The DOI matches its Crossref record; 17 of the 17 references it cites were found in a registry or an index.
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.
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“Together, these previous findings suggest that dampened neural response to social threat leads to greater sociability.”
From Effects of MDMA on sociability and neural response to social threat and social reward (2009) · cites this paper as Meyer-Lindenberg et al. 2005
In the citing paper
“patients with Williams-Beuren syndrome, characterized by hypersociability, demonstrate attenuated amygdala responses to social threat (Meyer-Lindenberg et al. 2005).”
From Effects of MDMA on sociability and neural response to social threat and social reward (2009) · cites this paper as Meyer-Lindenberg et al. 2005
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Cites
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Anxiety, Fears, and Phobias in Persons With Williams Syndrome
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Neural Basis of Genetically Determined Visuospatial Construction Deficit in Williams Syndrome
Meyer‐Lindenberg, A., Kohn, P. D., Mervis, C. Β., Kippenhan, J. S., Olsen, R. K., Morris, C. A., & Berman, K. F. (2004) · Neuron · doi:10.1016/j.neuron.2004.08.014 · Cited by 287
Self-citationAn Experiment of Nature: Brain Anatomy Parallels Cognition and Behavior in Williams Syndrome
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Increased social fear and decreased fear of objects in monkeys with neonatal amygdala lesions
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Self-citationTowards the neural basis for hypersociability in a genetic syndrome
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Kirsch, P., Esslinger, C., Chen, Q., Mier, D., Lis, S., Siddhanti, S., Gruppe, H., Mattay, V. S., Gallhofer, B., & Meyer-Lindenberg, A. (2005) · The Journal of Neuroscience · doi:10.1523/jneurosci.3984-05.2005 · Cited by 1,639
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Metadata
- Authors
- Meyer-Lindenberg, A., Hariri, A. R., Munoz, K. E., Mervis, C. B., Mattay, V. S., Morris, C. A., & Berman, K. F.
- Affiliations
- National Institutes of Health (US)
- University of Nevada, Las Vegas (US)
- Venue
- Nature Neuroscience
- Published
- 2005-07-10
- Volume
- 8
- Issue
- 8
- Pages
- 991-993
- ISSN
- 1097-6256 (ISSN-L)
- 1546-1726
- OpenAlex
- W2044271964
- Cited by
- 357
- References
- 17
- Citations by year
- 2026: 1 · 2025: 3 · 2024: 3 · 2023: 5 · 2022: 8 · 2021: 14 · 2020: 12 · 2019: 7 · 2018: 11 · 2017: 20 · 2016: 27 · 2015: 20 · 2014: 25 · 2013: 20 · 2012: 26
- FWCI
- 6.25
- Type
- journal article
- Language
- en
- Open access
- closed
- Licence
- www.springer.com/tdm (tdm)
- Locations
- Nature Neuroscience (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Institute of Neurological Disorders and Stroke (R01NS035102, NS35102)
- Topics
- Life Sciences › Neuroscience › Developmental Neuroscience › Williams Syndrome Research
- Life Sciences › Neuroscience › Cognitive Neuroscience › Face Recognition and Perception
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Genetics and Neurodevelopmental Disorders
- Keywords
- Williams syndrome, social cognition, amygdala, orbitofrontal cortex, threatening faces, hypersociability, chromosome 7q11.23 microdeletion, prefrontal cortex activation
- MeSH terms
- Amygdala, Anxiety, Brain, Brain Mapping, Cognition, Frontal Lobe, Humans, Magnetic Resonance Imaging, Social Behavior, Case-Control Studies, Prefrontal Cortex, Williams Syndrome
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