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66 results for “CGRP”
Migraine monoclonal antibodies against CGRP change brain activity depending on ligand or receptor target – an fMRI study
<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 2–3 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. </p> <p>Clinical trial number: The basic science study was preregistered in the Open Science Framework (https://osf.io/m2rc6).</p>
Antagonism of CGRP Receptor: Central and Peripheral Mechanisms and Mediators in an Animal Model of Chronic Migraine
<p>This dataset includes the findings obtained in the study aimed at investigating in more depth the interplay between the neuropeptide CGRP and the inflammatory mediators within the mechanisms of neuronal sensitization in an animal model of chronic migraine, using olcegepant as a pharmacological probe. Male Sprague-Dawley rats were exposed to nitroglycerin (NTG, 10 mg/kg, i.p.) or NTG vehicle and treated with the CGRP receptor antagonist olcegepant (1 or 2 mg/kg, i.p.) or vehicle (1 ml/kg, i.p.) 1h before the orofacial formalin test. Additionally, sets of rats received NTG (5 mg/kg, i.p.) or vehicle (equivalent volume) co-administered with olcegepant (2 mg/kg i.p.) or its vehicle every other day over a 9-day period. Twenty-four hours after the last injection of NTG (or vehicle), a first set of rats underwent the orofacial formalin test. In a second set, we evaluated the gene expression of CGRP and gene and protein expression of pro-inflammatory cytokines in specific areas involved in migraine pain. We also assessed the CGRP and cytokine levels in serum.</p> <p>The in vivo and ex vivo assessments were:</p> <p>1) Pain-related behavior in the orofacial formalin test: the face rubbing was measured counting the seconds the animal spent grooming the injected area (upper lip, lateral to the nose) with the ipsilateral forepaw or hindpaw 0–6 min (Phase I) or 12–45 min (Phase II) after formalin injection (50 µl, s.c.). The observation time was divided into 15 blocks of 3 min each.</p> <p>2) mRNA expression levels: CGRP, tumor necrosis factor-alpha (TNF-alpha), interleukin-1beta (IL-1beta), transient receptor potential ankyrin 1 (TRPA1) in cervical spinal cord (CSC), medulla-pons and trigeminal ganglia (TGs). mRNA levels were measured by rt-PCR. The same RNA was used for miRNAs (Mir-34a-5p, Mir-382-5p, Mir-155-5p) extraction in the same areas. All samples were assayed in triplicate and gene expression levels were calculated according to 2−∆∆Ct = 2− (∆Ct gene − ∆Ct housekeeping gene) formula by using Ct (cycle threshold) values.</p> <p>3) Pro-inflammatory cytokines in medulla-pons, CSC and TGs were evaluated using ELISA procedure. CGRP, TNF-alpha and IL-1beta serum levels were measured using commercial ELISA kits.</p> <p>Results in brief</p> <p>Olcegepant attenuated nitroglycerin-induced trigeminal hyperalgesia in the second phase of the orofacial formalin test. Interestingly, it also reduced gene expression and protein levels of CGRP, pro-inflammatory cytokines, inflammatory-associated miRNAs (miR-155-5p, miR-382-5p and miR-34a-5p) and TRPA1 channels in medulla-pons area, cervical spinal cord and trigeminal ganglia. Similarly, olcegepant reduced the NTG-induced increase of CGRP and inflammatory.</p>
Erenumab-aooe for Temporomandibular Disorders Management: TMD Cgrp Antibody RElief (TMD CARE)
ClinicalTrials.gov study NCT05162027. IPD Sharing: Not stated. Countries: 1. Publications: 39.
CGRP, Estrogen, Cortisol, VIP, α-Amylase, PGE2, PGI2 and ß-Endorphin Levels in Menstrual Migraine Before and After Treximet
ClinicalTrials.gov study NCT01329562. IPD Sharing: Not stated. Countries: 1. Publications: 6.
