Department of Neurobiology
 

 


Aizenman, Elias

Professor, Neurobiology
7020 BST3
   3501 Fifth Avenue
   Pittsburgh, PA 15213-3301
Telephone: 412-648-9434
Fax: 412-648-1441
redox@pitt.edu

Elias' Lab Website
PIND Website

Cellular & molecular mechanisms of neurodegeneration

Research in Dr. Aizenman's laboratory is directed towards investigating cellular signaling processes leading to neuronal cell death.

Acute and chronic injurious processes in the brain lead to the activation of signaling cascades that eventually result in the demise of neurons. In Dr. Aizenman's laboratory, cellular pathways leading to cell death are molecularly dissected in order to provide novel therapeutic targets to treat neurodegenerative disorders. This laboratory works on potential common final mediators of cell death signaling events that can be effectively targeted to treat neural disorders. This work is primarily focused on acute neuronal injury, such as stroke, although the results obtained from these studies could have broader applications to more chronic neurodegenerative conditions. Over the last several years, the laboratory has investigated redox and photic regulation of NMDA receptors, excitotoxicity, dopamine oxidation pathways, zinc-mediated neurotoxicity, and Kv2.1 potassium channel facilitated forms of neuronal apoptosis, among other topics.

Most recent publications:

Li, D., H. Yuan, X.R. Ortiz-Gonzales, E.D. Marsh, L. Tian, E.M. McCormick, G.J. Kosobucki, W. Chen, A.J. Schulien, R. Chiavacci, A. Tankovic, C. Naase, F. Bruckner, C. von Stulpnagel-Hortnagel, E. Aizenman, J.R. Lemke, H. Hakonarson, S.F. Traynelis and M.J. Falk. GRIN2D recurrent de novo mutation is an autosomal dominant cause of severe epileptic encephalopathy treatable with NMDA receptor channel blockers. American Journal of Human Genetics 2016 (in press).

Kumar, M., N. Reed, R. Liu, E. Aizenman, P. Wipf and T. Tzounopoulos. Synthesis and evaluation of potent KCNQ2/3-specific channel activators. Molecular Pharmacology 2016 89:667-677.

Schulien, A.J., J.A. Justice, R. Di Maio, Z.P. Wills, N.H. Shah and E. Aizenman. Zinc-induced calcium release via ryanodine receptors triggers calcineurin-dependent redistribution of cortical neuronal Kv2.1 K+ channels. Journal of Physiology 2016 594:2647-2659.

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