ArticleJournal of neuroinflammation2012
Alteration of astrocytes and Wnt/β-catenin signaling in the frontal cortex of autistic subjects.
Article in Journal of neuroinflammation, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 23 papers, 1 of them a synthesis that pooled it.
What it found
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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.
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.
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Who cites it
23 citing papers in PubMed, 1 synthesis or guideline pooled it, 45 citations in OpenAlex.
- Postmortem Studies of Neuroinflammation in Autism Spectrum Disorder: a Systematic Review.Molecular neurobiology · 2020Pooled it
- Blood-Brain Barrier Dysfunction Predicts Microglial Activation After Traumatic Brain Injury in Juvenile Rats.Neurotrauma reports · 2024Article
- Comparisons of quantitative approaches for assessing microglial morphology reveal inconsistencies, ecological fallacy, and a need for standardization.Scientific reports · 2022Article
- A perspective on molecular signalling dysfunction, its clinical relevance and therapeutics in autism spectrum disorder.Experimental brain research · 2022Review
- Downregulation of TGIF2 is possibly correlated with neuronal apoptosis and autism-like symptoms in mice.Brain and behavior · 2022Article
- Impaired calcium signaling in astrocytes modulates autism spectrum disorder-like behaviors in mice.Nature communications · 2021Article
- Decreased microglial Wnt/β-catenin signalling drives microglial pro-inflammatory activation in the developing brain.Brain : a journal of neurology · 2019Article
- Downregulation of Oxytocin Receptor Decreases the Length of Projections Stimulated by Retinoic Acid in the U-87MG Cells.Neurochemical research · 2017Article
- Valproic Acid Exposure during Early Postnatal Gliogenesis Leads to Autistic-like Behaviors in Rats.Clinical psychopharmacology and neuroscience : the official scientific journal of the Korean College of Neuropsychopharmacology · 2016Article
- Three-Dimensional Environment Sustains Morphological Heterogeneity and Promotes Phenotypic Progression During Astrocyte Development.Tissue engineering. Part A · 2016Article
- Retraction Note: Alteration of astrocytes and Wnt/β-catenin signaling in the frontal cortex of autistic subjects.Journal of neuroinflammation · 2016Article
- Language Impairments in ASD Resulting from a Failed Domestication of the Human Brain.Frontiers in neuroscience · 2016Article
- Coordinated Action of Biological Processes during Embryogenesis Can Cause Genome-Wide Linkage Disequilibrium in the Human Genome and Influence Age-Related Phenotypes.Annals of gerontology and geriatric research · 2016Article
- Shared Pathways Among Autism Candidate Genes Determined by Co-expression Network Analysis of the Developing Human Brain Transcriptome.Journal of molecular neuroscience : MN · 2015Article
- Review
- Mechanisms of astrocyte development and their contributions to neurodevelopmental disorders.Current opinion in neurobiology · 2014Review
- Dominant β-catenin mutations cause intellectual disability with recognizable syndromic features.The Journal of clinical investigation · 2014Article
- Redox Regulation and the Autistic Spectrum: Role of Tryptophan Catabolites, Immuno-inflammation, Autoimmunity and the Amygdala.Current neuropharmacology · 2014Article
- Altered glial marker expression in autistic post-mortem prefrontal cortex and cerebellum.Molecular autism · 2014Article
- An evo-devo approach to thyroid hormones in cerebral and cerebellar cortical development: etiological implications for autism.Frontiers in endocrinology · 2014Review
Corrections and comments
- Retraction · 2016-05-13Investigation by Company/Institution · Unreliable Image · Unreliable Results and/or Conclusions ·
- Retracted
Authors and funding
12 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundAutism is a neurodevelopmental disorder characterized by impairments in social interaction, verbal communication and repetitive behaviors. To date the etiology of this disorder is poorly understood. Studies suggest that astrocytes play critical roles in neural plasticity by detecting neuronal activity and modulating neuronal networks. Recently, a number of studies suggested that an abnormal function of glia/astrocytes may be involved in the development of autism. However, there is yet no direct evidence showing how astrocytes develop in the brain of autistic individuals.
methodsStudy subjects include brain tissue from autistic subjects, BTBR T + tfJ (BTBR) and Neuroligin (NL)-3 knock-down mice. Western blot analysis, Immunohistochemistry and confocal microscopy studies have be used to examine the density and morphology of astrocytes, as well as Wnt and β-catenin protein expression.
resultsIn this study, we demonstrate that the astrocytes in autisitcsubjects exhibit significantly reduced branching processes, total branching length and cell body sizes. We also detected an astrocytosis in the frontal cortex of autistic subjects. In addition, we found that the astrocytes in the brain of an NL3 knockdown mouse exhibited similar alterations to what we found in the autistic brain. Furthermore, we detected that both Wnt and β-catenin proteins are decreased in the frontal cortex of autistic subjects. Wnt/β-catenin pathway has been suggested to be involved in the regulation of astrocyte development.
conclusionsOur findings imply that defects in astrocytes could impair neuronal plasticity and partially contribute to the development of autistic-like behaviors in both humans and mice. The alteration of Wnt/β-catenin pathway in the brain of autistic subjects may contribute to the changes of astrocytes.
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Registered trials
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.