- PhD, Johns Hopkins University (1985)
Education & Training
Cellular and molecular mechanisms of neurodegeneration and neuroprotection
Please note that we are no longer accepting new students or postdocs to our group.
Research in Elias’s laboratory has been directed towards investigating cellular signaling processes leading to neuronal cell death. Cellular pathways leading to cell death have been molecularly dissected in order to provide novel therapeutic targets to treat neurodegenerative disorders. This laboratory has worked on potential common final mediators of cell death signaling events that can be effectively targeted to treat neural disorders. This work has been primarily focused on acute neuronal injury, such as stroke, although the results obtained from these studies have broader applications to more chronic/progressive neurodegenerative conditions.
Currently, Elias is participating on an NIH SBIR-funded collaboration with Julie Coleman (Celdara Medical, Lebanon, NH) and Brad Molyneaux (Brigham and Women's Hospital, Boston, MA) to move two of his patented, Kv2.1-directed neuroprotective peptides (CM-EA1 and CM-EA2, formerly TAT-C1aB and TAT-DP2) towards clinical use in acute stroke.
Finally, in addition to his position at Pitt, Elias also holds an adjunct appointment in the Department of Cell Biology and Physiology at Ben Gurion University. He collaborates there with Michal Hershfinkel and Israel Sekler, along with Thanos Tzounopoulos at Pitt, on all things zinc.
Kok M, Aizenman E, Guerriero CJ, Brodsky JL. Regulated degradation of KCC2, a potassium-chloride co-transporter required for synaptic transmission and neurodevelopment. Channels (Austin). 2026 Dec;20(1):2607247. doi: 10.1080/19336950.2025.2607247. Epub 2025 Dec 23. PMID: 41433127.
Kok M, Singh I, Aizenman E, Brodsky JL. Inefficient maturation of disease-linked mutant forms of the KCC2 potassium-chloride cotransporter correlates with predicted pathogenicity. J Biol Chem. 2025 Mar 10:108399. doi: 10.1016/j.jbc.2025.108399. Epub ahead of print. PMID: 40074080.
Hernandez-Espinosa DR, Medina-Ruiz GI, Scrabis MG, Thathiah A, Aizenman E. Proinflammatory microglial activation impairs in vitro cortical tissue repair via zinc-dependent ADAM17 cleavage of the CSF-1 receptor. J Neurochem. 2025 Feb;169(2):e16239. doi: 10.1111/jnc.16239. PMID: 39387604; PMCID: PMC11810582.
Bai Q, Shao E, Ma D, Jiao B, Scheetz SD, Hartnett-Scott KA, Ilin VA, Aizenman E, Kofler J, Burton EA. A human Tau expressing zebrafish model of progressive supranuclear palsy identifies Brd4 as a regulator of microglial synaptic elimination. Nat Commun. 2024 Sep 18;15(1):8195. doi: 10.1038/s41467-024-52173-0. PMID: 39294122.
Gale J, Aizenman E. The physiological and pathophysiological roles of copper in the nervous system. Eur J Neurosci. 2024 May 15. doi: 10.1111/ejn.16370. Epub ahead of print. PMID: 38747014.
Kok M, Hartnett-Scott K, Happe CL, MacDonald ML, Aizenman E, Brodsky JL. The expression system influences stability, maturation efficiency, and oligomeric properties of the potassium-chloride co-transporter KCC2. Neurochem Int. 2024 Mar;174:105695. doi: 10.1016/j.neuint.2024.105695. Epub 2024 Feb 17. PMID: 38373478; PMCID: PMC10923169.
