Department of Neurobiology

Aizenman, Elias

Professor, Neurobiology
The Johns Hopkins University (Ph.D. 1985)
7020 BST3
   3501 Fifth Avenue
   Pittsburgh, PA 15213-3301
Telephone: 412-648-9434
Fax: 412-648-1441

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.

Recent publications:

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

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.

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.. 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.

Hara, H. and E. Aizenman. Oxidative stress and neuronal zinc signaling. In: Zinc Signals in Cellular Functions and Disorders. Fukada, T. and T. Kambe, eds. Springer Japan 2014; Chapter 4, pp. 55-87.

McCord, M.C., P.H. Kullmann, K. He, K.A. Hartnett, J.P. Horn, I. Lotan and E. Aizenman. Syntaxin-binding domain of Kv2.1 is essential for the expression of apoptotic K+ currents. Journal of Physiology 2014; 592:3511-3521.

McCord, M.C. and E. Aizenman. The role of intracellular zinc release in aging, oxidative stress, and Alzheimer's disease. Frontiers in Aging Neuroscience 2014; doi:10.3389/fnagi.2014.00077

Shah, N.H., A.J. Schulien, K. Clemens, T.D. Aizenman, T.M. Hageman, Z.P. Wills and E. Aizenman. Cyclin E1 regulates Kv2.1 channel phospohorylation and localization in neuronal ischemia. Journal of Neuroscience 2014; 34:4326-4331.

Shah, N.H. and E. Aizenman. Voltage-gated potassium channels at the crossroads of neuronal function, ischemic tolerance, and neurodegeneration. Translational Stroke Research 2014; 5:38-58.

PubMed Search for "Aizenman E"
Link to Google Scholar

© Copyright 2001 - University of Pittsburgh Department of Neurobiology
Webmaster S Hunter Simpson