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An acetylated derivative of aspartate found in the brain. Used as a marker in brain nuclear magnetic resonance and in neuroimaging.
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Right dorsolateral frontal lobe N-acetyl aspartate and myoinositol concentration estimation in Type 2 diabetes with magnetic resonance spectroscopy.
Magnetic response spectroscopy sampling in bilateral hippocampi showed a similar appearance with decreased N-acetyl aspartate peak height.
Decreased N-acetyl aspartate (NAA) and increased or normal choline levels, suggestive of neuronal loss, is seen in RE.
Many researchers have reported decreases in hippocampal volume (Gilbertson et al., 2002; Villarreal et al., 2002) as well as reduced concentrations of the neuronal marker N-acetyl aspartate (Schuff et al., 2001) in PTSD patients.
(5) However, contrast enhancement does not occur in Canavan disease, and the typical raised N-acetyl aspartate (NAA) peak on MR spectroscopy was absent in our patient.
Halbower reported, "the N-acetyl aspartate to choline (NAA/Cho) ratios in the left hippocampus and left frontal cortex were significantly decreased in [OSA] patients, compared with healthy controls, and the [OSA] patients had significant decreases in the executive function of working memory, attention, and verbal memory."
Increases in mean childhood blood lead levels were associated with a decrease in N-acetyl aspartate, creatine, and phos-phocreatine levels in the basal ganglia; decreased choline (Cho) concentrations in the cerebellar hemisphere; decreased glutamate and glutamine (GLX) levels in the vermis; decreased Cho and GLX concentrations in parietal white matter; and decreased Cho concentrations in frontal white-matter.
One-way ANOVA was used to compare the P values among different regions tNAA; N-acetyl aspartate + NAAG; dipeptide N-acetylaspartylglutamate, Cr; Creatine, PCr; phosphocreatine Cho; Choline containing compound, Glx; glutamate (Glu) and glutamine (Gln); myo-inositol (mI) Table IV.
A decrease in N-acetyl aspartate, a marker or neuronal function, also may play a role.
From her post at UC, Delbello and her team examine neuro-chemical abnormalities of affected children and adolescents and have found that certain neuro-chemicals, such as myo-inositol, which is associated with second-messenger cellular signaling pathways, and N-acetyl aspartate, which is a potential marker of neuronal function and structure, are abnormal in patients with BD.
(Montreal Neurological Institute, Quebec, Canada) investigated the connection between fatigue and brain levels of n-acetyl aspartate (NAA), a chemical marker that indicates whether nerve fibers are intact and functioning properly.
The most remote study from December 2004 shows elevated choline (Cho) peaks relative to creatine (Cr) and N-acetyl aspartate (NAA) (Figure 2).
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