Elias Aizenman, PhD

Professor, Neurobiology

Contact

E1456 Biomedical Science Tower
412-648-9434
F: 412-648-1441
redox@pitt.edu
Website >

Education

PhD, Johns Hopkins University (1985)

Focus

Cellular and molecular signaling processes in neurodegeneration.

Research Summary

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, molecular pathways leading to cell death are being carefully 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 22 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.

Link to Dr. Aizenman's Lab

Publications

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. 

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; 99:802-816. 

Ogden, K.K., W. Chen, S.A. Swanger, M.J. McDaniel, L.Z. Fan, C. Hun, A. Tankovic, H. Kusumoto, G.J. Kosobucki, A.J. Schulien, Z. Su, J. Pecha, S. Bhattacharya, S. Petrovski, A.E. Cohen, E. Aizenman, S.F. Traynelis and H. Yuan. Molecular mechanism of disease-associated mutations in the pre-M1 helix of NMDA receptors and potential rescue pharmacology. PLOS Genetics 2017; 13:e1006536. 

Justice, J.A., A.J. Schulien, K. He, K.A. Hartnett, E. Aizenman and N.H. Shah. Disruption of Kv2.1 somato-dendritic clusters prevents the apoptogenic increase of potassium currents. Neuroscience 2017 (in press). 

Link to all of Dr. Aizenman's Publications