Hilmar Bading
Hilmar Bading (born 1958) is a German physician and neuroscientist. His work on neuronal calcium signaling and gene regulation in the nervous system has been widely cited. He described the role of extrasynaptic NMDA receptors in neurodegenerative disorders and identified small molecule neuprotectants, named NMDAR/TRPM4 interface inhibitors (also known as ‘interface inhibitors’). He is a member of the German National Academy of Science Leopoldina. Education and career. Hilmar Bading was born in Berlin on 3 November 1958. He studied medicine from 1978 to 1984 at Heidelberg University (MD in 1984) and carried out his MD Thesis at  the Max Planck Institute for Medical Research, Heidelberg, with on the calcium transport ATPase in skeletal muscle. He received postdoctoral training in the laboratory of Karin Mölling at the Max Planck Institute for Molecular Genetics, Berlin, Germany (1985–1989) and in the laboratory of Michael E. Greenberg at Harvard Medical School, Boston, US (1989–1993). From 1993 to 2001 he was a staff scientist at the MRC Laboratory of Molecular Biology, Cambridge, UK. Since 2001 he has been professor of neurobiology and director of the Neurobiology Institute and the Interdisciplinary Center for Neurosciences (IZN) at Heidelberg University. He is co-founder of  FundaMental Pharma GmbH, Heidelberg. He founded the Foundation BrainAid. Research. Hilmar Bading is noted for his work on neuronal calcium signaling and gene regulation in the nervous system. He identified calcium as the principal second messenger in the coupling of neuronal activity to gene expression and characterized the processes that mediate the dialogue between the synapse and the nucleus. His work highlighted the spatial aspects of calcium signals and in particular the importance of nuclear calcium in governing activity-dependent gene expression and adaptations in the nervous system that include memory formation and acquired neuroprotection. The discovery of toxic signaling  by extrasynaptic NMDA receptors which antagonizes gene regulation by synaptic activity and causes neuronal dysfunction and cell death contributed to the understanding of neurodegenerative disorders including Huntington's disease, Alzheimer's disease, and amyotrophic lateral sclerosis (ALS). Hilmar Bading and his co-workers uncovered the importance of a death signaling complex consisting of extrasynaptic NMDA receptors (NMDARs) and TRPM4 for excitotoxicity and identified a class of neuroprotective small molecules (known as NMDAR/TRPM4 interaction interface inhibitors or short ‚interface inhibitors‘) that disrupt the NMDAR/TRPM4 complex and protect against cell death in mouse models of stroke and retinal ganglion cell  degeneration. Awards and honors. 2001: Wolfgang-Paul Prize of the Alexander von Humboldt Foundation 2016: Innovation Prize of the German BioRegions 2019: Elected to the German National Academy of Science Leopoldina