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Background and purpose Tai Chi is a mind-body exercise that has been shown to improve both mental and physical health. As a result, recent literature suggests the use of Tai Chi to treat both physical and psychological disorders. However, the underlying physiological changes have not been characterized. The aim of this pilot study is to assess the changes in brain metabolites and muscle energetics after Tai Chi training in an aging population using a combined brain-muscle magnetic resonance spectroscopy (MRS) examination. Methods Six healthy older adults were prospectively recruited and enrolled into a 12-week Tai Chi program. A brain 1 H MRS and a muscle 31 P MRS were scanned before and after the training, and postprocessed to measure N-acetylaspartate to creatine (NAA/Cr) ratios and phosphocreatine (PCr) recovery time. Wilcoxon-signed rank tests were utilized to assess the differences between pre- and post-Tai Chi training. Results A significant within-subject increase in both the NAA/Cr ratios (P = .046) and the PCr recovery time (P = .046) was observed between the baseline and the posttraining scans. The median percentage changes were 5.38% and 16.51% for NAA/Cr and PCr recovery time, respectively. Conclusions Our pilot study demonstrates significant increase of NAA/Cr ratios in posterior cingulate gyrus and significantly improved PCr recovery time in leg muscles in older adults following short-term Tai Chi training, and thus provides insight into the beneficial mechanisms.

Canavan disease is caused by inactivating ASPA (aspartoacylase) mutations that prevent cleavage of N-acetyl-L-aspartate (NAA), resulting in marked elevations in central nervous system (CNS) NAA and progressively worsening leukodystrophy. We now report that ablating NAA synthesis by constitutive genetic disruption of Nat8l (N-acetyltransferase-8 like) permits normal CNS myelination and prevents leukodystrophy in a murine Canavan disease model.

In this study, concentrations of free amino acids (FAA) and amino group containing compounds (AGCC) following graded diffuse traumatic brain injury (mild TBI, mTBI; severe TBI, sTBI) were evaluated. After 6, 12, 24, 48 and 120 hr aspartate (Asp), glutamate (Glu), asparagine (Asn), serine (Ser), glutamine (Gln), histidine (His), glycine (Gly), threonine (Thr), citrulline (Cit), arginine (Arg), alanine (Ala), taurine (Tau), γ‐aminobutyrate (GABA), tyrosine (Tyr), S‐adenosylhomocysteine (SAH), l‐cystathionine (l‐Cystat), valine (Val), methionine (Met), tryptophane (Trp), phenylalanine (Phe), isoleucine (Ile), leucine (Leu), ornithine (Orn), lysine (Lys), plus N‐acetylaspartate (NAA) were determined in whole brain extracts (n = 6 rats at each time for both TBI levels). Sham‐operated animals (n = 6) were used as controls. Results demonstrated that mTBI caused modest, transient changes in NAA, Asp, GABA, Gly, Arg. Following sTBI, animals showed profound, long‐lasting modifications of Glu, Gln, NAA, Asp, GABA, Ser, Gly, Ala, Arg, Citr, Tau, Met, SAH, l‐Cystat, Tyr and Phe. Increase in Glu and Gln, depletion of NAA and Asp increase, suggested a link between NAA hydrolysis and excitotoxicity after sTBI. Additionally, sTBI rats showed net imbalances of the Glu‐Gln/GABA cycle between neurons and astrocytes, and of the methyl‐cycle (demonstrated by decrease in Met, and increase in SAH and l‐Cystat), throughout the post‐injury period. Besides evidencing new potential targets for novel pharmacological treatments, these results suggest that the force acting on the brain tissue at the time of the impact is the main determinant of the reactions ignited and involving amino acid metabolism.

Concentration of the neuronal marker, N-acetylaspartate (NAA), a quantitative metric for the health and density of neurons, is currently obtained by integration of the manually defined peak in whole-head proton ((1) H)-MRS. Our goal was to develop a full spectral modeling approach for the automatic estimation of the whole-brain NAA concentration (WBNAA) and to compare the performance of this approach with a manual frequency-range peak integration approach previously employed. MRI and whole-head (1) H-MRS from 18 healthy young adults were examined. Non-localized, whole-head (1) H-MRS obtained at 3 T yielded the NAA peak area through both manually defined frequency-range integration and the new, full spectral simulation. The NAA peak area was converted into an absolute amount with phantom replacement and normalized for brain volume (segmented from T1 -weighted MRI) to yield WBNAA. A paired-sample t test was used to compare the means of the WBNAA paradigms and a likelihood ratio test used to compare their coefficients of variation. While the between-subject WBNAA means were nearly identical (12.8 ± 2.5 mm for integration, 12.8 ± 1.4 mm for spectral modeling), the latter's standard deviation was significantly smaller (by ~50%, p = 0.026). The within-subject variability was 11.7% (±1.3 mm) for integration versus 7.0% (±0.8 mm) for spectral modeling, i.e., a 40% improvement. The (quantifiable) quality of the modeling approach was high, as reflected by Cramer-Rao lower bounds below 0.1% and vanishingly small (experimental - fitted) residuals. Modeling of the whole-head (1) H-MRS increases WBNAA quantification reliability by reducing its variability, its susceptibility to operator bias and baseline roll, and by providing quality-control feedback. Together, these enhance the usefulness of the technique for monitoring the diffuse progression and treatment response of neurological disorders.

