Nicotinamide adenine dinucleotide is a key player of cell metabolism. Previously we demonstrated the feasibility of in vivo NAD measurement, by 31P-MRS, in mouse brain. Actually we established the profile of cerebral NAD+, NADH and NAD+/NADH in a mouse model relevant for schizophrenia and we followed the metabolites regulation during the development by a combination of 1H-31P-MRS. We highlighted redox dysregulation associated with glutathione deficit, from 20 to 250 days old animals. This study provides prospective for understanding the molecular mechanism affecting brain development and regulation together with identification of potential therapeutic biomarker relevant for the pathophysiology of schizophrenia.
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