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Glob Adv Health Med. 2013 Nov;2(6):68-73. doi: 10.7453/gahmj.2013.087.

Autism: a redox/methylation disorder.

Author information

1
Northeastern University, Boston, Massachusetts, United States.

Abstract

While autism is still a mysterious developmental disorder, expansion of research efforts over the past 10 to 15 years has yielded a number of important clues implicating both genetic and environmental factors. We can now assert with a measure of confidence that contemporary autism reflects the combined impact of multiple environmental factors on the processes that regulate development in genetically vulnerable individuals. Since epigenetic regulation of gene expression is acknowledged as the most critical factor in development and DNA methylation (the addition of a carbon atom at discrete locations) is the fundamental event for epigenetic regulation, dysfunctional methylation can be considered as a likely cause of autism. Since methylation activity is highly sensitive to oxidative stress (an abnormal redox state) and many environmental factors promote oxidative stress, we have proposed a redox/methylation hypothesis for autism causation. The narrative herein describes the evolution of this hypothesis, which is essentially a series of linked discoveries about how the brain uniquely relies on oxidation and methylation to guide its development and to carry out its cognitive functions.

KEYWORDS:

ADHD; Attention deficit hyperactivity disorder; D4 dopamine receptor; epigenetic; glutathione; methylation; schizophrenia

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