Aerobic exercise is a promising form of prevention for cognitive decline; however, little is known about the molecular mechanisms by which exercise and fitness impacts the human brain. Several studies have postulated that increased regional brain volume and function are associated with aerobic fitness because of increased vascularization rather than increased neural tissue per se. We tested this position by examining the relationship between cardiorespiratory fitness and N-acetylaspartate (NAA) levels in the right frontal cortex using magnetic resonance spectroscopy. NAA is a nervous system specific metabolite found predominantly in cell bodies of neurons. We reasoned that if aerobic fitness was predominantly influencing the vasculature of the brain, then NAA levels should not vary as a function of aerobic fitness. However, if aerobic fitness influences the number or viability of neurons, then higher aerobic fitness levels might be associated with greater concentrations of NAA. We examined NAA levels, aerobic fitness, and cognitive performance in 137 older adults without cognitive impairment. Consistent with the latter hypothesis, we found that higher aerobic fitness levels offset an age-related decline in NAA. Furthermore, NAA mediated an association between fitness and backward digit span performance, suggesting that neuronal viability as measured by NAA is important in understanding fitness-related cognitive enhancement. Since NAA is found exclusively in neural tissue, our results indicate that the effect of fitness on the human brain extends beyond vascularization; aerobic fitness is associated with neuronal viability in the frontal cortex of older adults.

This study reports in vivo MRS findings in 11 patients with histologically diagnosed central neurocytomas, which are rare intraventricular tumors of neuronal origin. Single-voxel 1H MRS was carried out prior to surgery using a point-resolved spectroscopy sequence with TR = 6 s, TE = 135 ms and 128 scans. In vitro high-resolution 1H spectroscopy was also carried out on two surgically excised samples. The striking features of the spectra from the central neurocytomas were the presence of high glycine, decreased N-acetylaspartate, increased choline and alanine. Retrospective, blind analysis of the spectra by two independent observers correctly identified all but one central neurocytoma based on the presence of glycine. The presence of glycine and prominent choline in the 1H MR spectrum is a characteristic feature of the central neurocytomas, and could be used to characterize and differentiate them from other brain tumors. Copyright © 2011 John Wiley & Sons, Ltd.

WOS: 000268101000008, PubMed ID: 19531109, Aim: To date, despite possible neuroanatomical importance, no magnetic resonance spectroscopy (MRS) study on hippocampus has been performed in obsessive-compulsive disorder (OCD). The purpose of the present study was therefore to compare hippocampal chemicals in patients with OCD with those in healthy subjects with no psychopathology. Methods: Eighteen patients meeting DSM-IV criteria for OCD and 18 healthy controls were studied. The patients and controls underwent proton magnetic resonance spectroscopy ((1)H-MRS), and measures of N-acetyl-l-aspartate (NAA), choline (CHO), and creatine (CRE) in hippocampal regions were obtained. Results: Both NAA/CRE and NAA/CHO ratios in the hippocampus in patients with OCD were reduced relative to healthy controls. The ANOVA showed a near-significant effect of diagnosis for NAA/CRE and a significant effect for NAA/CHO, but the ANOVA did not show any significant effect even at a trend level for CHO/CRE. No main effect of hemisphere was found for any metabolite ratio. Conclusions: The presence of neuronal degeneration is suggested in OCD. Future longitudinal neuroimaging and neuropsychological studies with larger patient samples are warranted in order to confirm these preliminary findings to better characterize the relevance of neurochemical abnormalities in hippocampus in the pathophysiology of OCD.

A series of chiral ferrocene-containing thiourea derivatives have been synthesized, and their enantioselective recognition properties were investigated by UV/Vis titration. Receptors 5a and 6a exhibit excellent chiral recognition abilities towards N-acetylaspartate. The differences in solution colour can be observed directly by the naked eye. The minimum energy structures of 5a and 6a were also obtained by theoretical DFT calculations. (© Wiley-VCH Verlag GmbH & Co. KGaA, 69451 Weinheim, Germany, 2009)

The most consistent change in SVD is a reduction in NAA, a marker of neuronal integrity. The lack of correlation with cognition does not support the use of MRS as a surrogate disease marker.

BACKGROUND AND PURPOSE To characterize the cerebral metabolic changes in dementia with Lewy bodies patients. METHODS The metabolic ratios of NAA/Cr and Cho/Cr in bilateral hippocampus were determined by proton magnetic resonance spectroscopy in 8 patients and 8 age-matched healthy controls. RESULTS Dementia with Lewy bodies patients showed significantly lower NAA/Cr ratios in bilateral hippocampus, while the Cho/Cr ratio did not differ from the control group. CONCLUSIONS Our data show relatively decrease of N-acetylaspartate in the hippocampus of patients with early or intermediate stage DLB. Hence, damage of neurons seems to be an early alteration in DLB.

