Mechanisms and consequences of a defect redox control of Kv4.3 channels in Morbus Parkinson (A13)

• Subject Area: Molecular Biology and Physiology of Neurons and Glial Cells ; Anatomy and Physiology
• Term: from 2009 to 2020
• Project identifier: Deutsche Forschungsgemeinschaft (DFG) - Project number 61867463

We aim to clarify the mechanisms that lead to an altered redox-state of Kv4.3 potassium channels and in turn to hyperactivity in dopamine substantia nigra (DA SN) neurons in a transgenic mutant alpha-synuclein mouse model of Parkinson disease (PD). By comparison with a CRISP/Cas-mediated redox-insensitive Kv4.3 mutant (C110), we aim to define the causal role of redox-mediated hyperactivity for selective neurodegeneration of DA SN neurons in PD.

• DFG Programme: Collaborative Research Centres
• Subproject of: SFB 815: Redox-Regulation: Generating Systems and Functional Consequences
• Applicant Institution: Goethe-Universität Frankfurt am Main
• Project Head: Professor Dr. Jochen Roeper