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Genetic and environmental influences on cortical surface area and cortical thickness in bipolar disorder

Published online by Cambridge University Press:  28 May 2014

F. Bootsman*
Affiliation:
Brain Center Rudolf Magnus, University Medical Center Utrecht, Utrecht, The Netherlands
R. M. Brouwer
Affiliation:
Brain Center Rudolf Magnus, University Medical Center Utrecht, Utrecht, The Netherlands
H. G. Schnack
Affiliation:
Brain Center Rudolf Magnus, University Medical Center Utrecht, Utrecht, The Netherlands
G. C. M. van Baal
Affiliation:
Julius Center, University Medical Center Utrecht, Utrecht, The Netherlands
A. C. van der Schot
Affiliation:
Brain Center Rudolf Magnus, University Medical Center Utrecht, Utrecht, The Netherlands
R. Vonk
Affiliation:
Reinier van Arkel Group, 's-Hertogenbosch, The Netherlands
H. E. Hulshoff Pol
Affiliation:
Brain Center Rudolf Magnus, University Medical Center Utrecht, Utrecht, The Netherlands
W. A. Nolen
Affiliation:
Department of Psychiatry, University Medical Center Groningen, Groningen, The Netherlands
R. S. Kahn
Affiliation:
Brain Center Rudolf Magnus, University Medical Center Utrecht, Utrecht, The Netherlands
N. E. M. van Haren
Affiliation:
Brain Center Rudolf Magnus, University Medical Center Utrecht, Utrecht, The Netherlands
*
*Address for correspondence: Dr F. Bootsman, University Medical Center Utrecht, Brain Center Rudolf Magnus, Internal address: A.01.126, PO Box: 85500, 3508 GA Utrecht, The Netherlands. (Email: [email protected])

Abstract

Background

The risk of developing bipolar disorder (BD) has been linked to structural brain abnormalities. The degree to which genes and environment influence the association of BD with cortical surface area remains to be elucidated. In this twin study, genetic and environmental contributions to the association between liability to develop BD and surface area, thickness and volume of the cortex were examined.

Method

The study cohort included 44 affected monozygotic (nine concordant, 12 discordant) and dizygotic (four concordant, 19 discordant) twin pairs, and seven twins from incomplete discordant monozygotic and dizygotic discordant twin pairs. In addition, 37 monozygotic and 24 dizygotic healthy control twin pairs, and six twins from incomplete monozygotic and dizygotic control pairs were included.

Results

Genetic liability to develop BD was associated with a larger cortical surface in limbic and parietal regions, and a thicker cortex in central and parietal regions. Environmental factors related to BD were associated with larger medial frontal, parietal and limbic, and smaller orbitofrontal surfaces. Furthermore, thinner frontal, limbic and occipital cortex, and larger frontal and parietal, and smaller orbitofrontal volumes were also associated with environmental factors related to BD.

Conclusions

Our results suggest that unique environmental factors play a prominent role in driving the associations between liability to develop BD and cortical measures, particularly those involving cortical thickness. Further evaluation of their influence on the surface and thickness of the cortical mantle is recommended. In addition, cortical volume appeared to be primarily dependent on surface and not thickness.

Type
Original Articles
Copyright
Copyright © Cambridge University Press 2014 

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