2026-07-16T02:58:53Z https://www.fdr.uni-hamburg.de/oai2d

oai:fdr.uni-hamburg.de:13397 2023-09-26T07:33:30Z user-sfb936 user-uhh

true 3.1 UHH.FDR 10.5061/dryad.w3r2280t2 Basedau, Hauke 0000-0002-4605-0172 University Medical Center Hamburg-Eppendorf Sturm, Lisa-Marie University Medical Center Hamburg-Eppendorf Mehnert, Jan University Medical Center Hamburg-Eppendorf Peng, Kuan-Po University Medical Center Hamburg-Eppendorf Schellong, Marlene 0000-0002-6499-2024 University Medical Center Hamburg-Eppendorf May, Arne 0000-0002-3499-1506 University Medical Center Hamburg-Eppendorf Universität Hamburg 2022 Hypothalamus Migraine Other medical sciences CGRP antibodies functional imaging General Biochemistry, Genetics and Molecular Biology General Immunology and Microbiology General Medicine General Neuroscience pathophysiology 2022-06-01 en https://www.fdr.uni-hamburg.de/record/oai:fdr.uni-hamburg.de:13397 Creative Commons Attribution 4.0 International Open Access <p>Background: Monoclonal antibodies (mAbs) against calcitonin gene-related peptides (CGRP) are novel treatments for migraine prevention. Based on a previous functional imaging study which investigated the CGRP receptor mAb (erenumab), we hypothesized that (i) the CGRP ligand mAb galcanezumab would alter central trigeminal pain processing; (ii) responders to galcanezumab treatment would show specific hypothalamic modulation in contrast to non-responders; and (iii) the ligand and the receptor antibody differ in brain responses.</p> <p>Methods: Using an established trigeminal nociceptive functional magnetic imaging paradigm, 26 migraine patients were subsequently scanned twice: before and 2&ndash;3 weeks after administration of galcanezumab.</p> <p>Results: We found that galcanezumab decreases hypothalamic activation in all patients and that the reduction was stronger in responders than in non-responders. Contrasting erenumab and galcanezumab showed that both antibodies activate a distinct network. We also found that pre-treatment activity of the spinal trigeminal nucleus (STN) and coupling between the STN and the hypothalamus covariates with the response to galcanezumab.</p> <p>Conclusions: These data suggest that despite relative impermeability of the blood-brain barrier for CGRP mAb, mAb treatment induces certain and highly specific brain effects which may be part of the mechanism of their efficacy in migraine treatment.</p> <p>Funding: This work was supported by the German Ministry of Education and Research (BMBF) of ERA-Net Neuron under the project code BIOMIGA (01EW2002 to AM) and by the German Research Foundation (SFB936-178316478-A5 to AM). The funding sources did not influence study conduction in any way.&nbsp;</p> <p>Clinical trial number: The basic science study was preregistered in the Open Science Framework (https://osf.io/m2rc6).</p> <p><strong>Direct link to the published dataset:&nbsp;<a href="https://datadryad.org/stash/dataset/doi:10.5061/dryad.w3r2280t2">https://datadryad.org/stash/dataset/doi:10.5061/dryad.w3r2280t2</a></strong></p> <p>&nbsp;</p> Funding: Bundesministerium für Bildung und Forschung, Award: BIOMIGA (01EW2002 to AM); Deutsche Forschungsgemeinschaft, Award: SFB936- 178316478 - A5 (AM) {"references": ["Hauke Basedau, Lisa-Marie Sturm, Jan Mehnert, Kuan-Po Peng, Marlene Schellong, Arne May (2022) Migraine monoclonal antibodies against CGRP change brain activity depending on ligand or receptor target \u2013 an fMRI study eLife 11:e77146 https://doi.org/"]}