ArticleMolecular neurobiology2016
Up-Regulation of Oligodendrocyte Lineage Markers in the Cerebellum of Autistic Patients: Evidence from Network Analysis of Gene Expression.
Article in Molecular neurobiology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 34 citations in OpenAlex.
- Myelin, white matter, and social deficits in autism spectrum disorder.Neural regeneration research · 2026Article
- Chromatin remodeling factor BAF155 coordinates oligodendroglial-neuronal communications linked to regional myelination and autism-like behavioral deficits in mice.Nature communications · 2025Article
- Neuroactive steroid exposure impacts neurodevelopment: Comparison of human and rodent placental contribution.Journal of neuroendocrinology · 2025Review
- Decoding the peripheral transcriptomic and meta-genomic response to music in autism spectrum disorder via saliva-based RNA sequencing.Frontiers in molecular biosciences · 2025Article
- Immune signature of gene expression pattern shared by autism spectrum disorder and Huntington's disease.IBRO neuroscience reports · 2024Article
- Placental endocrine function shapes cerebellar development and social behavior.Nature neuroscience · 2021Article
- Role of Oligodendrocytes and Myelin in the Pathophysiology of Autism Spectrum Disorder.Brain sciences · 2020Review
- A diffusion-weighted imaging tract-based spatial statistics study of autism spectrum disorder in preschool-aged children.Journal of neurodevelopmental disorders · 2019Article
- Hyperexcitability and Hyperplasticity Disrupt Cerebellar Signal Transfer in theThe Journal of neuroscience : the official journal of the Society for Neuroscience · 2019Article
- Novel Gene-Based Analysis of ASD GWAS: Insight Into the Biological Role of Associated Genes.Frontiers in genetics · 2019Article
- Network-Based Identification of Altered Stem Cell Pluripotency and Calcium Signaling Pathways in Metastatic Melanoma.Medical sciences (Basel, Switzerland) · 2018Article
- Neuroglia in the autistic brain: evidence from a preclinical model.Molecular autism · 2018Article
- Gene-set analysis shows association between FMRP targets and autism spectrum disorder.European journal of human genetics : EJHG · 2017Article
- A brain proteomic investigation of rapamycin effects in theMolecular autism · 2017Article
- Rho GTPase RAC1 at the Molecular Interface Between Genetic and Environmental Factors of Autism Spectrum Disorders.Neuromolecular medicine · 2015Article
Corrections and comments
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Authors and funding
7 authors at 5 institutions in 6 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Autism is a neurodevelopmental disorder manifested by impaired social interaction, deficits in communication skills, restricted interests, and repetitive behaviors. In neurodevelopmental, neurodegenerative, and psychiatric disorders, glial cells undergo morphological, biochemical, and functional rearrangements, which are critical for neuronal development, neurotransmission, and synaptic connectivity. Cerebellar function is not limited to motor coordination but also contributes to cognition and may be affected in autism. Oligodendrocytes and specifically oligodendroglial precursors are highly susceptible to oxidative stress and excitotoxic insult. In the present study, we searched for evidence for developmental oligodendropathy in the context of autism by performing a network analysis of gene expression of cerebellar tissue. We created an in silico network model (OLIGO) showing the landscape of interactions between oligodendrocyte markers and demonstrated that more than 50 % (16 out of 30) of the genes within this model displayed significant changes of expression (corrected p value <0.05) in the cerebellum of autistic patients. In particular, we found up-regulation of OLIG2-, MBP-, OLIG1-, and MAG-specific oligodendrocyte markers. We postulate that aberrant expression of oligodendrocyte-specific genes, potentially related to changes in oligodendrogenesis, may contribute to abnormal cerebellar development, impaired myelination, and anomalous synaptic connectivity in autism spectrum disorders (ASD).
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