N-acetyl-aspartate

Moore GJ, Hasanat K, Chen G, Seraji-Bozorgzad N, Wilds IB, Faulk MW, Koch S, Jolkovsky L, Manji HK. Lithium Increases N-Acetyl-Aspartate in the Human Brain In Vivo Evidence in Support of bcl-2 s Neurotrophic Effects. Biol Psychiatry 2000 48 1-8. 

D., and Ketter, T.A. (2000) Decreased dorsolateral prefrontal N-acetyl aspartate in bipolar disorder. Biol Psychiatry 47 475 81. 

Magnetic resonance spectroscopy studies of COS patients revealed decreases in the ratio of N-acetyl aspartate to creatine (a putative marker of neuronal density) in the frontal cortex (Thomas et ah, 1998) and hippocampus (Bertolino et ah, 1998). These results were similar in direction and extent to those seen in adult patients. 

A magnetic resonance spectroscopy (MRS) study examined correlates of repetitive violence in 13 mildly mentally retarded individuals and 14 controls (Critch-ley et al., 2000). Concentrations and ratios of N-acetyl aspartate (NAA) and creatine phosphocreatine (Cr-l-PCr) were assayed. The NAA and CR-I-CR concentrations reflect neuronal density and high-energy phosphate metabolism, respectively. Violent patients had lower prefrontal concentrations of NAA and Cr-l-PCr and a lower NAA/Cr-l-PCr ratio in the amyg-dalohippocampal complex than that in controls. Within the violent group, prefrontal NAA concentration correlated with aggression frequency. 

J. W. Pan and K. Takahashi, Interdependence of N-acetyl aspartate and high-energy phosphates in healthy human brain. Ann. Neurol, 2005, 57(1), 92-97. 

Battistuta J., Bjartmar C., and Trapp B. D. (2001). Postmortem degradation of N-acetyl aspartate and N-acetyl aspartylglutamate an HPLC analysis of different rat CNS regions. Neurochem. Res. 26 695-702. 

Fig. 4.15. Perfusion images (PI) and spectroscopic imaging maps of lactate and N-acetyl-aspartate (NAA) before and after embolic occlusion of the middle cerebral artery. Thrombolysis was applied 1.5 h after embolism and lead to a partial reperfusion of the affected territory (upper row). There was a clear increase in lactate that was partially reversed upon thrombolytic reperfusion. NAA maps showed a decreased signal in the ischemic hemisphere that did not recover. [Reproduced with permission from Franke et al. (2000)]...

Sager TN, Laursen H, Hansen AJ (1995) Changes in N-acetyl-aspartate content during focal and global brain ischemia of the rat. J Cereb Blood Flow Metab 15 639-646 Sappey-Marinier D, Hubesch B, Matson GB, Weiner MW (1992) Decreased phosphorus metabolite concentrations and alkalosis in chronic cerebral infarction. Radiology 182 29-34... 

Heales SJ, Davies SE, Bates TE, Clark JB. 1995. Depletion of brain glutathione is accompanied by impaired mitochondrial function and decreased N-acetyl aspartate concentration. Neurochem Res 20 31-38. 

Block W, Bayer TA, Tepest R, Traber F, Rietschel M, et al. 2000. Decreased frontal lobe ratio of N-acetyl aspartate to choline... 

Callicott JH, Egan MF, Bertolino A, Mattay VS, Langheim FJ, et al. 1998. Hippocampal N-acetyl aspartate in unaffected siblings of patients with schizophrenia A possible intermediate neurobiological phenotype. Biol Psychiatry 44 941 -950. 

Clark JB. 1998. N-acetyl aspartate A marker for neuronal loss or mitochondrial dysfunction. Dev Neurosci 20 271-276. 

Ende G, Braus DF, Walter S, Weber-Fahr W, Soher B, et al. 2000. Effects of age, medication, and illness duration on the N-acetyl aspartate signal of the anterior cingulate region in schizophrenia. Schizophr Res 41 389-395. 

Molina V, Sanz J, Sarramea F, Luque R, Benito C, et al. 2006. No association between dorsolateral prefrontal gray matter deficit and N-acetyl aspartate ratios in schizophrenia. Neuropsychobiology 54 171-178. 

Stanley JA, Vemulapalli M, Nutche J, Montrose DM, Sweeney JA, et al. 2007. Reduced N-acetyl-aspartate levels in schizophrenia patients with a younger onset age A singlevoxel lh spectroscopy study. Schizophr Res 93 23-32. 

Li SJ, Wang Y, Pankiewicz J, Stein EA. Neurochemical adaptation to cocaine abuse reduction of N-acetyl aspartate in thalamus of human cocaine abusers. Biol Psychiatry 1999 45(11) 1481—7. 

Cerebral damage following stroke has also been assessed by MR spectroscopy. This technique uses the same methods as MRI but the signal obtained is converted into chemical as opposed to spatial information. Proton MR spectroscopy allows in vivo measurement of N-acetyl-containing compounds, creatine, choline and lactate. The majority of the N-acetyl signal comes from N-acetyl aspartate (NAA), which is present in high concentrations in the brain. The function of NAA is unclear, but it is of particular interest in studies of the brain since it is located almost exclusively in neurons in the adult. Decreases in the NAA resonance peak in vivo indicate neuronal or axonal injury or loss. 

Fig. 23.2. Axial T2-weighted image showing location of a spectroscopy voxel over the posterior limb of the internal capsule of each hemisphere together with the spectra obtained from the right and left internal capsules of a patient with subcortical stroke (Pendlebury et at. 1999). The N-acetyl aspartate (NAA) peak is reduced on the side of the affected right hemisphere consistent with damage to the descending motor pathways.

C2- and D2-symmetric dioxatetraaza 18-membered macrocycles such as 14 and 15 have been prepared by a chemoenzymatic method involving ( )-fraiw-diaminocyclohexane as starting material (eq 26). Good enantiomeric discrimination was observed with tetraprotonated species (/ ,/ )-14 and the D-enantiomer of N-acetyl aspartate. 

Relative decrease in N-acetyl aspartate, N-acetyl glutamate, creatine... 

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