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Rapid Detection of Neurodevelopmental Phenotypes in Human Neural Precursor Cells (NPCs)
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Prenatal and Postnatal Epigenetic Programming: Implications for GI, Immune, and Neuronal Function in Autism.

Mostafa I Waly1, Mady Hornig, Malav Trivedi

  • 1Department of Food Science and Nutrition, Sultan Qaboos University, Alkoudh 123, Muscat, Oman.

Autism Research and Treatment
|August 31, 2012
PubMed
Summary

Autism may stem from impaired cysteine absorption in the gut, leading to low antioxidant levels. This impacts brain development and function, potentially linking gastrointestinal, immune, and neurological issues in autism.

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Area of Science:

  • Neuroscience
  • Immunology
  • Gastroenterology
  • Biochemistry

Background:

  • Autism spectrum disorder (ASD) often presents with co-occurring gastrointestinal (GI) and immune system dysfunction, suggesting shared underlying mechanisms.
  • Systemic deficiencies in glutathione and its precursor, cysteine, are observed in ASD, correlating with oxidative stress and impaired methylation.
  • Epigenetic regulation via DNA and histone methylation is critical for prenatal and postnatal development, influenced by maternal environment and nutritional intake.

Purpose of the Study:

  • To propose a unifying hypothesis linking neurodevelopmental, GI, and immune aspects of autism.
  • To investigate the role of impaired cysteine absorption and subsequent antioxidant deficits in ASD.
  • To explore how genetic and environmental factors affecting antioxidant capacity may disrupt epigenetic programming in ASD.

Main Methods:

  • Review and synthesis of existing literature on autism, oxidative stress, methylation, and nutrient absorption.
  • Hypothesizing the role of excitatory amino acid transporter 3 (EAAT3) in cysteine uptake for key cell types.
  • Connecting impaired EAAT3 function under oxidative stress to systemic cysteine deficits.

Main Results:

  • Systemic deficits in glutathione and cysteine in ASD likely result from impaired GI cysteine absorption.
  • Reduced activity of EAAT3, crucial for cysteine uptake, may underlie these deficits, particularly under oxidative stress.
  • Inadequate antioxidant capacity, driven by impaired cysteine uptake, could disrupt prenatal and postnatal epigenetic programming, increasing autism vulnerability.

Conclusions:

  • Neurodevelopmental, GI, and immune dysfunctions in autism may be manifestations of inadequate antioxidant capacity due to impaired GI cysteine uptake.
  • This impaired uptake, potentially mediated by EAAT3 dysfunction, affects crucial cellular functions in the gut, brain, and immune system.
  • Factors compromising antioxidant capacity can disrupt epigenetic programming, contributing to the complex etiology of autism.