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Migraine and neuroinflammation: the inflammasome perspective
Oguzhan Kursun1, Muge Yemisci2,3, Arn M J M van den Maagdenberg4,5
1Department of Neurology, City Hospital, Ankara, Turkey.
The Journal of Headache and Pain
|June 11, 2021
Summary
Neuroinflammation, particularly inflammasomes, plays a key role in migraine pathophysiology. Targeting these inflammasome pathways offers potential new treatments and biomarkers for migraine pain.
Area of Science:
- Neuroscience
- Immunology
- Pain Research
Background:
- Migraine is a complex neuro-glio-vascular disorder involving significant neuroinflammation.
- Cortical spreading depolarization (CSD) is a key event in migraine pathophysiology, triggering neuroinflammatory signaling.
- Inflammasomes, crucial innate immune system components, are increasingly implicated in migraine pathogenesis.
Purpose of the Study:
- To review inflammasome-mediated neuroinflammatory signaling in response to CSD in migraine.
- To explore the role of inflammasomes in trigeminovascular system activation and migraine pain generation.
- To discuss inflammasome links with migraine comorbidities like stroke, epilepsy, and COVID-19.
Main Methods:
- Review of current literature on inflammasomes and migraine.
- Focus on nucleotide-binding domain (NOD)-like receptor family pyrin domain containing 3 (NLRP3) inflammasome.
- Analysis of CSD-induced neuroinflammation and its connection to pain pathways.
Main Results:
- CSD triggers neuroinflammatory signaling in the brain parenchyma via inflammasomes.
- Activated inflammasomes produce cytokines that stimulate trigeminal neurons, contributing to migraine pain.
- Emerging evidence links NLRP3 inflammasome activation to migraine and other inflammatory pain conditions.
Conclusions:
- Neuroinflammatory pathways involving inflammasome proteins are promising therapeutic targets for migraine.
- Inflammasome proteins may serve as potential biomarkers for migraine diagnosis or treatment response.
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