ReviewAutism research and treatment2013
Epigenetics and autism.
Review in Autism research and treatment, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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.
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.
Who cites it
17 citing papers in PubMed, 31 citations in OpenAlex.
- Essential element and toxic metal dyshomeostasis in childhood autism spectrum disorder: a comprehensive narrative review of correlations, tissue-specific distribution, and multifactorial regulation.Frontiers in behavioral neuroscience · 2026Review
- Review
- Phytochemical, In Silico, In Vitro, and In Vivo Research on Piptadeniastrum africanum (Fabaceae) Unveiling Anti-Stereotypic, Anxiolytic, and Analgesic Effects in a Sodium Valproate-Induced Autistic Disorders Model.Brain and behavior · 2025Article
- Diverse Applications of the Anti-Diabetic Drug Metformin in Treating Human Disease.Pharmaceuticals (Basel, Switzerland) · 2024Review
- Circadian clock crosstalks with autism.Brain and behavior · 2023Article
- Diet-induced dysbiosis of the maternal gut microbiome in early life programming of neurodevelopmental disorders.Neuroscience research · 2021Review
- The maternal body as environment in autism science.Social studies of science · 2016Article
- Hypothesis on supine sleep, sudden infant death syndrome reduction and association with increasing autism incidence.World journal of clinical pediatrics · 2016Article
- Dietary glycemic index modulates the behavioral and biochemical abnormalities associated with autism spectrum disorder.Molecular psychiatry · 2016Article
- From Genetics to Epigenetics: New Perspectives in Tourette Syndrome Research.Frontiers in neuroscience · 2016Review
- Epigenetics of Aging and Alzheimer's Disease: Implications for Pharmacogenomics and Drug Response.International journal of molecular sciences · 2015Review
- Gastrointestinal symptoms and autism spectrum disorder: links and risks - a possible new overlap syndrome.Pediatric health, medicine and therapeutics · 2015Review
- Epigenetic regulation of persistent pain.Translational research : the journal of laboratory and clinical medicine · 2015Review
- A Pooled Genome-Wide Association Study of Asperger Syndrome.PloS one · 2015Article
- The APOE Gene is Differentially Methylated in Alzheimer's Disease.Journal of Alzheimer's disease : JAD · 2015Article
- Epigenetic effect of testosterone in the behavior of C. elegans. A clue to explain androgen-dependent autistic traits?Frontiers in cellular neuroscience · 2014Article
- Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
This review identifies mechanisms for altering DNA-histone interactions of cell chromatin to upregulate or downregulate gene expression that could serve as epigenetic targets for therapeutic interventions in autism. DNA methyltransferases (DNMTs) can phosphorylate histone H3 at T6. Aided by protein kinase C β 1, the DNMT lysine-specific demethylase-1 prevents demethylation of H3 at K4. During androgen-receptor-(AR-) dependent gene activation, this sequence may produce AR-dependent gene overactivation which may partly explain the male predominance of autism. AR-dependent gene overactivation in conjunction with a DNMT mechanism for methylating oxytocin receptors could produce high arousal inputs to the amygdala resulting in aberrant socialization, a prime characteristic of autism. Dysregulation of histone methyltransferases and histone deacetylases (HDACs) associated with low activity of methyl CpG binding protein-2 at cytosine-guanine sites in genes may reduce the capacity for condensing chromatin and silencing genes in frontal cortex, a site characterized by decreased cortical interconnectivity in autistic subjects. HDAC1 inhibition can overactivate mRNA transcription, a putative mechanism for the increased number of cerebral cortical columns and local frontal cortex hyperactivity in autistic individuals. These epigenetic mechanisms underlying male predominance, aberrant social interaction, and low functioning frontal cortex may be novel targets for autism prevention and treatment strategies.
Identifiers
What OpenQuestion holds
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.