The research by Associate Professor Debbie Hay and Research Fellow Dr Christopher Walker of the School of Biological Sciences is published in Annals of Clinical and Translational Neurology.
Migraine, a debilitating but common neurological disorder, has puzzled scientists for centuries and while drugs have been developed to treat it, for many people they are ineffective or have significant side effects.
Current strategies for developing new migraine treatments are based on the knowledge that people who suffer from the disorder have elevated levels of a pain-causing hormone called CGRP, or calcitonin gene-related peptide.
Migraine medication developed in recent years to block acute migraine attacks, a class of drugs called “gepants”, work by blocking CGRP activity at the CGRP receptor.
But Associate Professor Hay and Dr Walker believe the reason the gepants are less effective than was hoped is because their research shows that another receptor, called AMY1, also plays a critical role in CGRP activity during migraine attacks.
“We have discovered that CGRP activates a second target on the surface of pain-sensing nerve cells, called AMY1, which the gepants are not designed to block,” Associate Professor Hay says.
“This may be the key to treating migraine and opens the door for the design of new drugs that block this second target.”
“CGRP-blocking drugs have been the great hope in the treatment of migraine for a long time,” Dr Walker says. “It turns out there is a second receptor involved and this may be why the gepants are not as effective as we might have expected.”
More research is required into exactly how CGRP and AMY1 work in nerves that are involved in pain in the head.
“We need to try and understand how these two receptors are working together and exactly what role both play in migraine,” Associate Professor Hay says.
“But we are excited about the possibilities that AMY1 holds for treating migraine and even other types of pain,” adds Dr Walker.
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