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, 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.
Regulation of neuronal pro-apoptotic potassium currents by the hepatitis C virus non-structural protein 5A.
SNARE-dependent upregulation of potassium chloride co-transporter 2 activity after metabotropic zinc receptor activation in rat cortical neurons in vitro.
The neurophysiology and pathology of brain zinc.
Upregulation of KCC2 Activity by Zinc-Mediated Neurotransmission via the mZnR/GPR39 Receptor.
Redox regulation of intracellular zinc: molecular signaling in the life and death of neurons.
Complex role of zinc in methamphetamine toxicity in vitro.
Zinc bells rang in Jerusalem!
ERK signaling leads to mitochondrial dysfunction in extracellular zinc-induced neurotoxicity.
Zn2+ regulates Kv2.1 voltage-dependent gating and localization following ischemia.
Regulation of apoptotic potassium currents by coordinated zinc-dependent signaling.
Protein kinase C regulation of neuronal zinc signaling mediates survival during preconditioning.
Intracellular zinc inhibits KCC2 transporter activity.
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of Pittsburgh Department of Neurobiology