The authors report they have no financial relationships within the past 3 years to disclose.
Pilot multimodal twin imaging study of generalized anxiety disorder
Article first published online: 12 OCT 2011
© 2011 Wiley-Liss, Inc.
Depression and Anxiety
Volume 29, Issue 3, pages 202–209, March 2012
How to Cite
Hettema, J. M., Kettenmann, B., Ahluwalia, V., McCarthy, C., Kates, W. R., Schmitt, J. E., Silberg, J. L., Neale, M. C., Kendler, K. S. and Fatouros, P. (2012), Pilot multimodal twin imaging study of generalized anxiety disorder. Depress. Anxiety, 29: 202–209. doi: 10.1002/da.20901
Preliminary results from this study were presented at the 30th Annual Anxiety Disorders Association of America Conference, March 4-7, 2010, Baltimore, MD.
- Issue published online: 17 APR 2012
- Article first published online: 12 OCT 2011
- Manuscript Accepted: 22 AUG 2011
- Manuscript Revised: 17 AUG 2011
- Manuscript Received: 22 JUN 2011
- NIH. Grant Number: K08 MH-66277
- National Center for Research Resources. Grant Number: UL1RR031990
- anxiety disorders;
- depressive disorder;
- twin study;
- magnetic resonance spectroscopy;
- diffusion tensor imaging
Generalized anxiety disorder (GAD) is a common chronic condition that is relatively understudied compared to other psychiatric syndromes. Neuroimaging studies have begun to implicate particular neural structures and circuitry in its pathophysiology; however, no genetically informative research has examined the potential sources of reported brain differences.
We acquired spectroscopic, volumetric, and diffusion tensor magnetic resonance imaging data from a pilot study of 34 female subjects selected from monozygotic twin pairs based upon their affection status for GAD, and examined brain regions previously implicated in fear and anxiety for their relationship with affection status and genetic risk.
Lifetime GAD associated with increased creatine levels in the amygdala, smaller left hippocampal volume, and lower fractional anisotropy in the uncinate fasciculus which connects amygdala and frontal cortex. In addition, GAD genetic risk predicted increases in myo-inositol in the amygdala and, possibly, glutamate/glutamine/GABA alterations in the hippocampus. The association of lifetime GAD with smaller hippocampal volume was independent of major depression and might represent a common genetic risk marker for internalizing disorders.
These preliminary data suggest that GAD and its genetic risk factors are likely correlated with volumetric and spectroscopic changes in fear-related limbic structures and their connections with the frontal cortex. Depression and Anxiety 0:1–8, 2011. © 2011 Wiley-Liss, Inc.