Richard Deth, PhD

Nova Southeastern University


Dr. Richard Deth is a molecular neuroscientist with a research interest in a number of brain disorders, including autism. His laboratory has a particular focus on the molecular mechanisms underlying neurodevelopment and changes that occur during aging, as well as the mechanisms which provide the capacity for attention and learning.

This work involves an appreciation of unique metabolic features of neurons, especially factors influencing levels of the antioxidant glutathione (GSH) and its influence over methylation reactions, including DNA methylation. Methylation of DNA is a fundamental event in epigenetic regulation of gene expression, which drives development and allows adaptive responses to oxidation across the lifespan.

Dr. Deth published a monograph entitled: Molecular Origins of Human Attention: The Dopamine-Folate Connection. During the past 10 years Dr. Deth has worked closely with autism families and several parent-supported autism organizations. Dr. Deth’s lab recently reported the ability of casein and gluten-derived opiate peptides, as well as morphine, to impair transport of the amino acid cysteine, which adversely affects antioxidant levels and leads to epigenetic consequences.

His ongoing research incudes studies of the effects of neurotoxic substances on antioxidant and methylation status and autism-related changes in antioxidant and methylation status, as well as vitamin B12 levels in post mortem brain tissues. These same factors are involved in other a number of neurological and neuroimmune conditions.

BRAIN Funded Projects

NLRP3 inflammasome activity in autism spectrum disorder: Relationship to oxidative stress status and inhibition by cobinamide

Project’s aim: illuminate the connection between inflammation and antioxidant deficits in autism, namely oxidative stress and impaired methylation, with the aim of identifying a potential new target for developing a new treatment.

Selected Publications

Terhune TD, Deth RC. A role for impaired regulatory T cell function in adverse responses to aluminum adjuvant-containing vaccines in genetically susceptible individuals. Vaccine. 32(40):5149-55 (2014).

Trivedi MS, Shah JS, Al-Mughairy S, Hodgson NW, Simms B, Trooskens GA, Van Criekinge W, Deth RC. Food-derived opioid peptides inhibit cysteine uptake with redox and epigenetic consequences. J Nutr Biochem. 25(10):1011-8 (2014).

Raymond LJ, Deth RC, Ralston NV. Potential Role of Selenoenzymes and Antioxidant Metabolism in relation to Autism Etiology and Pathology. Autism Res Treat. 2014:164938 (2014).

Hodgson NW, Waly MI, Al-Farsi YM, Al-Sharbati MM, Al-Farsi O, Ali A, Ouhtit A, Zang T, Zhou ZS, Deth RC. Decreased glutathione and elevated hair mercury levels are associated with nutritional deficiency-based autism in Oman. Exp Biol Med (Maywood). 239(6):697-706 (2014).

Trivedi M, Shah J, Hodgson N, Byun HM, Deth R. Morphine induces redox-based changes in global DNA methylation and retrotransposon transcription by inhibition of excitatory amino acid transporter type 3-mediated cysteine uptake. Mol Pharmacol. 85(5):747-57 (2014).

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