Scientists at the University of Copenhagen have demonstrated that the trigeminal nerve, a cranial nerve whose activation underlies migraine pain, has direct access to cerebrospinal fluid (CSF) transported by the glymph system. Furthermore, in the run-up to a migraine, levels of multiple proteins in the CSF changed. One of them was calcitonin gene-related peptide (CGRP), a driver of migraine pain and target of several approved drugs for both treatment and prevention of migraine.

Wound healing is a highly specialized dynamic process for the repair of damaged/injured tissues through an intricate mechanism. Any failure in the normal wound healing process results in abnormal scar formation, and a chronic state which is more susceptible to infections. Researchers from Monash University in Australia and Osaka University in Japan have demonstrated that the removal of a specific subtype of sensory neurons containing the Nav1.8+ ion channel significantly impairs skin wound repair and muscle regeneration following injury.

Two studies published this week have reported new insights into the role of the nervous system in tumors outside of the brain. Researchers at the Shanghai Jiao Tong University School of Medicine have identified a role for pain-sensing neurons in helping oral carcinomas cope with nutrient starvation, and that this interaction could be blocked by the calcitonin gene-related peptide (CGRP)-targeting migraine drug Nurtec ODT (rimegepant; Biohaven Pharmaceutical Holding Co. Ltd.).

With the FDA approval of Abbvie Inc.’s Qulipta (atogepant) to prevent episodic migraine in adults, the oral calcitonin gene-related peptide (CGRP) receptor antagonist became the first specifically developed for preventing migraine.