ArticleBrain sciences2018
Decreased Neuron Density and Increased Glia Density in the Ventromedial Prefrontal Cortex (Brodmann Area 25) in Williams Syndrome.
Article in Brain sciences, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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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.
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Who cites it
4 citing papers in PubMed, 10 citations in OpenAlex.
- Inhibitory Systems in Brain Evolution: Pathways of Vulnerability in Neurodevelopmental Disorders.Brain, behavior and evolution · 2025Review
- Co-Treatment With Verapamil and Curcumin Attenuates the Behavioral Alterations Observed in Williams-Beuren Syndrome Mice by Regulation of MAPK Pathway and Microglia Overexpression.Frontiers in pharmacology · 2021Article
- Identification of emotions and physiological response in individuals with moderate intellectual disability.International journal of developmental disabilities · 2021Article
- Decreased density of cholinergic interneurons in striatal territories in Williams syndrome.Brain structure & function · 2020Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
Williams Syndrome (WS) is a neurodevelopmental disorder caused by a deletion of 25⁻28 genes on chromosome 7 and characterized by a specific behavioral phenotype, which includes hypersociability and anxiety. Here, we examined the density of neurons and glia in fourteen human brains in Brodmann area 25 (BA 25), in the ventromedial prefrontal cortex (vmPFC), using a postmortem sample of five adult and two infant WS brains and seven age-, sex- and hemisphere-matched typically developing control (TD) brains. We found decreased neuron density, which reached statistical significance in the supragranular layers, and increased glia density and glia to neuron ratio, which reached statistical significance in both supra- and infragranular layers. Combined with our previous findings in the amygdala, caudate nucleus and frontal pole (BA 10), these results in the vmPFC suggest that abnormalities in frontostriatal and frontoamygdala circuitry may contribute to the anxiety and atypical social behavior observed in WS.
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