Evidence map›Paper›PMID 23709644›Full record

ArticleCerebral cortex (New York, N.Y. : 1991)2014

Altered microstructure within social-cognitive brain networks during childhood in Williams syndrome.

Brian W Haas, Naama Barnea-Goraly, Kristen E Sheau, Bun Yamagata, Shruti Ullas, Allan L Reiss

Abstract read
In one paragraph

Article in Cerebral cortex (New York, N.Y. : 1991), 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

18 citing papers in PubMed.

  1. Friendships in Children with Williams Syndrome: Parent and Child Perspectives.Journal of autism and developmental disorders · 2024
    Article
  2. Article
  3. Article
  4. Autism and Williams syndrome: truly mirror conditions in the socio-cognitive domain?International journal of developmental disabilities · 2022
    Review
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Aberrant white matter microstructure in children with 16p11.2 deletions.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2014
    Article
  18. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

6 authors.

Brian W HaasDepartment of Psychology, University of Georgia, Center for Interdisciplinary Brain Sciences Research (CIBSR), Department of Psychiatry and Behavioral Sciences, Stanford University School of Medicine, Palo Alto, CA, USA.
Naama Barnea-GoralyCenter for Interdisciplinary Brain Sciences Research (CIBSR), Department of Psychiatry and Behavioral Sciences, Stanford University School of Medicine, Palo Alto, CA, USA.
Kristen E SheauCenter for Interdisciplinary Brain Sciences Research (CIBSR), Department of Psychiatry and Behavioral Sciences, Stanford University School of Medicine, Palo Alto, CA, USA.
Bun YamagataCenter for Interdisciplinary Brain Sciences Research (CIBSR), Department of Psychiatry and Behavioral Sciences, Stanford University School of Medicine, Palo Alto, CA, USA.
Shruti UllasDepartment of Psychology, University of California, Los Angeles, Los Angeles, CA 90095, USA.
Allan L ReissCenter for Interdisciplinary Brain Sciences Research (CIBSR), Department of Radiology, and Department of Pediatrics, Stanford University School of Medicine, 401 Quarry Rd. Palo Alto, CA 94305-5795, USA.

Funding

TRAINING FOR CHILD PSYCHIATRY AND CHILD DEVELOPMENTT32MH019908 · NIMH · STANFORD UNIVERSITY · PI IAN H GOTLIB, DAVID S HONG · 1993 to 2026
$6.3M
NIMH NIH HHS T32 MH019908NIMH NIH HHS T32 MH19908
6 · The paper itself

Abstract

Williams syndrome (WS) is a neurodevelopmental condition caused by a hemizygous deletion of ∼26-28 genes on chromosome 7q11.23. WS is associated with a distinctive pattern of social cognition. Accordingly, neuroimaging studies show that WS is associated with structural alterations of key brain regions involved in social cognition during adulthood. However, very little is currently known regarding the neuroanatomical structure of social cognitive brain networks during childhood in WS. This study used diffusion tensor imaging to investigate the structural integrity of a specific set of white matter pathways (inferior fronto-occipital fasciculus [IFOF] and uncinate fasciculus [UF]) and associated brain regions [fusiform gyrus (FG), amygdala, hippocampus, medial orbitofrontal gyrus (MOG)] known to be involved in social cognition in children with WS and a typically developing (TD) control group. Children with WS exhibited higher fractional anisotropy (FA) and axial diffusivity values and lower radial diffusivity and apparent diffusion coefficient (ADC) values within the IFOF and UF, higher FA values within the FG, amygdala, and hippocampus and lower ADC values within the FG and MOG compared to controls. These findings provide evidence that the WS genetic deletion affects the development of key white matter pathways and brain regions important for social cognition.

Indexed as

AdolescentBrainChildCognition DisordersDiffusion Tensor ImagingEmotionsFemaleHumansMaleNerve NetSocial BehaviorWhite MatterWilliams SyndromeDTIgeneticssocial cognitionWilliams syndrome

Identifiers

PMID23709644
PMCPMC4207879

What OpenQuestion holds

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Registered trials

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.