We found no significant variation in neurometabolites concentration between the whole 22q11DS patient group and the healthy control group. This might be explained by group differences in the proportion of gray matter/white matter within the DLPFC and hippocampal voxels. Also, we found no evidence for altered Myoseverin B glutamate in the DLPFC of 22q11DS patients vs. healthy controls. In patients with chronic schizophrenia, 1H-MRS studies of the frontal cortex have shown increased and reduced glutamate concentrations. Perhaps, brain dysfunction MRS 1845 associated with psychosis in 22q11DS involves specific regions of the temporal lobe. Furthermore, it is also possible that abnormalities in glutamatergic function in this brain region may exist at the level of NMDA receptor or in second messenger signaling without alterations in glutamate concentration. An interesting observation is that most of the metabolite contents are in the order of 22q11DS SCZ2,HC,22q11DS SCZ+. We are not aware of an existing explanation for this relation in the literature. However, we hypothesize that prior to the development of schizophrenia patients with 22q11DS in general may have decreased neuronal metabolism as has been observed for glutamate in individuals with increased vulnerability to schizophrenia. On the other hand, an instable neuronal metabolism may predispose a subgroup of 22q11DS patients to psychotic decompensation. Another possibility is that higher metabolites in the 22q11DS patients are the result of the transition to psychosis instead of the cause. This would mean that high metabolic rates in 22q11DS are state- instead of trait-related. Due to the cross-sectional design of our study we are unable to confirm this hypothesis. Longitudinal research in 22q11DS patients before and after transition to psychosis is therefore warranted. The strengths of this study include the evaluation of neuronal integrity in 22q11DS according to psychiatric status of 22q11DS SCZ2 and 22q11DS SCZ+ and in comparison to age matched healthy controls. Also, all MRS spectra were carefully inspected and were included only if fulfilling the quality criteria of LCmodel. We have to acknowledge some limitations of the study; unfortunately at the time of the study we were not able to analyze plasma samples of proline and glutamine of healthy controls.