Vestibular migraine (VM) is characterized by recurrent episodes of headache and vertigo, and its pathogenesis is closely associated with neuroinflammation and central sensitization. C-X-C motif chemokine ligand 10 (CXCL10) plays a critical role in neuroinflammation and pain modulation; however, its specific involvement in VM remains unclear.
No actionable change at this time; this is an animal study identifying a potential drug target for vestibular migraine, and findings require replication in human trials before any clinical guidance can be derived.
Vestibular migraine is a common and under-treated cause of episodic dizziness seen in audiology and neurotology clinics, and identifying a specific molecular target (CXCL10/PI3K pathway) could eventually lead to new therapies.
- 01CXCL10 knockdown (reducing the activity of a specific inflammation-signaling protein) reduced vestibular migraine symptoms in rats.
- 02The mechanism involves the PI3K pathway, which controls neuroinflammation (brain inflammation) and central sensitization (heightened nerve sensitivity).
- 03This is a preclinical animal study only — no human data are included.
- 04Vestibular migraine is a major cause of episodic vertigo relevant to audiologists and vestibular specialists.
- 05Results suggest CXCL10 could be a future therapeutic target but require substantial further research.
CXCL10 knockdown attenuates vestibular migraine symptoms in a rat model.
studysupportedThe PI3K pathway mediates CXCL10-driven neuroinflammation and central sensitization in vestibular migraine.
studypartially supported- PMID
- 42363060
- DOI
- 10.1186/s10194-026-02437-5.
- Journal
- The Journal of Headache and Pain
- Publication type
- research_article
- Evidence level
- 4
- Population
- Rat model of vestibular migraine
- Intervention
- CXCL10 gene knockdown
- Comparator
- Control rats without CXCL10 knockdown
Primary outcomes
Vestibular migraine symptom severity; Markers of neuroinflammation; Central sensitization indicators