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Elias Aizenman

Professor of Neurobiology
Ph.D., The Johns Hopkins University
Address: 7020 BST3
Telephone: 412-648-9434
Fax: 412-648-1441
E-mail: redox@pitt.edu

Cellular and molecular mechanisms of neurodegeneration

Pittsburgh Institute for Neurodegenerative Diseases

Link to Carlos Aizenman's website at Brown

Link to International Society for Zinc Biology



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

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 being molecularly dissected in order to provide novel therapeutic targets to treat neurodegenerative disorders. This laboratory works on potential final common mediators of cell death signaling events that can be effectively targeted to treat neuronal disorders. This work is primarily focused on acute neuronal injury, such as stroke, although the results from these studies could have broader applications to more chronic neurodegenerative conditions, such as Parkinson's disease, ALS and Alzheimer's disease. Over the last several years, the laboratory has investigated redox and photic regulation of NMDA receptors, excitotoxicity, dopamine oxidation pathways, zinc-mediated neurotoxicity, and potassium channel facilitated forms of neuronal apoptosis, among other topics.


News! Elias Aizenman and Michael Palladino (Pharmacology) receive 2016 Kaufman Foundation Initiative Award to generate a new fruit fly model of neuroprotection more

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; 99:802-816.

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.

Aizenman E. and P.G. Mastroberardino. Metals and Neurodegeneration (Editorial: Introduction to Special Issue). Neurobiology of Disease 2015 81:1-3.

Ganay, T., H. Asraf, E. Aizenman, M. Bogdanovic, I. Sekler and M. Hershfinkel. Regulation of neuronal pH by the metabotropic zinc receptor mZnR/GPR39. Journal of Neurochemistry 2015; 135:897-907.

Clemens, K., C.Y. Yeh and E. Aizenman. Critical role of casein kinase 2 in hepatitis C NS5A-mediated inhibition of Kv2.1 K+ channel function. Neuroscience Letters 2015; 609:48-52.

Hershfinkel, M., D. Ford, S. Kelleher and E. Aizenman. Seashells by the zinc shore: a meeting report of the international society for zinc biology, Asilomar, CA 2014. Metallomics 2015; 7:1299-304.

He, K., M.C. MCord, K.A. Hartnett and E. Aizenman. Regulation of pro-apoptotic phosphorylation of Kv2.1 K+ channels. PLoS One 2015; 10(6):e0129498.

Gilad, D., S. Shorer, M. Ketzef, A. Friedman, I. Sekler, E. Aizenman and M. Hershfinkel. Homeostatic regulation of KCC2 activity by the zinc receptor mZnR/GPR39 during seizures. Neurobiology of Disease 2015; 81:4-13.

Link to Google Scholar