NPY-Y2R driven neuroimmune signaling as a potential therapeutic target for trigeminal neuralgia: clinical and experimental evidence - PubMed
5 hours ago
- #Neuropeptide-Y
- #Neuroimmune signaling
- #Trigeminal neuralgia
- Trigeminal neuralgia (TN), a painful orofacial condition, lacks effective, long-lasting treatments as current options don't address mechanisms of chronic pain.
- CSF NPY levels are elevated in TN patients and correlate with pain intensity, making it a candidate biomarker with clinical relevance.
- In a mouse model, injured trigeminal ganglion neurons release NPY, activating Y2R on nociceptors and recruiting macrophages that release TNF-α.
- This creates a neuron-macrophage feedback loop, amplifying neuroinflammation and mechanical allodynia, with Y2R blockade, its genetic deletion, or macrophage depletion effectively reversing pain responses.
- NPY-Y2R targeting demonstrates promise as a therapeutic strategy for TN, aligning treatment with underlying disease mechanisms.