Neuron-glia crosstalk and inflammatory mediators in migraine pathophysiology.

Migraine is a complex neurological disorder with neuroinflammation playing a crucial role in its pathogenesis. This review provides an overview of the neuroinflammation mechanisms in migraine, focusing on both cellular and molecular aspects. At the cellular level, we examine the role of glial cells, including astrocytes, microglia, oligodendrocytes in the central nervous system, and Schwann cells and satellite glial cells in the peripheral nervous system. On the molecular level, we explore the signaling pathways, including IL-1β, TNF-α, IL-6, and non-coding RNAs, that mediate cell interactions or independent actions. Some of the molecular signaling pathways mentioned, such as TNF-α and IL-1β, have been investigated as druggable targets. Recent advancements, such as [11C] PBR28-targeted imaging for visualizing astrocyte activation and single-cell sequencing for exploring cellular heterogeneity, represent breakthroughs in understanding the mechanisms of neuroinflammation in migraine. By considering factors for personalized treatments, estrogen and TRPM8 emerge as promising therapeutic targets regarding sexual dimorphism. These advancements may help bridge the gap between preclinical findings and clinical applications, ultimately leading to more precise and personalized options for migraine patients.