Neuronal connectivity as a convergent target of gene × environment interactions that confer risk for Autism Spectrum Disorders
Open accessAbstract
Evidence implicates environmental factors in the pathogenesis of Autism Spectrum Disorders (ASD). However, the identity of specific environmental chemicals that influence ASD risk, severity or treatment outcome remains elusive. The impact of any given environmental exposure likely varies across a population according to individual genetic substrates, and this increases the difficulty of identifying clear associations between exposure and ASD diagnoses. Heritable genetic vulnerabilities may amplify adverse effects triggered by environmental exposures if genetic and environmental factors converge to dysregulate the same signaling systems at critical times of development. Thus, one strategy for identifying environmental risk factors for ASD is to screen for environmental factors that modulate the same signaling pathways as ASD susceptibility genes. Recent advances in defining the molecular and cellular pathology of ASD point to altered patterns of neuronal connectivity in the developing brain as the neurobiological basis of these disorders. Studies of syndromic ASD and rare highly penetrant mutations or CNVs in ASD suggest that ASD risk genes converge on several major signaling pathways linked to altered neuronal connectivity in the developing brain. This review briefly summarizes the evidence implicating dysfunctional signaling via Ca(2+)-dependent mechanisms, extracellular signal-regulated kinases (ERK)/phosphatidylinositol-3-kinases (PI3K) and neuroligin-neurexin-SHANK as convergent molecular mechanisms in ASD, and then discusses examples of environmental chemicals for which there is emerging evidence of their potential to interfere with normal neuronal connectivity via perturbation of these signaling pathways.
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Molecular and pathological evidence implicates later pregnancy and early postnatal life, pointing to altered neuronal connectivity and signaling pathways under intense development in these periods.
“Later pregnancy and early postnatal life are additionally implicated by accumulating molecular and pathological evidence pointing to altered neuronal connectivity and a resultant perturbation in signaling pathways, systems under intense development in these periods.25,26”
From Environmental Chemical Exposures and Autism Spectrum Disorders: A Review of the Epidemiological Evidence (2014) · cites this paper as [25]
Diverse environmental factors have been implicated as risk factors for ASD, including maternal stress and drug use, paternal age, nutritional status, hormones, and environmental chemicals.
“Diverse environmental factors have been implicated as risk factors for ASD, including maternal stress and drug use, paternal age, nutritional status, hormones, and environmental chemicals [ 14 , 25–29 ].”
From DNA methylation: a mechanism linking environmental chemical exposures to risk of autism spectrum disorders? (2016) · cites this paper as [27]
Data from experimental models suggest that PCB developmental neurotoxicity is mediated predominantly by NDL PCBs.
“This is of significant concern because data from experimental models suggest that PCB developmental neurotoxicity is mediated predominantly by NDL PCBs [ 27 , 104 ].”
From DNA methylation: a mechanism linking environmental chemical exposures to risk of autism spectrum disorders? (2016) · cites this paper as [27]
NDL PCBs have been reported to activate calcium-dependent signaling pathways implicated in the pathogenesis of ASD.
“Third, NDL PCBs have been reported to activate calcium- dependent signaling pathways implicated in the pathogenesis of ASD [ 27 ].”
From DNA methylation: a mechanism linking environmental chemical exposures to risk of autism spectrum disorders? (2016) · cites this paper as [27]
These pathways are also dysregulated in ASD.
“These are pathways that are also dysregulated in ASD [ 27 , 105 , 123 ].”
From DNA methylation: a mechanism linking environmental chemical exposures to risk of autism spectrum disorders? (2016) · cites this paper as [27]
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Flagged first, then by citations
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- Authors
- Stamou, M., Streifel, K. M., Goines, P. E., & Lein, P. J.
- Affiliations
- University of California, Davis (US)
- Corresponding author
- Lein, Pamela J.
- Venue
- Neurotoxicology and Teratology
- Publisher
- Elsevier BV
- Published
- 2013-03
- Volume
- 36
- Pages
- 3-16
- ISSN
- 0892-0362 (ISSN-L)
- PMC
- PMC3610799
- OpenAlex
- W2160229277
- Cited by
- 128
- References
- 265
- Citations by year
- 2026: 6 · 2025: 6 · 2024: 8 · 2023: 6 · 2022: 12 · 2021: 8 · 2020: 11 · 2019: 7 · 2018: 10 · 2017: 11 · 2016: 8 · 2015: 13 · 2014: 17 · 2013: 5
- FWCI
- 0.90
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Neurotoxicology and Teratology (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- eScholarship (California Digital Library) (submittedVersion)
- Funders
- National Institutes of Health (R01 ES014901, P01 ES011269, R01 ES017425, ES04699)
- University of California, Davis
- Johnson Foundation
- U.S. Environmental Protection Agency (R829388, R833292)
- Topics
- Life Sciences › Neuroscience › Cognitive Neuroscience › Autism Spectrum Disorder Research
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Genetics and Neurodevelopmental Disorders
- Health Sciences › Medicine › Psychiatry and Mental health › Child Nutrition and Feeding Issues
- Keywords
- autism spectrum disorder, gene-environment interaction, neuronal connectivity, environmental chemicals, ASD risk factors, calcium signaling, ERK signaling, PI3K signaling, copy number variation, syndromic autism, developmental neurotoxicity
- MeSH terms
- Animals, Child, Child Development Disorders, Pervasive, Humans, Neurons, Risk Factors, Signal Transduction, Genetic Predisposition to Disease, Gene-Environment Interaction
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
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