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Neuroanatomical markers of familial risk in adolescents with conduct disorder and their unaffected relatives

Published online by Cambridge University Press:  05 October 2021

Graeme Fairchild*
Affiliation:
Department of Psychology, University of Bath, Bath, UK
Kate Sully
Affiliation:
School of Psychology, University of Southampton, Southampton, UK
Luca Passamonti
Affiliation:
Department of Clinical Neurosciences, University of Cambridge, Cambridge, UK Institute of Bioimaging and Molecular Physiology, National Research Council, Milan, Italy
Marlene Staginnus
Affiliation:
Department of Psychology, University of Bath, Bath, UK
Angela Darekar
Affiliation:
Department of Medical Physics, University Hospital Southampton NHS Foundation Trust, Southampton, UK
Edmund J. S. Sonuga-Barke
Affiliation:
Department of Child and Adolescent Psychiatry, King's College London, London, UK
Nicola Toschi
Affiliation:
Department of Biomedicine and Prevention, University of Rome “Tor Vergata”, Rome, Italy Martinos Center for Biomedical Imaging, Boston, USA Harvard Medical School, Boston, USA
*
Author for correspondence: Graeme Fairchild, E-mail: g.fairchild@bath.ac.uk

Abstract

Background

Previous studies have reported brain structure abnormalities in conduct disorder (CD), but it is unclear whether these neuroanatomical alterations mediate the effects of familial (genetic and environmental) risk for CD. We investigated brain structure in adolescents with CD and their unaffected relatives (URs) to identify neuroanatomical markers of familial risk for CD.

Methods

Forty-one adolescents with CD, 24 URs of CD probands, and 38 healthy controls (aged 12–18), underwent structural magnetic resonance imaging. We performed surface-based morphometry analyses, testing for group differences in cortical volume, thickness, surface area, and folding. We also assessed the volume of key subcortical structures.

Results

The CD and UR groups both displayed structural alterations (lower surface area and folding) in left inferior parietal cortex compared with controls. In contrast, CD participants showed lower insula and pars opercularis volume than controls, and lower surface area and folding in these regions than controls and URs. The URs showed greater folding in rostral anterior cingulate and inferior temporal cortex than controls and greater medial orbitofrontal folding than CD participants. The surface area and volume differences were not significant when controlling for attention-deficit/hyperactivity disorder comorbidity. There were no group differences in subcortical volumes.

Conclusions

These findings suggest that alterations in inferior parietal cortical structure partly mediate the effects of familial risk for CD. These structural changes merit investigation as candidate endophenotypes for CD. Neuroanatomical changes in medial orbitofrontal and anterior cingulate cortex differentiated between URs and the other groups, potentially reflecting neural mechanisms of resilience to CD.

Type
Original Article
Copyright
Copyright © The Author(s), 2021. Published by Cambridge University Press

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Footnotes

*

Joint first and last authorship.

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