ArticleAutism research and treatment2012
Prenatal and Postnatal Epigenetic Programming: Implications for GI, Immune, and Neuronal Function in Autism.
Article in Autism research and treatment, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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
10 citing papers in PubMed, 23 citations in OpenAlex.
- Clinical and Molecular Characteristics of Mitochondrial Dysfunction in Autism Spectrum Disorder.Molecular diagnosis & therapy · 2018Review
- Early Disruption of the Microbiome Leading to Decreased Antioxidant Capacity and Epigenetic Changes: Implications for the Rise in Autism.Frontiers in cellular neuroscience · 2018Review
- Immune system transcriptome in gingival tissues of young nonhuman primates.Journal of periodontal research · 2016Article
- Epigenetic effects of casein-derived opioid peptides in SH-SY5Y human neuroblastoma cells.Nutrition & metabolism · 2015Article
- The glutathione system: a new drug target in neuroimmune disorders.Molecular neurobiology · 2014Review
- Food-derived opioid peptides inhibit cysteine uptake with redox and epigenetic consequences.The Journal of nutritional biochemistry · 2014Article
- Redox Regulation and the Autistic Spectrum: Role of Tryptophan Catabolites, Immuno-inflammation, Autoimmunity and the Amygdala.Current neuropharmacology · 2014Article
- SLC1 glutamate transporters.Pflugers Archiv : European journal of physiology · 2014Review
- Autism: a redox/methylation disorder.Global advances in health and medicine · 2013Article
- Redox metabolism abnormalities in autistic children associated with mitochondrial disease.Translational psychiatry · 2013Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Although autism is first and foremost a disorder of the central nervous system, comorbid dysfunction of the gastrointestinal (GI) and immune systems is common, suggesting that all three systems may be affected by common molecular mechanisms. Substantial systemic deficits in the antioxidant glutathione and its precursor, cysteine, have been documented in autism in association with oxidative stress and impaired methylation. DNA and histone methylation provide epigenetic regulation of gene expression during prenatal and postnatal development. Prenatal epigenetic programming (PrEP) can be affected by the maternal metabolic and nutritional environment, whereas postnatal epigenetic programming (PEP) importantly depends upon nutritional support provided through the GI tract. Cysteine absorption from the GI tract is a crucial determinant of antioxidant capacity, and systemic deficits of glutathione and cysteine in autism are likely to reflect impaired cysteine absorption. Excitatory amino acid transporter 3 (EAAT3) provides cysteine uptake for GI epithelial, neuronal, and immune cells, and its activity is decreased during oxidative stress. Based upon these observations, we propose that neurodevelopmental, GI, and immune aspects of autism each reflect manifestations of inadequate antioxidant capacity, secondary to impaired cysteine uptake by the GI tract. Genetic and environmental factors that adversely affect antioxidant capacity can disrupt PrEP and/or PEP, increasing vulnerability to autism.
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.