Following our first line of enquiry in the attempt to show that NAA can index neuronal pathology in schizophrenia, Bertolino et al. found in two separate groups of patients that NAA/Cre ratios were reduced in the medial temporal lobe and in the DLPFC independent of the medication status of the patients.10,11 The same phenomena was observed in patients with childhood onset schizophrenia.12 These results have been confirmed by a number of other investigators around the world, but not by all.1 It is important to note that NAA/Cre reductions in the DLPFC are not as consistently found as are changes in the hippocampal region, most likely due to variations in the degree of chronicity and age of the cohorts, as well as possible effects of medication.13 Another variable that may be able to explain some of the variation in patient samples is clinical symptomatology: Callicott et al.14 found that the lower the NAA/Cre in the DLPFC, the higher the negative symptoms in 36 patients with schizophrenia. This finding, which implicates NAA measures as having functional correlates, is shown in Figure 2. Further attesting to the sensitivity of NAA/Cre ratios to important functional aspects of the pathophysiology of schizophrenia, especially in areas that have been implicated by other functional and post-mortem approaches (e.g. Xe, PET, fMRI915) is the finding that neuroleptic treatment seems to increase NAA/Cre measurements selectively in the DLPFC.16

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