Abstract
N-acetylaspartate (NAA) is an amino acid derivative primarily located in the neurons of the adult brain. The function of NAA is incompletely understood. Decrease in brain tissue NAA is presently considered symptomatic and a potential biomarker of acute and chronic neuropathological conditions. The aim of this study was to use microdialysis to investigate the behavior of extracellular NAA (eNAA) levels after traumatic brain injury (TBI). Sampling for this study was performed using cerebral microdialysis catheters (M Dialysis 71) perfused at 0.3 μL/min. Extracellular NAA was measured in microdialysates by high-performance liquid chromatography in 30 patients with severe TBI and for comparison, in radiographically “normal” areas of brain in six non-TBI neurosurgical patients. We established a detailed temporal eNAA profile in eight of the severe TBI patients. Microdialysate concentrations of glucose, lactate, pyruvate, glutamate, and glycerol were measured on an ISCUS clinical microdialysis analyzer. Here, we show that the temporal profile of microdialysate eNAA was characterized by highest levels in the earliest time-points post-injury, followed by a steady decline; beyond 70 h post-injury, average levels were 40% lower than those measured in non-TBI patients. There was a significant inverse correlation between concentrations of eNAA and pyruvate; eNAA showed significant positive correlations with glycerol and the lactate/pyruvate (L/P) ratio measured in microdialysates. The results of this on-going study suggest that changes in eNAA after TBI relate to the release of intracellular components, possibly due to neuronal death or injury, as well as to adverse brain energy metabolism.
Highlights
N-acetylaspartate (NAA) is an amino acid derivative primarily located in the neurons of the adult brain
Extracellular NAA concentrations were monitored in a detailed temporal profile in eight of the traumatic brain injury (TBI) patients, ages 20 to 69 years
We have analyzed the temporal profile of extracellular NAA (eNAA) in eight patients with severe traumatic brain injury
Summary
N-acetylaspartate (NAA) is an amino acid derivative primarily located in the neurons of the adult brain. There was a significant inverse correlation between concentrations of eNAA and pyruvate; eNAA showed significant positive correlations with glycerol and the lactate/pyruvate (L/P) ratio measured in microdialysates The results of this on-going study suggest that changes in eNAA after TBI relate to the release of intracellular components, possibly due to neuronal death or injury, as well as to adverse brain energy metabolism. The acetic acid from NAA becomes incorporated into CNS myelin.[10] Inherited ASPA gene mutations result in Canavan disease, showing ASPA deficiency in oligodendrocytes, abnormally high brain NAA levels, deficient axonal myelin sheath development, and spongy degeneration of white matter.[11,12,13,14] NAA plays a vital role as a precursor for the neurotransmitter N-acetylaspartylglutamate.[15] In addition, NAA traps excess aspartate and transports amino group nitrogen from mitochondria to the cytoplasm.[16,17] NAA may provide a store of energy metabolism precursors in neurons, astrocytes and oligodendrocytes in the absence of a sufficient store.
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