Review discusses GFAP's role in migraine mechanisms and its potential as a treatment target, indicating its therapeutic promise.
Glial fibrillary acidic protein (GFAP), a pivotal intermediate filament protein predominantly expressed in astrocytes, serves as a core structural and functional regulator in the central nervous system, and is deeply implicated in the pathological cascades underlying a wide spectrum of neurological disorders, ranging from neurodegenerative diseases to neuroinflammatory conditions and episodic neurological disorders. In this paper, we reviewed the current research progress on the biological function, expression regulation and involvement in the process of neuroinflammation of GFAP, and discussed the potential of GFAP as a new target for the treatment of migraine. We reviewed the epidemiological characteristics, complex pathophysiological mechanisms, and clinical burden of migraine, a highly prevalent neurovascular disorder, while underscoring the inherent limitations of current mainstream therapeutic approaches, including incomplete efficacy, frequent recurrence, and prominent adverse effects, which highlight the unmet clinical demand for novel, targeted, and mechanism-driven therapeutic strategies. Evidence from preclinical and clinical studies suggests that the regulation of GFAP may affect the key mechanisms of migraine, including glial cell activation, neuroinflammation and neuronal excitability. Although challenges associated with technical barriers in drug development remain, this review highlights the translational potential of targeting GFAP to improve patient outcomes. Future interdisciplinary research and collaborative efforts are crucial for the introduction of GFAP based therapy into clinical practice.
No takes yet. Share an insight, caveat, or question.
Liao et al. (2026) studied this question.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: