The University of Toledo

Youssef Sari

Assistant Professor of Pharmacology
Department of Pharmacology

419.383.1507 Office
419.383.1505 Lab
419.383.1909 FAX
HEB 282G
youssef.sari@utoledo.edu

Institutions/Degrees

• B.S. Cellular Biology, Denis Diderot University (Paris, France).
• M.S. Cellular Biology, Orsay University (Paris, France)
• Ph.D. Neuroscience, Pierre and Marie Curie University, Institute of Neuroscience (Paris, France).
• Postdoc and Associate Scientist: Indiana University

Research Interests

Two research projects are ongoing in my Neuroprotection and Drug Abuse Research Lab:

1. The first project is dealing with the investigation of the role of glutamate transport in alcohol dependence. While it has been clearly established that dopaminergic neurotransmission plays an important role in reward and drug addiction, increasing evidence suggests that many aspects of the plasticity of drug addiction involves changes in glutamatergic neurotransmission. I have recently identified an FDA-approved drug and other related compounds that can cross the brain blood barrier and facilitate glutamate neurotransmission. We have tested one of these drugs and found potential therapeutic effects in a model of drug abuse such as cocaine addiction. Our ongoing research projects focused on the identification and pharmacological studies of drugs known to upregulate the glutamate transporter 1 (termed also excitatory amino acid transporter 2, EAAT2) and their role for the treatment of alcohol dependence. We use animal model of alcohol dependence to determine the behavioral, molecular and pharmacological manipulations of all these therapeutic drugs. This project is currently funded by the National Institutes of Health-NIAAA (R01).
2. The second project is dealing with the use of derived neurotrophic peptides and other neuroprotective compounds in the treatment of diseases involving oxidative stress. Oxidative stress is the major cause for most of neurodegenerative diseases. We have tested the role of neurotrophic factors in a model of oxidative stress involving alcohol exposure in brain development and have shown neuroprotective effects. We have demonstrated that derived neurotrophic peptides prevent alcohol-induced mitochondrial dysfunction. Mitochondrion is a key play in oxidative stress, thus preventing its dysfunction will be a therapeutic useful tool to prevent or delay the progression of neurodegenerative diseases. Since my lab is focusing in Huntington’s disease, we are currently working in testing these novel trophic factors to prevent or slow the progression of the disease. We are using transgenic mice. that have the dysfunctional human huntingtin protein. We are also testing other compounds that have anti-oxidative effects. We aim to delineate the precise signaling pathways that mediate these trophic factors and other anti-oxidative compounds in neuroprotection using Huntington’s disease mouse models.