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Published on: September 12, 2011
White matter microstructural abnormalities in families multiply affected with bipolar I disorder: a diffusion tensor
L Emsell1, C Chaddock2, N Forde3
1Translational MRI, Department of Imaging and Pathology, KU Leuven and Radiology,University Hospitals Leuven,Belgium.
White matter abnormalities in bipolar disorder (BD) patients show reduced fractional anisotropy (FA) and increased radial diffusivity (RD). Alterations in specific tracts like the superior longitudinal fasciculus (SLF) and uncinate fasciculus (UF) may indicate genetic risk for BD.
Area of Science:
- Neuroimaging
- Neuroscience
- Psychiatry
Background:
- White matter (WM) abnormalities are potential endophenotypic markers for bipolar disorder (BD).
- Previous diffusion tensor imaging (DTI) voxel-based analysis (VBA) linked widespread fractional anisotropy (FA) abnormalities to BD and genetic liability.
- This study further explores WM abnormalities using DTI tractography to investigate tracts involved in BD pathophysiology.
Purpose of the Study:
- To investigate the endophenotypic potential of white matter (WM) abnormalities in bipolar disorder (BD).
- To analyze specific white matter tracts implicated in the pathophysiology of BD using DTI tractography.
- To examine the effects of participant group and genetic liability on WM microstructure.
Main Methods:
- Diffusion magnetic resonance imaging (MRI) data from 19 BD patients, 21 unaffected relatives, and 18 healthy volunteers.
- DTI tractography applied to identify key tracts: cingulum, uncinate fasciculus (UF), superior longitudinal fasciculus (SLF), inferior longitudinal fasciculus (ILF), corpus callosum, and anterior limb of the internal capsule (ALIC).
- Regression analyses to assess group and genetic liability effects on fractional anisotropy (FA) and radial diffusivity (RD).
Main Results:
- Significant group effects on FA and RD in the cingulum, SLF, callosal splenium, and ILF, with reduced FA and increased RD in BD patients.
- Genetic liability correlated with decreased FA and increased RD in the UF.
- Genetic liability was also associated with decreased FA in the SLF among patients.
Conclusions:
- WM microstructural abnormalities in limbic, temporal, and callosal pathways are associated with BD.
- Alterations in the SLF and UF may serve as potential endophenotypic markers for BD risk.
- DTI tractography provides insights into the neural underpinnings of BD and genetic susceptibility.
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