ArticlePsychopharmacology2015
Glutamatergic markers, age, intellectual functioning and psychosis in 22q11 deletion syndrome.
Article in Psychopharmacology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers, 1 of them a synthesis that pooled it.
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Who cites it
10 citing papers in PubMed, 1 synthesis or guideline pooled it, 20 citations in OpenAlex.
- Neural excitation/inhibition imbalance and neurodevelopmental pathology in human copy number variant syndromes: a systematic review.Journal of neurodevelopmental disorders · 2025Pooled it
- Glutamatergic and GABAergic reactivity and cognition in 22q11.2 deletion syndrome and healthy volunteers: A randomized double-blind 7-Tesla pharmacological MRS study.Journal of psychopharmacology (Oxford, England) · 2020Trial
- Article
- The 22q11.2 Microdeletion in Pediatric Patients with Cleft Lip, Palate, or Both and Congenital Heart Disease: A Systematic Review.Journal of pediatric genetics · 2020Review
- Neurobiological perspective of 22q11.2 deletion syndrome.The lancet. Psychiatry · 2019Review
- Abnormal development of early auditory processing in 22q11.2 Deletion Syndrome.Translational psychiatry · 2019Article
- A pilot study on machine learning approach to delineate metabolic signatures in intellectual disability.International journal of developmental disabilities · 2019Article
- Decreased Serum Glutamate Levels in Male Adults with Internet Gaming Disorder: A Pilot Study.Clinical psychopharmacology and neuroscience : the official scientific journal of the Korean College of Neuropsychopharmacology · 2018Article
- Deletion size analysis of 1680 22q11.2DS subjects identifies a new recombination hotspot on chromosome 22q11.2.Human molecular genetics · 2018Article
- The use of two different MLPA kits in 22q11.2 deletion syndrome.European journal of medical genetics · 2016Article
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Authors and funding
6 authors at 4 institutions in 1 country.
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No grant is acknowledged in the PubMed record.
Abstract
rationalePatients with 22q11 deletion syndrome (22q11DS) have a high prevalence of intellectual disabilities and psychiatric disorders, including psychosis. Haplo-insufficiency of genes in the deleted region may offer a partial explanation for the increased vulnerability for psychosis and intellectual disability. One gene of particular interest is the gene coding for proline dehydrogenase (PRODH), an enzyme responsible for the conversion of proline into glutamate.
objectivesBecause abnormalities in glutamatergic signaling are thought to be responsible for cognition and psychosis in the general population, we hypothesized that PRODH haplo-insufficiency may underlie some of the cognitive and psychotic features seen in 22q11DS.
methodsIn this explorative study, we investigated the relation between plasma proline, glutamate, and glutamine and age, intelligence, and psychosis in 64 adults with 22q11DS.
resultsHyperprolinemia was found in 31.3% of subjects with 22q11DS. A relation between glutamine, glutamate, proline, and presence of psychosis was not observed. Regression analysis revealed a positive relation between plasma glutamate and age, a positive relation of glutamate with antipsychotic drugs, a relation of glutamine and gender, and a positive relation of glutamine and mood stabilizing drugs, and a negative relation of the ratio glutamine/glutamate and age. The group with relatively lower IQ had higher glutamate levels compared to the group with relatively higher IQ.
conclusionsOur results suggest that 22q11DS is accompanied by abnormalities in glutamatergic metabolism. Future longitudinal studies are needed to further investigate the glutamatergic system in 22q11DS and how this affects the development of cognitive problems and psychopathology.
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