Year: 2011
Type: erratum
Abstract: Objective: People 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.Method: We employed proton magnetic resonance spectroscopy ( 1 H-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 SCZ2) schizophrenia and 23 age-matched healthy controls.Also, plasma proline levels were determined in the 22q11DS group.Results: We found significantly increased concentrations of glutamate and myo-inositol in the hippocampal region of 22q11DS SCZ+ compared to 22q11DS SCZ2.There were no significant differences in levels of plasma proline between 22q11DS SCZ+ and 22q11DS SCZ2.There was no relationship between plasma proline and cerebral glutamate in 22q11DS.Conclusion: This is the first in vivo 1 H-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.
Source: PLoS ONE
Language: English
Subfield: Psychiatry and Mental health
Field: Medicine
Domain: Health Sciences
Open Access status: gold
Estimated APC paid: $2,382
OpenAlex ID: W2059214465