Title:  Professor of Pharmacology

Department:  Department of Pharmaceutical Sciences

School/Center:  School of Pharmacy

Office Location:  312 Mugar Hall

Phone:  617.373.4064

Fax:  617.373.8886

Email:  r.deth@neu.edu

Education:  Ph.D. University of Miami

BS, State University of New York, Buffalo

Certification: 

Specializations:  Neuropharmacology

Research:  Role of impaired methylation and oxidative stress in neurological and neuropsychiatric disorders, including autism, ADHD, schizophrenia, and Alzheimer’s disease.

Our lab investigates the molecular events regulating the transfer of a single carbon methyl group (i.e. methylation), which is a major regulatory mechanism in all cells. Prompted by our discovery of dopamine-stimulated methylation of membrane phospholipids, we particularly focus on the folate and vitamin B12-dependent enzyme methionine synthase, which provides methyl groups for this process. The D4 dopamine receptor exclusively carries out this methylation, which appears to be critical for synchronization of neural networks during attention. Our recent work has revealed that a number of neurodevelopment toxins, including alcohol, lead, mercury and other heavy metals are potent inhibitors of methylation in neuronal cells, and this reflects their common ability to reduce levels of glutathione, the primary intracellular antioxidant, creating a condition of oxidative stress. Improved understanding of the link between oxidative stress and methylation can lead to new treatment approaches for neurodevelopmental and neuropsychiatric conditions.

Public Service: 

Courses: 

Publications:  Deth, R.C. “Molecular Origins of Attention: The Dopamine-Folate Connection” Kluwer Academic Publishers (2003)

Zhu Q., Qi, L-J., Abou-Samra, A., Shi, A. and Deth, R.C.: “Protein kinase C-dependent constitutive activity of alpha 2A/D-adrenergic receptors.” Pharmacol. 71: 80-90 (2004).

Waly, M., Banerjee, R., Choi, S.W., Mason, J., Benzecry, J., Power-Charnitsky, V.A, Deth, R.C. “PI3-kinase regulates methionine synthase: Activation by IGF-1 or dopamine and inhibition by heavy metals and thimerosal” Molecular Psychiatry 9: 358-370 (2004).

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