Proton magnetic resonance spectroscopy in 22q11 deletion syndrome |
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Authors: | da Silva Alves Fabiana Boot Erik Schmitz Nicole Nederveen Aart Vorstman Jacob Lavini Christina Pouwels Petra J Pouwels Petra de Haan Lieuwe Linszen Don van Amelsvoort Therese |
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Institution: | Department of Psychiatry, Academic Medical Centre Amsterdam, Amsterdam, The Netherlands. F.daSilvaAlves@amc.nl |
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Abstract: | ObjectivePeople with velo-cardio-facial syndrome or 22q11 deletion syndrome (22q11DS) have behavioral, cognitive and psychiatric problems. Approximately 30% of affected individuals develop schizophrenia-like psychosis. Glutamate dysfunction is thought to play a crucial role in schizophrenia. However, it is unknown if and how the glutamate system is altered in 22q11DS. People with 22q11DS are vulnerable for haploinsufficiency of PRODH, a gene that codes for an enzyme converting proline into glutamate. Therefore, it can be hypothesized that glutamatergic abnormalities may be present in 22q11DS.MethodWe employed proton magnetic resonance spectroscopy (1H-MRS) to quantify glutamate and other neurometabolites in the dorsolateral prefrontal cortex (DLPFC) and hippocampus of 22 adults with 22q11DS (22q11DS SCZ+) and without (22q11DS SCZ?) schizophrenia and 23 age-matched healthy controls. Also, plasma proline levels were determined in the 22q11DS group.ResultsWe found significantly increased concentrations of glutamate and myo-inositol in the hippocampal region of 22q11DS SCZ+ compared to 22q11DS SCZ?. There were no significant differences in levels of plasma proline between 22q11DS SCZ+ and 22q11DS SCZ?. There was no relationship between plasma proline and cerebral glutamate in 22q11DS.ConclusionThis is the first in vivo
1H-MRS study in 22q11DS. Our results suggest vulnerability of the hippocampus in the psychopathology of 22q11DS SCZ+. Altered hippocampal glutamate and myo-inositol metabolism may partially explain the psychotic symptoms and cognitive impairments seen in this group of patients. |
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