Hilmar Bading

He received postdoctoral training at the Max Planck Institute for Molecular Genetics, Berlin, Germany (1985–1989) and at Harvard Medical School, Boston, US (1989–1993).

[5] Hilmar Bading's work is focused on neuronal calcium signaling and gene regulation in the nervous system.

[6] 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.

[11][12][13][14] The discovery of toxic signaling by extrasynaptic NMDA receptors which antagonizes gene regulation by synaptic activity and causes neuronal dysfunction and cell death[15][16] contributed to the understanding of neurodegenerative disorders including Huntington's disease, Alzheimer's disease, and amyotrophic lateral sclerosis (ALS).

[15][16][17][18][19][20] 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.