Objectives: Studies have reported decreased N-acetylaspartate (NAA) in dorsolateral prefrontal cortex (DLPFC) of adults and children with bipolar disorder (BD), suggesting decreased neuronal density in this area. However, it is unclear if this finding represents neurodegeneration after or a trait marker present before BD onset. To address this question, we used proton magnetic resonance spectroscopy (1H-MRS) to compare DLPFC levels of NAA among bipolar offspring with early-onset BD, bipolar offspring with subsyndromal symptoms of BD and healthy children. Methods: Participants were 9–18 years old, and included 60 offspring of parents with bipolar I or II disorder (32 with BD and 28 with subsyndromal symptoms of BD), and 26 healthy controls. 1H-MRS at 3 T was used to study 8-cm3 voxels placed in left and right DLPFC. Results: There were no significant group differences in mean right or left DLPFC NAA/Cr ratios. Exploratory analyses of additional metabolites (myoinositol, choline) also yielded no significant group differences. NAA/Cr ratios were not correlated with age, duration of illness, or exposure to lithium or valproate. Conclusions: Our findings suggest that DLPFC NAA/Cr ratios cannot be used as a trait marker for BD. Although we did not find decreased DLPFC NAA/Cr ratios in children and adolescents with BD, it is still possible that such levels begin to decrease after longer durations of illness into adulthood. Longitudinal neuroimaging studies of patients with BD accounting for developmental and treatment factors are needed to further clarify the neurodegenerative aspects of BD.

N-Acetylaspartate (NAA) is one of the most important metabolites detectable by brain 1H-MRS being considered an index of neuronal integrity. At the low magnetic field used in most clinical settings β,γ-glutamate/glutamine (Glx) resonances are very close and partially overlap the methyl-NAA resonance interfering with NAA quantification especially at low TE and in the presence of increased Glx signals. NAA overestimation due to Glx on a set of model solutions containing NAA, glutamate, and glutamine in variable amounts was evaluated and the result tested in vivo in six healthy controls and five age- and sex-matched patients with hepatic encephalopathy (HE), the latter having an increased Glx content. A method to assess in vivo the NAA overestimation caused by Glx is proposed. A perfect match was obtained between the assessment of Glx contamination on the NAA of healthy controls and that obtained on the model solutions. However, a substantial difference in NAA overestimation was found between controls and HE patients that cannot be explained by our model. An interpretative hypothesis is provided. Magn Reson Med, 2005. © 2005 Wiley-Liss, Inc.

N-acetylaspartate (NAA) contributes to the most prominent signal in proton magnetic resonance spectroscopy (1H-MRS) of the adult human brain. We report the absence of NAA in the brain of a 3-year-old child with neurodevelopmental retardation and moderately delayed myelination. Since normal concentration of NAA in body fluids is hardly detectable, 1H-MRS is a noninvasive technique for identifying neurometabolic diseases with absent NAA. This report puts NAA as a neuronal marker to question. Ann Neurol 2001;49:518–521

N-acetylaspartate (NAA) is found exclusively in neurons and their processes in the adult brain. Since the regional distribution of NAA may be imaged using magnetic resonance spectroscopic imaging ( 1 H-MRSI), a regional measure of neuronal density may be noninvasively obtained. The technique may be particularly useful in the diagnosis of diseases where neurons are selectively injured, since these diseases do not result in definitive changes on conventional imaging studies. The goal of this study was to determine whether 1 H-MRSI measurement of NAA detects neuronal loss following global ischemia. 1 H-MRSI was performed in rats 24 h after global ischemia was induced by bilateral carotid occlusion plus hypotension. 1- H-MRSI showed that NAA was decreased by 29-74% in vulnerable regions, including the cortex, striatum, hippocampus, and, to a lesser extent, the thalamus. No change was observed in the brain stem or cerebellum. Regions where 1 H-MRSI observed NAA was decreased also had histological evidence of selective neuronal necrosis and showed marked increase of lactate and alanine. These results show that 1 H-MRSI detected loss of NAA in brain regions with selective neuronal loss, suggesting that 1 H-MRSI measurements of NAA could detect neuronal loss in a variety of disease states where there is selective neuronal necrosis.

High-resolution 1H and 13C NMR of N-acetylaspartic acid as its 2-(S)-butyl diester allows the two enantiomers to be unambiguously identified. Analysis of urine samples from five patients with Canavan disease (N-aspartoacylase deficiency) showed that more than 95% of the excreted N-acetylaspartate had the S-configuration.

Magnetic resonance spectroscopy (MRS) provides a non-invasive method of investigating disordered energy metabolism in vivo. Here, we briefly outline some MRS studies of skeletal muscle and brain metabolism that have been carried out in patients with inborn errors of energy metabolism. We concentrate in particular on the use of 1H MRS for the detection of elevated brain lactate in these patients.