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Hilmar Bading

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Hilmar Bading
Born (1958-11-03) November 3, 1958 (age 67)
Berlin, Germany
Alma materRuprecht-Karls-University Heidelberg
Scientific career
FieldsNeurobiology, NMDA receptor and calcium signaling
InstitutionsRuprecht-Karls-University Heidelberg
Academic advisors
Wilhelm Hasselbach, Karin Mölling, Michael E. Greenberg

Hilmar Bading (born 1958) is a German physician and neuroscientist. He is a member of the German National Academy of Science Leopoldina.[1]

Education and career

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Hilmar Bading 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 on calcium transport ATPase in skeletal muscle. He received postdoctoral training at the Max Planck Institute for Molecular Genetics in Berlin, Germany (1985–1989) and 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.[2][3]

He is co-founder of FundaMental Pharma GmbH, Heidelberg.[4]

He founded the Foundation BrainAid.[5]

Research

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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.[7][8] His work highlighted the spatial aspects of calcium signals[9][10] 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.[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 colleagues identified a signaling complex formed by extrasynaptic NMDA receptors (NMDARs) and TRPM4 that mediates excitotoxicity. They further described a class of neuroprotective small molecules, termed "NMDAR/TRPM4 interaction interface inhibitors" or "TwinF interface inhibitors", which disrupt the NMDAR/TRPM4 complex.[21] In mouse disease models, these compounds were reported to protect against neurodegeneration and cell death associated with stroke,[22][23] retinal ganglion cell degeneration,[21] Huntington's disease,[24] and Alzheimer's disease.[25] The compounds are being further developed for the therapy of treatment-resistant depression by FundaMental Pharma GmbH, based in Heidelberg.[26][27]

Awards and honors

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2001: Wolfgang-Paul Prize of the Alexander von Humboldt Foundation[28]

2016: Innovation Prize of the German BioRegions[29]

2019: Elected to the German National Academy of Science Leopoldina[1]

