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Hum Brain Mapp. 2017 May 23. doi: 10.1002/hbm.23660. [Epub ahead of print]

Brain structural alterations in obese children with and without Prader-Willi Syndrome.

Xu M1,2, Zhang Y3,4, von Deneen KM3,4, Zhu H2, Gao JH1,5,6,7.

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Center for MRI Research, Academy for Advanced Interdisciplinary Studies, Peking University, Beijing, 100871, China.
Department of Biomedical Engineering, Peking University, Beijing, 100871, China.
Center for Brain Imaging, Xidian University, Xi'an, 710071, China.
Department of Psychiatry & McKnight Brain Institute, University of Florida, Gainesville, Florida, 32610.
Beijing City Key Lab for Medical Physics and Engineering, Institution of Heavy Ion Physics, School of Physics, Peking University, Beijing, 100871, China.
McGovern Institute for Brian Research, Peking University, Beijing, 100871, China.
Shenzhen Institute of Neuroscience, Shenzhen, 518057, China.


Prader-Willi syndrome (PWS) is a genetic imprinting disorder that is mainly characterized by hyperphagia and childhood obesity. Previous neuroimaging studies revealed that there is a significant difference in brain activation patterns between obese children with and without PWS. However, whether there are differences in the brain structure of obese children with and without PWS remains elusive. In the current study, we used T1-weighted and diffusion tensor magnetic resonance imaging to investigate alterations in the brain structure, such as the cortical volume and white matter integrity, in relation to this eating disorder in 12 children with PWS, 18 obese children without PWS (OB) and 18 healthy controls. Compared with the controls, both the PWS and OB groups exhibited alterations in cortical volume, with similar deficit patterns in 10 co-varying brain regions in the bilateral dorsolateral and medial prefrontal cortices, right anterior cingulate cortex, and bilateral temporal lobe. The white matter integrities of the above regions were then examined with an analysis method based on probabilistic tractography. The PWS group exhibited distinct changes in the reduced fractional anisotropy of white matter fibers connected to the co-varying regions, whereas the OB group did not. Our findings indicated that PWS and OB share similar gray matter alterations that are responsible for the development of eating disorders. Additionally, the distinct white matter alterations might explain the symptoms associated with food intake in PWS, including excessive hyperphagia and constant hunger. Hum Brain Mapp, 2017. © 2017 Wiley Periodicals, Inc.


Prader-Willi syndrome; childhood obesity; cortical volume; eating disorder; tractography

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