Brief Communication abstract


Nature Neuroscience 8, 991 - 993 (2005)
Published online: 10 July 2005 | doi:10.1038/nn1494

Neural correlates of genetically abnormal social cognition in Williams syndrome

Andreas Meyer-Lindenberg1,2,3, Ahmad R Hariri3,6, Karen E Munoz2,3, Carolyn B Mervis4, Venkata S Mattay2,3, Colleen A Morris5 & Karen Faith Berman1,3

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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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  1. Section on Integrative Neuroimaging, National Institute of Mental Health, National Institutes of Health, Department of Health and Human Services, Bethesda, Maryland 20892, USA.
  2. Neuroimaging Core Facility of the Clinical Brain Disorders Branch, Genes, Cognition and Psychosis Program, National Institute of Mental Health, National Institutes of Health, Department of Health and Human Services, Bethesda, Maryland 20892, USA.
  3. Clinical Brain Disorders Branch, Genes, Cognition and Psychosis Program, National Institute of Mental Health, National Institutes of Health, Department of Health and Human Services, Bethesda, Maryland 20892, USA.
  4. Neurodevelopmental Sciences Laboratory, Department of Psychological and Brain Sciences, University of Louisville, Louisville, Kentucky 40292, USA.
  5. Department of Pediatrics, University of Nevada School of Medicine, Las Vegas, Nevada 89102, USA.
  6. Present address: Department of Psychiatry, University of Pittsburgh School of Medicine, Western Psychiatric Institute and Clinic, Pittsburgh, Pennsylvania 15213, USA.

Correspondence to: Andreas Meyer-Lindenberg1,2,3 e-mail: andreasml@nih.gov