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Response of neural reward regions to food cues in autism spectrum disorders

BACKGROUND: One hypothesis for the social deficits that characterize autism spectrum disorders (ASD) is diminished neural reward response to social interaction and attachment. Prior research using established monetary reward paradigms as a test of non-social reward to compare with social reward may...

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Autores principales: Cascio, Carissa J, Foss-Feig, Jennifer H, Heacock, Jessica L, Newsom, Cassandra R, Cowan, Ronald L, Benningfield, Margaret M, Rogers, Baxter P, Cao, Aize
Formato: Online Artículo Texto
Lenguaje:English
Publicado: BioMed Central 2012
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3436657/
https://www.ncbi.nlm.nih.gov/pubmed/22958533
http://dx.doi.org/10.1186/1866-1955-4-9
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author Cascio, Carissa J
Foss-Feig, Jennifer H
Heacock, Jessica L
Newsom, Cassandra R
Cowan, Ronald L
Benningfield, Margaret M
Rogers, Baxter P
Cao, Aize
author_facet Cascio, Carissa J
Foss-Feig, Jennifer H
Heacock, Jessica L
Newsom, Cassandra R
Cowan, Ronald L
Benningfield, Margaret M
Rogers, Baxter P
Cao, Aize
author_sort Cascio, Carissa J
collection PubMed
description BACKGROUND: One hypothesis for the social deficits that characterize autism spectrum disorders (ASD) is diminished neural reward response to social interaction and attachment. Prior research using established monetary reward paradigms as a test of non-social reward to compare with social reward may involve confounds in the ability of individuals with ASD to utilize symbolic representation of money and the abstraction required to interpret monetary gains. Thus, a useful addition to our understanding of neural reward circuitry in ASD includes a characterization of the neural response to primary rewards. METHOD: We asked 17 children with ASD and 18 children without ASD to abstain from eating for at least four hours before an MRI scan in which they viewed images of high-calorie foods. We assessed the neural reward network for increases in the blood oxygenation level dependent (BOLD) signal in response to the food images RESULTS: We found very similar patterns of increased BOLD signal to these images in the two groups; both groups showed increased BOLD signal in the bilateral amygdala, as well as in the nucleus accumbens, orbitofrontal cortex, and insula. Direct group comparisons revealed that the ASD group showed a stronger response to food cues in bilateral insula along the anterior-posterior gradient and in the anterior cingulate cortex than the control group, whereas there were no neural reward regions that showed higher activation for controls than for ASD. CONCLUSION: These results suggest that neural response to primary rewards is not diminished but in fact shows an aberrant enhancement in children with ASD.
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spelling pubmed-34366572012-09-08 Response of neural reward regions to food cues in autism spectrum disorders Cascio, Carissa J Foss-Feig, Jennifer H Heacock, Jessica L Newsom, Cassandra R Cowan, Ronald L Benningfield, Margaret M Rogers, Baxter P Cao, Aize J Neurodev Disord Research BACKGROUND: One hypothesis for the social deficits that characterize autism spectrum disorders (ASD) is diminished neural reward response to social interaction and attachment. Prior research using established monetary reward paradigms as a test of non-social reward to compare with social reward may involve confounds in the ability of individuals with ASD to utilize symbolic representation of money and the abstraction required to interpret monetary gains. Thus, a useful addition to our understanding of neural reward circuitry in ASD includes a characterization of the neural response to primary rewards. METHOD: We asked 17 children with ASD and 18 children without ASD to abstain from eating for at least four hours before an MRI scan in which they viewed images of high-calorie foods. We assessed the neural reward network for increases in the blood oxygenation level dependent (BOLD) signal in response to the food images RESULTS: We found very similar patterns of increased BOLD signal to these images in the two groups; both groups showed increased BOLD signal in the bilateral amygdala, as well as in the nucleus accumbens, orbitofrontal cortex, and insula. Direct group comparisons revealed that the ASD group showed a stronger response to food cues in bilateral insula along the anterior-posterior gradient and in the anterior cingulate cortex than the control group, whereas there were no neural reward regions that showed higher activation for controls than for ASD. CONCLUSION: These results suggest that neural response to primary rewards is not diminished but in fact shows an aberrant enhancement in children with ASD. BioMed Central 2012 2012-05-17 /pmc/articles/PMC3436657/ /pubmed/22958533 http://dx.doi.org/10.1186/1866-1955-4-9 Text en Copyright ©2012 Cascio et al; licensee BioMed Central Ltd. http://creativecommons.org/licenses/by/2.0 This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
spellingShingle Research
Cascio, Carissa J
Foss-Feig, Jennifer H
Heacock, Jessica L
Newsom, Cassandra R
Cowan, Ronald L
Benningfield, Margaret M
Rogers, Baxter P
Cao, Aize
Response of neural reward regions to food cues in autism spectrum disorders
title Response of neural reward regions to food cues in autism spectrum disorders
title_full Response of neural reward regions to food cues in autism spectrum disorders
title_fullStr Response of neural reward regions to food cues in autism spectrum disorders
title_full_unstemmed Response of neural reward regions to food cues in autism spectrum disorders
title_short Response of neural reward regions to food cues in autism spectrum disorders
title_sort response of neural reward regions to food cues in autism spectrum disorders
topic Research
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3436657/
https://www.ncbi.nlm.nih.gov/pubmed/22958533
http://dx.doi.org/10.1186/1866-1955-4-9
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