Cited by 325Autism Spectrum Disorder ResearchGenetics and Neurodevelopmental DisordersFolate and B Vitamins Research

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How environmental and genetic factors combine to cause autism: A redox/methylation hypothesis

Deth, Richard, Muratore, Christina, Benzecry, Jorge, Power-Charnitsky, Verna-Ann, Waly, Mostafa·2008·NeuroToxicology

DOI 10.1016/j.neuro.2007.09.010

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Abstract

Recently higher rates of autism diagnosis suggest involvement of environmental factors in causing this developmental disorder, in concert with genetic risk factors. Autistic children exhibit evidence of oxidative stress and impaired methylation, which may reflect effects of toxic exposure on sulfur metabolism. We review the metabolic relationship between oxidative stress and methylation, with particular emphasis on adaptive responses that limit activity of cobalamin and folate-dependent methionine synthase. Methionine synthase activity is required for dopamine-stimulated phospholipid methylation, a unique membrane-delimited signaling process mediated by the D4 dopamine receptor that promotes neuronal synchronization and attention, and synchrony is impaired in autism. Genetic polymorphisms adversely affecting sulfur metabolism, methylation, detoxification, dopamine signaling and the formation of neuronal networks occur more frequently in autistic subjects. On the basis of these observations, a "redox/methylation hypothesis of autism" is described, in which oxidative stress, initiated by environment factors in genetically vulnerable individuals, leads to impaired methylation and neurological deficits secondary to reductions in the capacity for synchronizing neural networks.

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Authors: Deth, R., Muratore, C., Benzecry, J., Power-Charnitsky, V.-A., & Waly, M.
Affiliations: Northeastern University (US)
Corresponding author: Deth, Richard
ORCID: Deth, Richard
Waly, Mostafa
Venue: NeuroToxicology
Publisher: Elsevier BV
Published: 2008-01
Volume: 29
Issue: 1
Pages: 190-201
ISSN: 0161-813X (ISSN-L)
DOI: 10.1016/j.neuro.2007.09.010
OpenAlex: W2167943688
Cited by: 325
References: 132
Citations by year: 2026: 5 · 2025: 7 · 2024: 12 · 2023: 13 · 2022: 12 · 2021: 16 · 2020: 17 · 2019: 11 · 2018: 17 · 2017: 16 · 2016: 15 · 2015: 28 · 2014: 27 · 2013: 20 · 2012: 34
FWCI: 1.26
Type: journal article
Language: en
Open access: closed
Licence: www.elsevier.com/tdm/userlicense/1.0/ (tdm)
Locations: NeuroToxicology (publishedVersion)
PubMed (publishedVersion)
Topics: Life Sciences › Neuroscience › Cognitive Neuroscience › Autism Spectrum Disorder Research
Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Genetics and Neurodevelopmental Disorders
Health Sciences › Nursing › Nutrition and Dietetics › Folate and B Vitamins Research
Keywords: autism spectrum disorder, oxidative stress, DNA methylation, sulfur metabolism, methionine synthase, vitamin B12, folic acid, dopamine signaling, dopamine D4 receptor, phospholipid methylation, neural network synchronization, genetic polymorphism, environmental toxic exposure
MeSH terms: Animals, Autistic Disorder, Environment, Humans, Methylation, Models, Biological, Oxidation-Reduction, Sulfur, Oxidative Stress, Receptors, Dopamine D4

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How environmental and genetic factors combine to cause autism: A redox/methylation hypothesis

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