Department of Psychiatry
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Patrizia De Sarno, Ph.D.

Desarno-Patrizia

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Education:

  • Ph.D. – Biological Sciences (110 cum laude/110), Major Advisor: Prof.GiancarloPepeu,Departimentodi Farmacologia, Mario Aiazzi Mancini, Universitá degli Studi di Firenze, Florence, Italy, 1985
  • Postdoctoral Trainee, Department of Pharmacology, School of Medicine, University of Firenze, Italy (Mentor: Dr. G. Pepeu), 1985-1986
  • Postdoctoral fellow, Department of Pharmacology, School of Medicine, Southern Illinois University, Springfield, IL (Mentor: Dr. E. Giacobini), 1986-1989
  • Postdoctoral fellow, Department of Pharmacological and Physiological Sciences,University of Chicago, Chicago, IL (Mentor: Dr. Nava Segev), 1990-1992
  • Postdoctoral fellow, Department of Psychiatry and Behavioral Neurobiology,University of Alabama at Birmingham, Birmingham, AL (Mentor: Dr. Richard Jope), 1997-2000

Academic Appointments with UAB:

  • Assistant Professor, Department of Psychiatry and Behavioral Neurobiology

People in the lab:

  • Amber Buel, Graduate Student, Department of Microbiology
  • Tethia Mbana, Research Assistant

Research Interests:
The role of Glycogen Synthase Kinase-3 (GSK3) in Experimental Autoimmune Encephalomyelitis

Multiple sclerosis (MS) is a chronic debilitating disease of the central nervous system (CNS), for which there is no adequate therapy. It is characterized by an immune-mediated inflammation of the CNS (neuroinflammation) which is linked to demyelination, neuronal degeneration and cell death. The mechanism(s) regulating neuroinflammation in MS is still largely unknown. Dr. De Sarno’s current research uses the mouse model of MS, experimental autoimmune encephalomyelitis (EAE), to test the hypothesis that glycogen synthase kinase-3 (GSK3), a protein that is linked to many pathophysiological processes, plays a proinflammatory role in EAE. GSK3 has an important role in regulating cell death and cell survival, the activities of proteins involved in gene transcription, and recently it was revealed to be a major regulator of inflammation. Our recent studies revealed that pretreating mice with the GSK3 inhibitor lithium renders them resistant to developing EAE, and treating them after disease onset attenuates EAE and inhibits relapsing episodes, supporting the premise that GSK3 is proinflammatory in EAE. The goal of Dr. De Sarno’s research is to determine the proinflammatory role of GSK3 in EAE and to define the pathophysiological mechanism and cell target of its action that lead to neurological damage. These studies set the framework for better understanding of the inflammatory events that lead to neurological damage in multiple sclerosis and other inflammatory diseases of the central nervous system. Because inflammation is linked not only to multiple sclerosis, but also to several other neurodegenerative, and psychiatric diseases, the identification of the enzyme GSK3 as a central regulator of the inflammatory processes in the brain will open a possibility for developing more specific targeted therapy for treatment of multiple sclerosis and other diseases of the CNS that involve inflammatory components.

Recent Publications:

  • Axtell, R. C., de Jong, B. A., Boniface, K., van der Voort,, L. F., Bhat, R., De Sarno, P, Naves, R., Han, M., Zhong, F., Castellanos, J. G., Mair, R., Christakos, T., Kolkowitz, I., Katz, L., Killestein, J., Polman, C. H., de Waal Malefyt, R., Steinman, L and Raman, C. 2010. T-helper types 1 and 17 determine efficacy of interferon-β in multiple sclerosis and experimental encephalomyelitis. Nat. Medicine 16:406:412.
  • De Sarno, P., Axtell, R.C., Raman, C., Roth, K.A., Alessi, D.R., and Jope, R. S. 2008. Lithium prevents and ameliorates experimental autoimmune encephalomyelitis (EAE). J. Immunol. 181(1): 338-345.
  • De Sarno, P., Bijur, G.N., Zmijewska, A.A., Li, X., and Jope, R.S. 2006. In vivo regulation of GSK3 phosphorylation by cholinergic and NMDA receptor. Neurobiology of Aging. 27: 413-422.
  • Clodfelder-Miller, B., De Sarno, P., Zmijewska, A.A., Song, L., Jope, R.S. 2005. Physiological and pathological changes in glucose regulate brain Akt and glycogen synthase kinase-3. J. Biol. Chem. 280: 39723-39731.
  • De Sarno, P., Shestopal, S.A., Zmijewska, A.A. Jope, R.S. 2005. Anti-apoptotic effects of muscarinic receptor activation are mediated by Rho kinase. Brain Res. 1401: 112-115.
  • De Sarno, P., Shestopal, S., King, T., Zmijewska, A.A., Song, L., and Jope, R., S. 2003. Muscarinic receptor activation protects cells from apoptotic effects of DNA damage, oxidative stress, and mitochondrial inhibition. J. Biol. Chem. 278: 11086-11093.
  • De Sarno, P., Li, X., and Jope, R.S. Regulation of Akt and glycogen synthase kinase-3b phosphorylation by sodium valproate and lithium. 2002. Neuropharmacology. 43: 1158-1164.
  • De Sarno, P., Bijur, G.N., Lu, R., Davis, R.E., and Jope, R.S. 2000. Alterations in muscarinic receptor-coupled phosphoinositide hydrolysis and AP-1 activation in Alzheimer’s disease cybrid cells. Neurobiol. Aging. 21: 31-38.