Redox Abnormalities as a Vulnerability Phenotype for Autism and Related Alterations in CNS Development
Final rept. 15 Sep 2008 - 14 Sep 2012
ARKANSAS CHILDREN'S HOSPITAL LITTLE ROCK AR
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We hypothesize that low systemic redox potential GSHGSSG cysteinecystine reflects a vulnerability phenotype that is associated with regressive autism and is predictive of the risk of developing autism. The redox vulnerability phenotype is associated with epigenetic alterations in primary immune cells that may be reversible with restoration of intracellular redox potential. The hypothesis predicts that children with regressive autism and high risk developmentally-delayed children who are subsequently diagnosed with autism will exhibit lower redox potential compared to age-matched unaffected control children. It also predicts that low redox potential from these children will be associated with epigenetic modifications in DNA methylation and histone acetylationmethylation that are reversible with treatment to restore redox potential. In Aim 1 we will determine whether redox potential in immune cells can be used as a biomarker for regressive autism and whether it is predictive of the subsequent diagnosis of autism. We will also evaluate immune redox potential from high risk developmentally delayed children to determine whether redox status is predictive of subsequent development of autism. In Aim 2, we will determine whether immune cells from autistic children are associated with altered cytokine patterns, macrophageT cell DNA methylation, and chromatin histone methylation compared to control children.
- Anatomy and Physiology