Genetic and environmental influences on cortical surface area and cortical thickness in bipolar disorder. Issue 1 (28th May 2014)

• Record Type: Journal Article
• Authors: Bootsman, F.; Brouwer, R. M.; Schnack, H. G.; van Baal, G. C. M.; van der Schot, A. C.; Vonk, R.; Hulshoff Pol, H. E.; Nolen, W. A.; Kahn, R. S.; van Haren, N. E. M.
• Is Part Of: Psychological medicine. Volume 45:Issue 1(2015)
• Page Start: 193
• Page End: 204
• Publication Date: 2014-05-28
• Subjects: Bipolar disorder, -- cortical surface area, -- cortical thickness, -- heritability, -- magnetic resonance imaging, -- twin studies, -- unique environmental factors; Psychiatry -- Periodicals; Medicine and psychology -- Periodicals; Clinical psychology -- Periodicals; 616.89
• DOI: 10.1017/S0033291714001251
• Languages: English
• ISSNs: 0033-2917

Abstract

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.