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Neural correlates of reward processing in adults with 22q11 deletion syndrome

BACKGROUND: 22q11.2 deletion syndrome (22q11DS) is caused by a microdeletion on chromosome 22q11.2 and associated with an increased risk to develop psychosis. The gene coding for catechol-O-methyl-transferase (COMT) is located at the deleted region, resulting in disrupted dopaminergic neurotransmiss...

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Autores principales: van Duin, Esther D. A., Goossens, Liesbet, Hernaus, Dennis, da Silva Alves, Fabiana, Schmitz, Nicole, Schruers, Koen, van Amelsvoort, Therese
Formato: Online Artículo Texto
Lenguaje:English
Publicado: BioMed Central 2016
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Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4946156/
https://www.ncbi.nlm.nih.gov/pubmed/27429661
http://dx.doi.org/10.1186/s11689-016-9158-5
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author van Duin, Esther D. A.
Goossens, Liesbet
Hernaus, Dennis
da Silva Alves, Fabiana
Schmitz, Nicole
Schruers, Koen
van Amelsvoort, Therese
author_facet van Duin, Esther D. A.
Goossens, Liesbet
Hernaus, Dennis
da Silva Alves, Fabiana
Schmitz, Nicole
Schruers, Koen
van Amelsvoort, Therese
author_sort van Duin, Esther D. A.
collection PubMed
description BACKGROUND: 22q11.2 deletion syndrome (22q11DS) is caused by a microdeletion on chromosome 22q11.2 and associated with an increased risk to develop psychosis. The gene coding for catechol-O-methyl-transferase (COMT) is located at the deleted region, resulting in disrupted dopaminergic neurotransmission in 22q11DS, which may contribute to the increased vulnerability for psychosis. A dysfunctional motivational reward system is considered one of the salient features in psychosis and thought to be related to abnormal dopaminergic neurotransmission. The functional anatomy of the brain reward circuitry has not yet been investigated in 22q11DS. METHODS: This study aims to investigate neural activity during anticipation of reward and loss in adult patients with 22q11DS. We measured blood-oxygen-level dependent (BOLD) activity in 16 patients with 22q11DS and 12 healthy controls during a monetary incentive delay task using a 3T Philips Intera MRI system. Data were analysed using SPM8. RESULTS: During anticipation of reward, the 22q11DS group alone displayed significant activation in bilateral middle frontal and temporal brain regions. Compared to healthy controls, significantly less activation in bilateral cingulate gyrus extending to premotor, primary motor and somatosensory areas was found. During anticipation of loss, the 22q11DS group displayed activity in the left middle frontal gyrus and anterior cingulate cortex, and relative to controls, they showed reduced brain activation in bilateral (pre)cuneus and left posterior cingulate. Within the 22q11DS group, COMT Val hemizygotes displayed more activation compared to Met hemizygotes in right posterior cingulate and bilateral parietal regions during anticipation of reward. During anticipation of loss, COMT Met hemizygotes compared to Val hemizygotes showed more activation in bilateral insula, striatum and left anterior cingulate. CONCLUSIONS: This is the first study to investigate reward processing in 22q11DS. Our preliminary results suggest that people with 22q11DS engage a fronto-temporal neural network. Compared to healthy controls, people with 22q11DS primarily displayed reduced activity in medial frontal regions during reward anticipation. COMT hemizygosity affects responsivity of the reward system in this condition. Alterations in reward processing partly underlain by the dopamine system may play a role in susceptibility for psychosis in 22q11DS.
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spelling pubmed-49461562016-07-16 Neural correlates of reward processing in adults with 22q11 deletion syndrome van Duin, Esther D. A. Goossens, Liesbet Hernaus, Dennis da Silva Alves, Fabiana Schmitz, Nicole Schruers, Koen van Amelsvoort, Therese J Neurodev Disord Research BACKGROUND: 22q11.2 deletion syndrome (22q11DS) is caused by a microdeletion on chromosome 22q11.2 and associated with an increased risk to develop psychosis. The gene coding for catechol-O-methyl-transferase (COMT) is located at the deleted region, resulting in disrupted dopaminergic neurotransmission in 22q11DS, which may contribute to the increased vulnerability for psychosis. A dysfunctional motivational reward system is considered one of the salient features in psychosis and thought to be related to abnormal dopaminergic neurotransmission. The functional anatomy of the brain reward circuitry has not yet been investigated in 22q11DS. METHODS: This study aims to investigate neural activity during anticipation of reward and loss in adult patients with 22q11DS. We measured blood-oxygen-level dependent (BOLD) activity in 16 patients with 22q11DS and 12 healthy controls during a monetary incentive delay task using a 3T Philips Intera MRI system. Data were analysed using SPM8. RESULTS: During anticipation of reward, the 22q11DS group alone displayed significant activation in bilateral middle frontal and temporal brain regions. Compared to healthy controls, significantly less activation in bilateral cingulate gyrus extending to premotor, primary motor and somatosensory areas was found. During anticipation of loss, the 22q11DS group displayed activity in the left middle frontal gyrus and anterior cingulate cortex, and relative to controls, they showed reduced brain activation in bilateral (pre)cuneus and left posterior cingulate. Within the 22q11DS group, COMT Val hemizygotes displayed more activation compared to Met hemizygotes in right posterior cingulate and bilateral parietal regions during anticipation of reward. During anticipation of loss, COMT Met hemizygotes compared to Val hemizygotes showed more activation in bilateral insula, striatum and left anterior cingulate. CONCLUSIONS: This is the first study to investigate reward processing in 22q11DS. Our preliminary results suggest that people with 22q11DS engage a fronto-temporal neural network. Compared to healthy controls, people with 22q11DS primarily displayed reduced activity in medial frontal regions during reward anticipation. COMT hemizygosity affects responsivity of the reward system in this condition. Alterations in reward processing partly underlain by the dopamine system may play a role in susceptibility for psychosis in 22q11DS. BioMed Central 2016-07-15 /pmc/articles/PMC4946156/ /pubmed/27429661 http://dx.doi.org/10.1186/s11689-016-9158-5 Text en © The Author(s). 2016 Open AccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.
spellingShingle Research
van Duin, Esther D. A.
Goossens, Liesbet
Hernaus, Dennis
da Silva Alves, Fabiana
Schmitz, Nicole
Schruers, Koen
van Amelsvoort, Therese
Neural correlates of reward processing in adults with 22q11 deletion syndrome
title Neural correlates of reward processing in adults with 22q11 deletion syndrome
title_full Neural correlates of reward processing in adults with 22q11 deletion syndrome
title_fullStr Neural correlates of reward processing in adults with 22q11 deletion syndrome
title_full_unstemmed Neural correlates of reward processing in adults with 22q11 deletion syndrome
title_short Neural correlates of reward processing in adults with 22q11 deletion syndrome
title_sort neural correlates of reward processing in adults with 22q11 deletion syndrome
topic Research
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4946156/
https://www.ncbi.nlm.nih.gov/pubmed/27429661
http://dx.doi.org/10.1186/s11689-016-9158-5
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