Linking genetics to epigenetics: The role of folate and folate‐related pathways in neurodevelopmental disorders
Abstract
There is growing evidence that epigenetic dysregulation plays a role in neurodevelopmental disorders. In humans, folate is one of the main donors of the methyl group required for the synthesis of S‐adenosylmethionine, which in turn is needed for DNA and histone methylation as key neurodevelopment processes. Folate deficiency during pregnancy has been correlated with neural tube defects and with a higher incidence of neurocognitive and/or neurobehavioral deficits. A similar outcome may be exerted by gene polymorphisms in folate or folate‐related pathways. This has been documented by numerous case/control association studies performed on neurodevelopmental disorders such as autism spectrum disorder and attention deficit hyperactivity disorder. In this regard, the folate cycle represents a “perfect model” of how genetics influences epigenetics. Gene variants in folate and folate‐related pathways can be considered risk factors for neurodevelopmental disorders and should therefore be assessed by genetic testing in pregnant women. High‐risk women should be considered for folate supplementation during pregnancy. Here, we review all published case/control association studies on gene polymorphisms in folate and folate‐related pathways performed on neurodevelopmental disorders, provide an overview of neurodevelopment and DNA methylation changes occurring at this time, and describe the biological basis of neurodevelopmental disorders and recent evidence of their epigenetic dysregulation.
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There is wide evidence that pre and periconceptional folate supplementation supports neural and neurobehavioral development, bolstering social, cognitive and verbal functioning.
“There is wide evidence that pre and periconceptional folate supplementation supports neural and neurobehavioral development, bolstering social, cognitive and verbal functioning [235–237].”
From The contribution of environmental exposure to the etiology of autism spectrum disorder (2019) · cites this paper as [237]
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Dutta, S., Shaw, J., Chatterjee, A., Sarkar, K., Rajamma, U., Chatterjee, A., Sinha, S., & Mukhopadhyay, K. (2011) · Nutritional Neuroscience · doi:10.1179/1476830511y.0000000016 · Cited by 15 · see citing works
Oxytocin Receptor (OXTR) Methylation and Cognition in Psychotic Disorders
Grove, T. B., Burghardt, K. J., Kraal, A. Z., Dougherty, R. J., Taylor, S. F., & Ellingrod, V. L. (2016) · Complex Psychiatry · doi:10.1159/000448173 · Cited by 15 · see citing works
A Pilot Study on the Contribution of Folate Gene Variants in the Cognitive Function of ADHD Probands
Saha, T., Dutta, S., Rajamma, U., Sinha, S., & Mukhopadhyay, K. (2014) · Neurochemical Research · doi:10.1007/s11064-014-1393-0 · Cited by 14 · see citing works
Mahmuda, N. A., Yokoyama, S., Huang, J., Liu, L., Munesue, T., Nakatani, H., Hayashi, K., Yagi, K., Yamagishi, M., & Higashida, H. (2016) · International Journal of Molecular Sciences · doi:10.3390/ijms17050772 · Cited by 12 · see citing works
Dutta, S., Bhowmik, A. D., Sinha, S., et al. (2008) · Nutritional Neuroscience · doi:10.1179/147683008x301351 · Cited by 9 · see citing works
Pjetri, E., & Zeisel, S. H. (2017) · Behavioural Brain Research · doi:10.1016/j.bbr.2017.05.051 · Cited by 9 · see citing works
Infant C677T MTHFR polymorphism and severe mental retardation
Shaw, G. M., Jelliffe‐Pawlowski, L. L., Nelson, V. E., et al. (2006) · Birth Defects Research Part A Clinical and Molecular Teratology · doi:10.1002/bdra.20321 · Cited by 8 · see citing works
Dutta, S., Sinha, S., & Mukhopadhyay, K. (2007) · Psychiatric Genetics · doi:10.1097/ypg.0b013e32809c2f88 · Cited by 5 · see citing works
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The contribution of environmental exposure to the etiology of autism spectrum disorder
Bölte, S., Girdler, S., & Marschik, P. B. (2019) · Cellular and Molecular Life Sciences · doi:10.1007/s00018-018-2988-4 · Cited by 509 · see citing works
- Authors
- Lintas, C.
- Affiliations
- Università Campus Bio-Medico (IT)
- Corresponding author
- Lintas, C.
- ORCID
- Lintas, C.
- Venue
- Clinical Genetics
- Publisher
- Wiley
- Published
- 2018-09-03
- Volume
- 95
- Issue
- 2
- Pages
- 241-252
- ISSN
- 0009-9163 (ISSN-L)
- 1399-0004
- OpenAlex
- W2883210979
- Cited by
- 62
- References
- 100
- Citations by year
- 2026: 8 · 2025: 8 · 2024: 12 · 2023: 6 · 2022: 10 · 2021: 7 · 2020: 6 · 2019: 4 · 2018: 1
- FWCI
- 0.75
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Clinical Genetics (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Health Sciences › Medicine › Rheumatology › Folate and B Vitamins Research
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Epigenetics and DNA Methylation
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Genetics and Neurodevelopmental Disorders
- Keywords
- folic acid, epigenetics, neurodevelopmental disorders, DNA methylation, histone methylation, S-adenosylmethionine, folate cycle, genetic polymorphism, autism spectrum disorder, attention deficit hyperactivity disorder, neural tube defects, folic acid supplementation, epigenetic dysregulation
- MeSH terms
- Animals, Diet, Folic Acid, Gene Expression Regulation, Humans, Genetic Variation, Biomarkers, DNA Methylation, Genetic Predisposition to Disease, Epigenesis, Genetic, Metabolic Networks and Pathways, Neurogenesis, Neurodevelopmental Disorders
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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