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Neural correlates of genetically abnormal social cognition in Williams syndrome

Nature Neuroscience volume 8, pages 991–993 (2005)Cite this article

Abstract

Williams-Beuren syndrome (WBS), caused by a microdeletion of approximately 21 genes on chromosome 7q11.23, is characterized by unique hypersociability combined with increased non-social anxiety. Using functional neuroimaging, we found reduced amygdala activation in individuals with WBS for threatening faces but increased activation for threatening scenes, relative to matched normal controls. Activation and interactions of prefrontal regions linked to amygdala, especially orbitofrontal cortex, were abnormal, suggesting a genetically controlled neural circuitry for regulating human social behavior.

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Figure 1: Amygdala activation by task.
Figure 2: Differential activation and interaction in a network regulating amygdala.

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Acknowledgements

We thank N. Dixit, A. Bonner-Jackson, R. Olsen and J. Holt for research assistance; A. Goldman and Q. Chen for single-subject analyses and D. Weinberger for helpful discussion. This work was supported by the US National Institute of Mental Health intramural program and National Institute on Neurological Disorders and Stroke grant NS35102 to C.B.M.

Author information

Author notes

  1. Ahmad R Hariri

    Present address: Department of Psychiatry, University of Pittsburgh School of Medicine, Western Psychiatric Institute and Clinic, Pittsburgh, Pennsylvania, 15213, USA

Authors and Affiliations

  1. Department of Health and Human Services, Section on Integrative Neuroimaging, National Institute of Mental Health, National Institutes of Health, Bethesda, 20892, Maryland, USA

    Andreas Meyer-Lindenberg & Karen Faith Berman

  2. Department of Health and Human Services, Neuroimaging Core Facility of the Clinical Brain Disorders Branch, Genes, Cognition and Psychosis Program, National Institute of Mental Health, National Institutes of Health, Bethesda, 20892, Maryland, USA

    Andreas Meyer-Lindenberg, Karen E Munoz & Venkata S Mattay

  3. Department of Health and Human Services, Clinical Brain Disorders Branch, Genes, Cognition and Psychosis Program, National Institute of Mental Health, National Institutes of Health, Bethesda, 20892, Maryland, USA

    Andreas Meyer-Lindenberg, Ahmad R Hariri, Karen E Munoz, Venkata S Mattay & Karen Faith Berman

  4. Department of Psychological and Brain Sciences, Neurodevelopmental Sciences Laboratory, University of Louisville, Louisville, 40292, Kentucky, USA

    Carolyn B Mervis

  5. Department of Pediatrics, University of Nevada School of Medicine, Las Vegas, 89102, Nevada, USA

    Colleen A Morris

Authors
  1. Andreas Meyer-Lindenberg
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Corresponding author

Correspondence to Andreas Meyer-Lindenberg.

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The authors declare no competing financial interests.

Supplementary information

Supplementary Fig. 1

Single-subject analyses in native space of activation during the face-matching task. (PDF 3219 kb)

Supplementary Fig. 2

Single-subject analyses in native space of activation during the scene-matching task. (PDF 3325 kb)

Supplementary Table 1

Demographics and behavioral data. (PDF 50 kb)

Supplementary Table 2

Amygdala activation in the faces and IAPS matching tasks. (PDF 40 kb)

Supplementary Table 3

Cortical activation in the faces and IAPS matching tasks. (PDF 55 kb)

Supplementary Methods (PDF 122 kb)

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Meyer-Lindenberg, A., Hariri, A., Munoz, K. et al. Neural correlates of genetically abnormal social cognition in Williams syndrome. Nat Neurosci 8, 991–993 (2005). https://doi.org/10.1038/nn1494

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