervals. These markers were correlated with survival and a 6-month Glasgow Outcome Score. Eleven patients died and eight survived. A linear mixed model analysis showed a significant effect of outcome and of the interaction between time of injury and outcome on NAA levels (p = 0.009 and p = 0.004, respectively). Overall, extracellular NAA was 34% lower in non-survivors. A significant non-recoverable fall was observed in this group from day 4 onwards, with a concomitant rise in lactate-pyruvate ratio and glycerol. These results suggest that mitochondrial dysfunction is a significant contributor to poor outcome following TBI and propose extracellular NAA as a potential marker for monitoring interventions aimed at preserving mitochondrial function.
Pubblicato
Rilevanza internazionale
Articolo
Sì, ma tipo non specificato
Settore MED/27 - Neurochirurgia
English
microdialysis; mitochondria; N-acetylaspartate; traumatic brain injury
Belli A., S.J. (2006). Extracellular N-acetylaspartate depletion in traumatic brain injury. JOURNAL OF NEUROCHEMISTRY, 96(3), 861-869 [10.1111/j.1471-4159.2005.03602.x].
Belli, A; Sen, J; Petzold, A; Russo, S; Kitchen, N; Smith, M; Tavazzi, B; Vagnozzi, R; Signoretti, S; Amorini, Am; Bellia, F; Lazzarino, G
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Utilizza questo identificativo per citare o creare un link a questo documento: http://hdl.handle.net/2108/35541
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