References

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  1. ^ a b "List of Members". Nationale Akademie der Wissenschaften Leopoldina. Retrieved 2020-10-29.
  2. ^ "Neurobiology". Heidelberg University. Retrieved 2016-10-18.
  3. ^ "Interdisciplinary Center for Neurosciences (IZN)". Heidelberg University. Retrieved 2016-10-18.
  4. ^ https://fundamentalpharma.com/
  5. ^ "Foundation Brainaid". www.foundationbrainaid.org. Retrieved 2020-10-29.
  6. ^ Forschung, biotechnologie.de - Initiative des Bundesministeriums für Bildung und Forschung. "Biotechnologie.de - Menschen". www.biotechnologie.de (in German). Retrieved 2016-09-07.
  7. ^ Bading, H.; Ginty, D. D.; Greenberg, M. E. (1993-04-09). "Regulation of gene expression in hippocampal neurons by distinct calcium signaling pathways". Science. 260 (5105): 181–186. Bibcode:1993Sci...260..181B. doi:10.1126/science.8097060. ISSN 0036-8075. PMID 8097060.
  8. ^ Hagenston, Anna M.; Bading, Hilmar (2011-11-01). "Calcium signaling in synapse-to-nucleus communication". Cold Spring Harbor Perspectives in Biology. 3 (11) a004564. doi:10.1101/cshperspect.a004564. ISSN 1943-0264. PMC 3220353. PMID 21791697.
  9. ^ Ginty, D. D. (1997-02-01). "Calcium regulation of gene expression: isn't that spatial?". Neuron. 18 (2): 183–186. doi:10.1016/s0896-6273(00)80258-5. ISSN 0896-6273. PMID 9052789. S2CID 15833933.
  10. ^ Hardingham, G. E.; Chawla, S.; Johnson, C. M.; Bading, H. (1997-01-16). "Distinct functions of nuclear and cytoplasmic calcium in the control of gene expression". Nature. 385 (6613): 260–265. Bibcode:1997Natur.385..260H. doi:10.1038/385260a0. ISSN 0028-0836. PMID 9000075. S2CID 4328815.
  11. ^ Bading, Hilmar (2013-09-01). "Nuclear calcium signalling in the regulation of brain function". Nature Reviews. Neuroscience. 14 (9): 593–608. doi:10.1038/nrn3531. ISSN 1471-0048. PMID 23942469. S2CID 14896252.
  12. ^ "Heidelberg Researchers Identify Neuron Survival Programmes - University of Heidelberg". www.uni-heidelberg.de. Retrieved 2016-09-07.
  13. ^ "Mediaserver – Universität Heidelberg: Audio". archiv.ub.uni-heidelberg.de. Retrieved 2016-09-07.
  14. ^ Campus TV: Dem Langzeitgedächtnis auf der Spur, retrieved 2016-09-07
  15. ^ a b Milnerwood, Austen J.; Gladding, Clare M.; Pouladi, Mahmoud A.; Kaufman, Alexandra M.; Hines, Rochelle M.; Boyd, Jamie D.; Ko, Rebecca W.Y.; Vasuta, Oana C.; Graham, Rona K. (2010-01-28). "Early Increase in Extrasynaptic NMDA Receptor Signaling and Expression Contributes to Phenotype Onset in Huntington's Disease Mice". Neuron. 65 (2): 178–190. doi:10.1016/j.neuron.2010.01.008. ISSN 1097-4199. PMID 20152125. S2CID 12987037.
  16. ^ a b Talantova, Maria; Sanz-Blasco, Sara; Zhang, Xiaofei; Xia, Peng; Akhtar, Mohd Waseem; Okamoto, Shu-ichi; Dziewczapolski, Gustavo; Nakamura, Tomohiro; Cao, Gang (2013-07-02). "Aβ induces astrocytic glutamate release, extrasynaptic NMDA receptor activation, and synaptic loss". Proceedings of the National Academy of Sciences of the United States of America. 110 (27): E2518–2527. Bibcode:2013PNAS..110E2518T. doi:10.1073/pnas.1306832110. ISSN 1091-6490. PMC 3704025. PMID 23776240.
  17. ^ "Proteins Produced by Activated Neurons Could Protect Against Neurodegeneration". 2015-08-24. Retrieved 2016-09-07.
  18. ^ Okamoto, Shu-ichi; Pouladi, Mahmoud A.; Talantova, Maria; Yao, Dongdong; Xia, Peng; Ehrnhoefer, Dagmar E.; Zaidi, Rameez; Clemente, Arjay; Kaul, Marcus (2009-12-01). "Balance between synaptic versus extrasynaptic NMDA receptor activity influences inclusions and neurotoxicity of mutant huntingtin". Nature Medicine. 15 (12): 1407–1413. doi:10.1038/nm.2056. ISSN 1546-170X. PMC 2789858. PMID 19915593.
  19. ^ Hardingham, Giles E.; Bading, Hilmar (2010-10-01). "Synaptic versus extrasynaptic NMDA receptor signalling: implications for neurodegenerative disorders". Nature Reviews. Neuroscience. 11 (10): 682–696. doi:10.1038/nrn2911. ISSN 1471-0048. PMC 2948541. PMID 20842175.
  20. ^ Parsons, Matthew P.; Raymond, Lynn A. (2014). "Extrasynaptic NMDA Receptor Involvement in Central Nervous System Disorders". Neuron. 82 (2): 279–293. doi:10.1016/j.neuron.2014.03.030. PMID 24742457.
  21. ^ a b Yan, Jing; Wang, Yu Meng; Hellwig, Andrea; Bading, Hilmar (February 2024). "TwinF interface inhibitor FP802 stops loss of motor neurons and mitigates disease progression in a mouse model of ALS". Cell Reports Medicine. 5 (2) 101413. doi:10.1016/j.xcrm.2024.101413. PMC 10897598. PMID 38325382.[non-primary source needed]
  22. ^ Yan, Jing; Bengtson, C. Peter; Buchthal, Bettina; Hagenston, Anna M.; Bading, Hilmar (9 October 2020). "Coupling of NMDA receptors and TRPM4 guides discovery of unconventional neuroprotectants". Science. 370 (6513) eaay3302. doi:10.1126/science.aay3302. PMID 33033186.[non-primary source needed]
  23. ^ Sun, Meiling; Wang, Lin; Cao, Qiaofeng; Wang, Xuechun; Zhang, Ying; Guo, Manyu; Chen, Jie; Ma, Yuchen; Niu, Le; Zhang, Yanping; Hu, Mengdie; Gu, Mengli; Zhu, Zhihui; Yao, Xinyi; Yao, Junchen; Zhao, Chen; Wu, Jin; Liu, Xiuxiu; Lu, Yingmei; Wang, Zhen; Xiang, Qiuping; Han, Feng; Zhu, Dongsheng (23 January 2025). "Discovery of HZS60 as a Novel Brain Penetrant NMDAR/TRPM4 Interaction Interface Inhibitor with Improved Activity and Pharmacokinetic Properties for the Treatment of Cerebral Ischemia". Journal of Medicinal Chemistry. 68 (2): 2008–2043. doi:10.1021/acs.jmedchem.4c02772. PMID 39745498.[non-primary source needed]
  24. ^ Oberländer, Kristin; Pruunsild, Priit; Koch, Philipp; Yan, Jing; Szafranski, Karol; Bading, Hilmar (3 December 2025). "Inhba, Homer1 and Bdnf are major targets of transcriptomic dysregulation by neurodegenerative disease-associated excitotoxic NMDA receptor signaling". Communications Biology. 8 (1) 1743. doi:10.1038/s42003-025-09074-9. PMC 12678830. PMID 41339520.[non-primary source needed]
  25. ^ Yan, Jing; Yang, Xiaohui; Li, Guilin; Ramirez, Omar A.; Hagenston, Anna M.; Chen, Zhe-Yu; Bading, Hilmar (February 2026). "The NMDAR/TRPM4 death complex is a major promoter of disease progression in the 5xFAD mouse model of Alzheimer's disease". Molecular Psychiatry. 31 (2): 635–648. doi:10.1038/s41380-025-03143-5. PMC 12815682. PMID 40858778.[non-primary source needed]
  26. ^ Beher, Dirk; Yan, Jing. "Why NMDA receptor modulation remains central to next-generation depression therapies". Drug Target Review.
  27. ^ https://fundamentalpharma.com/
  28. ^ "The Wolfgang Paul Award". Alexander von Humboldt Foundation. Retrieved 2016-10-18.
  29. ^ "Nasenspray gegen Nervenleiden, Organmodelle statt Tierversuche, Viren gegen Krebs: Innovationspreis der BioRegionen" [Nasal spray against nervous disorders, organ models instead of animal testing, virus against cancer: Innovation Award BioRegions]. Bio Deutschland (Press release) (in German). Retrieved 2016-10-18.
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