Migraine monoclonal antibodies against CGRP change brain activity depending on ligand or receptor target – an fMRI study
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Dissociable control of unconditioned responses and associative fear learning by parabrachial CGRP neurons
<p>Parabrachial CGRP neurons receive diverse threat-related signals and contribute to multiple phases of adaptive threat responses in mice, with their inactivation attenuating both unconditioned behavioral responses to somatic pain and fear-memory formation. Because CGRP<sup>PBN</sup> neurons respond broadly to multi-modal threats, it remains unknown how these distinct adaptive processes are individually engaged. We show that while three partially separable subsets of CGRP<sup>PBN</sup> neurons broadly collateralize to their respective downstream partners, individual projections accomplish distinct functions: hypothalamic and extended amygdalar projections elicit assorted unconditioned threat responses including autonomic arousal, anxiety, and freezing behavior, while thalamic and basal forebrain projections generate freezing behavior and, unexpectedly, contribute to associative fear learning. Moreover, the unconditioned responses generated by individual projections are complementary, with simultaneous activation of multiple sites driving profound freezing behavior and bradycardia that are not elicited by any individual projection. This semi-parallel, scalable connectivity schema likely contributes to flexible control of threat responses in unpredictable environments.</p>
CGRP-induced Migraine Attacks in Patients Who Have Tried Anti-CGRP Monoclonal Antibody Treatment
ClinicalTrials.gov study NCT03481400. IPD Sharing: NO. Countries: 1. Publications: 1.
Positron Emission Tomography (PET) Study of Brain Calcitonin Gene-Related Peptide (CGRP) Receptor Occupancy After Telcagepant Administration (MK-0974-067)
ClinicalTrials.gov study NCT01315847. IPD Sharing: YES. Countries: 0. Publications: 1.
Potential Osteocatabolic Effect Caused by Anti-CGRP mAbs in Migraine Patients Treated With Anti-CGRP mAbs - an Observational Pilot Project With Prospectively Collected Health Related Data
ClinicalTrials.gov study NCT06035458. IPD Sharing: NO. Countries: 1. Publications: 0.
Transcranial Direct Current Stimulation Plus Monoclonal Antibodies Acting on the CGRP Pathway for Migraine
ClinicalTrials.gov study NCT05161871. IPD Sharing: UNDECIDED. Countries: 1. Publications: 2.
Study of Two Digital Therapeutics for the Prevention of Episodic Migraine Receiving CGRP Therapy (ReMMiD-C)
ClinicalTrials.gov study NCT06004388. IPD Sharing: Not stated. Countries: 1. Publications: 0.
CGRP Inhibition, Autonomic Function, and Migraine
ClinicalTrials.gov study NCT04628429. IPD Sharing: NO. Countries: 1. Publications: 42.
Plasma Levels of CGRP and Expression of Specific microRNAs in Blood Cells of Episodic and Chronic Migraine Subjects
ClinicalTrials.gov study NCT04473976. IPD Sharing: NO. Countries: 1. Publications: 26.
Anti-CGRP Monoclonal Antibody Response After Switching (AMARAS)
ClinicalTrials.gov study NCT05785988. IPD Sharing: UNDECIDED. Countries: 1. Publications: 12.
Hypersensitivity to CGRP as a Predictive Biomarker of Migraine Prevention With Erenumab
ClinicalTrials.gov study NCT04592952. IPD Sharing: NO. Countries: 1. Publications: 4.
BIOmarkers of MIGraine: a Proof of Concept Study Based on the Stratification of Responders to CGRP Monoclonal Antibodies
ClinicalTrials.gov study NCT04503083. IPD Sharing: NO. Countries: 3. Publications: 17.
The Nordic Chronic Migraine Trial of CGRP Monoclonal Antibody and Onabotulinumtoxin A Dual Therapy Compared to CGRP mAbs Monotherapy
ClinicalTrials.gov study NCT07040813. IPD Sharing: UNDECIDED. Countries: 1. Publications: 35.
CGRP's Cluster Headache Inducing Abilities in Cluster Headache Patients
ClinicalTrials.gov study NCT02466334. IPD Sharing: UNDECIDED. Countries: 1. Publications: 1.
Correlation of Calcitonin Gene-Related Peptide (CGRP) Levels in Saliva With the Evolution of an Attack of Migraine
ClinicalTrials.gov study NCT00772473. IPD Sharing: Not stated. Countries: 1. Publications: 1.
HD-EEG Connectivity Changes in Migraine Patients Undergoing Treatment With Anti-CGRP mAbs
ClinicalTrials.gov study NCT06155123. IPD Sharing: Not stated. Countries: 1. Publications: 8.
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Allen Brain Atlas
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DANDI Archive for NWB datasets
DANDI is a BRAIN Initiative archive for publishing and sharing neurophysiology data, including electrophysiology, optophysiology, and behavioral data packaged as NWB and related standards.
International Brain Laboratory public data
The International Brain Laboratory public data releases expose standardized mouse decision-making experiments, including Neuropixels recordings, widefield calcium imaging, behavior, and session metadata accessed through the ONE API.
OpenNeuro
OpenNeuro is a free, open platform for sharing neuroimaging datasets, with public search, dataset pages, and download paths for web, S3, DataLad, and the OpenNeuro CLI.