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Neural correlates of reward processing in adults with 22q11 deletion syndrome.
J Neurodev Disord 2016; 8:25JN

Abstract

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.

Authors+Show Affiliations

Department of Psychiatry and Psychology, Maastricht University, Maastricht, The Netherlands.Department of Psychiatry and Psychology, Maastricht University, Maastricht, The Netherlands.Department of Psychiatry and Psychology, Maastricht University, Maastricht, The Netherlands.Department of Psychiatry, Academic Medical Centre Amsterdam, Amsterdam, The Netherlands.Department of Psychiatry, Academic Medical Centre Amsterdam, Amsterdam, The Netherlands.Department of Psychiatry and Psychology, Maastricht University, Maastricht, The Netherlands.Department of Psychiatry and Psychology, Maastricht University, Maastricht, The Netherlands.

Pub Type(s)

Journal Article

Language

eng

PubMed ID

27429661

Citation

van Duin, Esther D A., et al. "Neural Correlates of Reward Processing in Adults With 22q11 Deletion Syndrome." Journal of Neurodevelopmental Disorders, vol. 8, 2016, p. 25.
van Duin EDA, Goossens L, Hernaus D, et al. Neural correlates of reward processing in adults with 22q11 deletion syndrome. J Neurodev Disord. 2016;8:25.
van Duin, E. D. A., Goossens, L., Hernaus, D., da Silva Alves, F., Schmitz, N., Schruers, K., & van Amelsvoort, T. (2016). Neural correlates of reward processing in adults with 22q11 deletion syndrome. Journal of Neurodevelopmental Disorders, 8, p. 25. doi:10.1186/s11689-016-9158-5.
van Duin EDA, et al. Neural Correlates of Reward Processing in Adults With 22q11 Deletion Syndrome. J Neurodev Disord. 2016;8:25. PubMed PMID: 27429661.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Neural correlates of reward processing in adults with 22q11 deletion syndrome. AU - van Duin,Esther D A, AU - Goossens,Liesbet, AU - Hernaus,Dennis, AU - da Silva Alves,Fabiana, AU - Schmitz,Nicole, AU - Schruers,Koen, AU - van Amelsvoort,Therese, Y1 - 2016/07/15/ PY - 2015/12/25/received PY - 2016/07/05/accepted PY - 2016/7/19/entrez PY - 2016/7/19/pubmed PY - 2016/7/19/medline KW - 22q11 deletion syndrome KW - COMT KW - Psychosis KW - Reward SP - 25 EP - 25 JF - Journal of neurodevelopmental disorders JO - J Neurodev Disord VL - 8 N2 - 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. SN - 1866-1947 UR - https://www.unboundmedicine.com/medline/citation/27429661/Neural_correlates_of_reward_processing_in_adults_with_22q11_deletion_syndrome_ L2 - https://jneurodevdisorders.biomedcentral.com/articles/10.1186/s11689-016-9158-5 DB - PRIME DP - Unbound Medicine ER -