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Hilmar Bading is Professor of Neurobiology at Heidelberg University, where he has held the Chair of Neurobiology since 2001. He studied medicine at Heidelberg University from 1978 to 1984, earning his MD in 1984 with his thesis completed at the Max Planck Institute for Medical Research in Heidelberg. He received postdoctoral training at the Max Planck Institute for Molecular Genetics in Berlin from 1985 to 1989 and at Harvard Medical School in Boston from 1989 to 1993. From 1993 to 2001, he served as a staff scientist at the MRC Laboratory of Molecular Biology in Cambridge, UK. Since 2001, he has directed the Institute of Neurobiology and, since 2006, the Interdisciplinary Center for Neurosciences (IZN) at Heidelberg University. He is a member of the German National Academy of Sciences Leopoldina.
Bading's research centers on neuronal calcium signaling, synapse-to-nucleus communication, NMDA receptor functions in health and disease, and activity-dependent gene expression leading to neuroprotection and memory formation. His work has elucidated toxic signaling by extrasynaptic NMDA receptors and identified a signaling complex with TRPM4 that contributes to neuronal dysfunction and cell death in neurodegenerative conditions including Alzheimer's disease, Huntington's disease, and amyotrophic lateral sclerosis. This research has supported the development of novel neuroprotective small molecules known as TwinF interface inhibitors. He is co-founder of FundaMental Pharma GmbH and founder of the Foundation BrainAid. Bading received the Wolfgang-Paul Prize of the Alexander von Humboldt Foundation in 2001 and the Innovation Prize of the German BioRegions in 2016. Key contributions include publications on calcium regulation of gene expression and nuclear calcium signalling in brain function.
Heidelberg University researchers identify a neurotoxic 'death switch' fueling Alzheimer's neuron death and test FP802 compound to halt progression in mice, with implications for US higher education neuroscience.
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