CGRP

Aim: Methylcobalamin (MeCbl) is known to promote peripheral nerve regeneration and polarize macrophage to M2. In recent years, it has been reported that the regeneration of peripheral nerves and the polarization of macrophages to M2 are important for bone formation. The purpose of this research is to examine the effects of MeCbl on bone formation via peripheral nerves and macrophages. Methods: Effects of MeCbl were evaluated using rat skull defect models. Briefly, we created a bone hole in the rat skull, and evaluated the bone formation rate in the defect area in a group that received continuo

Migraine is a pain disorder that affects 10 – 15% of the population worldwide. Even though there is a wide choice of therapeutics that includes different classes of well-tolerated drugs, numerous patients are still not satisfied with their treatment. Trigeminal ganglion and nucleus caudalis are enriched with nociceptin/orphanin FQ (N/OFQ) receptor (NOP)-expressing cells. The general aim of the present study is to investigate the role of the N/OFQ – NOP system in the modulation of migraine. This study evaluated the phenotype of mice with genetically induced knockout of the NOP receptor gene (NO

…DOR with the pro-migraine peptide, CGRP. There is regional variation between the co-expression of DOR with CGRP or its receptor in the trigeminal complex. This work indicates that DOR agonists can moderate both CGRP release and signaling, thus regulating pro-migraine ef

In this presentation I will describe how the CGRP project started and culminated in the development of gepants and mAbs for successful therapy. The outstanding question regarding the preponderance of female migraineurs also remains. I will present views on the reason behind this and suggest that understanding the hormonal influence will pave the way to alleviating hormone related migraine.

Lifelong devotion to headache research has led to many discoveries. First a series of studies of brain blood flow during attacks of migraine. The results showed changes compatible with cortical spreading depression in migraine without aura effectively negating the then prevailing vasospastic/ischemic theory. In migraine without aura no changes in brain blood flow. This difference was crucial for the separation of migraine with aura and migraine without aura in the first and subsequent editions of the international headache classification headed by me. Then a human migraine provocation model th