Neural correlates of genetically abnormal social cognition in Williams syndrome

Andreas Meyer-Lindenberg; Ahmad R. Hariri; Karen E. Munoz; Carolyn B. Mervis; Venkata S. Mattay; Colleen A. Morris; Karen Faith Berman

doi:10.1038/nn1494

Neural correlates of genetically abnormal social cognition in Williams syndrome

Andreas Meyer-Lindenberg, Ahmad R. Hariri, Karen E. Munoz, Carolyn B. Mervis, Venkata S. Mattay, Colleen A. Morris, Karen Faith Berman

Research output: Contribution to journal › Article › peer-review

281 Scopus citations

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.

Original language	English (US)
Pages (from-to)	991-993
Number of pages	3
Journal	Nature neuroscience
Volume	8
Issue number	8
DOIs	https://doi.org/10.1038/nn1494
State	Published - Aug 2005
Externally published	Yes

ASJC Scopus subject areas

Neuroscience(all)

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title = "Neural correlates of genetically abnormal social cognition in Williams syndrome",

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.",

author = "Andreas Meyer-Lindenberg and Hariri, {Ahmad R.} and Munoz, {Karen E.} and Mervis, {Carolyn B.} and Mattay, {Venkata S.} and Morris, {Colleen A.} and Berman, {Karen Faith}",

note = "Funding Information: 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.",

year = "2005",

month = aug,

doi = "10.1038/nn1494",

language = "English (US)",

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T1 - Neural correlates of genetically abnormal social cognition in Williams syndrome

AU - Meyer-Lindenberg, Andreas

AU - Hariri, Ahmad R.

AU - Munoz, Karen E.

AU - Mervis, Carolyn B.

AU - Mattay, Venkata S.

AU - Morris, Colleen A.

AU - Berman, Karen Faith

N1 - Funding Information: 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.

PY - 2005/8

Y1 - 2005/8

N2 - 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.

AB - 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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Neural correlates of genetically abnormal social cognition in Williams syndrome

Abstract

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