ReviewCNS drugs2019
Pathophysiological Mechanisms in Migraine and the Identification of New Therapeutic Targets.
Review in CNS drugs, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 57 papers, 1 of them a synthesis that pooled it.
What it found
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The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
57 citing papers in PubMed, 1 synthesis or guideline pooled it, 109 citations in OpenAlex.
- Epidemiological linkage between migraine and diabetes mellitus: a systematic review and meta-analysis.The journal of headache and pain · 2024Pooled it
- Glibenclamide Posttreatment Does Not Inhibit Levcromakalim Induced Headache in Healthy Participants: A Randomized Clinical Trial.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2023Trial
- Acupuncture modulates migraine-related neural and neuroendocrine regulatory pathways.The journal of headache and pain · 2026Review
- Intranasal SARS-CoV-2 infection changes the transcriptome of the mouse trigeminal ganglion and brainstem: potential mechanisms underlying headache and trigeminal pain presentation in COVID-19.Journal of neuroinflammation · 2026Article
- Migraine-induced cochlear injury triggers ZBP1-mediated PANoptosis via CGRP signaling.The journal of headache and pain · 2026Article
- The role of non-coding RNAs in the pathogenesis of migraine: from molecular insights to potential biomarkers.Frontiers in neurology · 2026Review
- LPS-Induced Neuroinflammation Increases Serotonin-Evoked Activity of Trigeminal Afferents and Aggravates Mechanical Allodynia and Photophobic Behavior in Rat Migraine Model.International journal of molecular sciences · 2025Article
- Dual block evidence of the effects of topiramate, a sulfamate-substituted monosaccharide, on voltage-gated sodium current and hyperpolarization-activated cation current.BMC pharmacology & toxicology · 2025Article
- Dysregulated autophagy, neural signaling pathways and gut-brain axis in a novel vestibular migraine-like rat model: implications for pathogenesis.The journal of headache and pain · 2025Article
- Ex vivo stimulation of the trigeminal nucleus caudalis induces peripheral CGRP release in the trigeminal ganglion and reveals a distinct dopamine-endocannabinoid mechanism relevant to migraine.The journal of headache and pain · 2025Article
- Poly-IC Alleviates Nitroglycerin-Induced Migraine by Inhibiting Neuroinflammation via TLR3/TRIF Signaling Pathway.CNS neuroscience & therapeutics · 2025Article
- A Correlation Between Migraine and Endometriosis and Its Clinical Implications-A Systematic Literature Review.Journal of clinical medicine · 2025Review
- Up-regulation of MAPK14-related lncRNAs in the circulation of migraineurs.Scientific reports · 2025Article
- Differentially localizing isoforms of the migraine component calcitonin gene-related peptide (CGRP), in the mouse trigeminal ganglion: βCGRP is translated but, unlike αCGRP, not sorted into axons.The journal of headache and pain · 2025Article
- Pipeline for development of acylated peptide based CGRP receptor antagonist with extended half-life for migraine treatment.Scientific reports · 2025Article
- Role of Phytocompounds for Effective Management of Migraine: Current and Future Prospectives.Central nervous system agents in medicinal chemistry · 2025Review
- Informatics Approach Towards Targeting HTR1B Pathways in Neuropharmacology for Migraine Treatment.Current neuropharmacology · 2025Article
- Enhancing Acute Migraine Treatment: Exploring Solid Lipid Nanoparticles and Nanostructured Lipid Carriers for the Nose-to-Brain Route.Pharmaceutics · 2024Review
- Article
- Astrocyte-Microglia Crosstalk: A Novel Target for the Treatment of Migraine.Aging and disease · 2024Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Migraine is a strongly disabling disease characterized by a unilateral throbbing headache lasting for up to 72 h for each individual attack. There have been many theories on the pathophysiology of migraine throughout the years. Currently, the neurovascular theory dominates, suggesting clear involvement of the trigeminovascular system. The most recent data show that a migraine attack most likely originates in the hypothalamus and activates the trigeminal nucleus caudalis (TNC). Although the mechanisms are unknown, activation of the TNC leads to peripheral release of calcitonin gene-related protein (CGRP), most likely from C-fibers. During the past year monoclonal antibodies against CGRP or the CGRP receptor have emerged as the most promising targets for migraine therapy, and at the same time established the strong involvement of CGRP in the pathophysiology of migraine. The viewpoint presented here focuses further on the activation of the CGRP receptor on the sensory Aδ-fiber, leading to the sensation of pain. The CGRP receptor activates adenylate cyclase, which leads to an increase in cyclic adenosine monophosphate (cAMP). We hypothesize that cAMP activates the hyperpolarization-activated cyclic nucleotide-gated (HCN) channels, triggering an action potential sensed as pain. The mechanisms behind migraine pain on a molecular level, particularly their importance to cAMP, provide clues to potential new anti-migraine targets. In this article we focus on the development of targets related to the CGRP system, and further include novel targets such as the pituitary adenylate cyclase-activating peptide (PACAP) system, the serotonin 5-HT
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.