A migraine is neurogical disease that can cause intense throbbing or a pulsing sensation in one area of the head and is commonly accompanied by nausea, vomiting, and extreme sensitivity to light and sound. The pain of migraine and headache originates from those parts of the head, face and neck that lie outside the skull, not from brain’s blood vessel as was previously thought.

First line therapy was done through giving painkillers for pain relieving and drugs from a class called triptans such as: Sumatriptan, Rizatriptan, Frovitriptan etc. But because of theirs side effects profile, scientist were in searching for drugs with better therapeutic outcomes. In this way they started to study physiology of brain working and other unstudied aspects of biochemical events in migraine.

Migraine attacks could soon become less of a menace if hopes surrounding a Kiwi-led breakthrough are realized.

About one in 10 men and nearly two in 10 women experience migraines, and for many sufferers, existing treatments are ineffective and can trigger unpleasant and severe side effects.

For around 20 years, scientists have understood that migraine attacks occur in people who have elevated levels of a pain-causing hormone called CGRP, or calcitonin gene-related peptide.


A new class of drugs called gepants, which work by blocking CGRP activity at the hormone's receptor in nerves, has been tested to combat severe attacks. Yet they weren't as effective as expected.

University of Auckland researchers might have just discovered the missing piece of the puzzle.

They 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.

Despite this hormone having such a clear role in migraines, why it's been so hard to actually block it may be that they need to block two things and not just one.

Researchers, found that CGRP-receptor blocking drugs had been the great hope in migraine treatment for a long time, yet the presence of the second receptor may explain why targeting CGRP for migraine has been hard to grapple with.

Now, researchers needed to understand how the two receptors work together, and what role each plays in nerves related to pain in the head.

But they were excited about the possibilities that AMY1 holds for treating migraine and even other types of pain.

"We need a new class of painkillers that people can take regularly – opioids work but there are tolerance and addiction issues, and that's not good enough.", researchers said.

Their study, published in the journal Annals of Clinical and Translational Neurology, has been offered as open-access research in the hope it will help fast-track better treatments.

Sufferers of migraine disease welcomed this breakthrough and they are delighted to learn of the University of Auckland's breakthrough. They will feel themselves more comfortable and this s going to affect positively theirs lifestyle.

The World Health Organization also estimates about 12 per cent of men suffer from migraines – a disorder characterized by recurrent headaches, often preceded by a loss of vision and accompanied by flashing lights.

Related to first mentioned therapy, scientist also managed to block protein called calcitonin gene-related peptide (CGRP).

The new injection gives hope to the hundreds of thousands of people who suffer chronic migraines – the most debilitating type of headaches.

The jab is made from monoclonal blood protein compounds. These are antibodies – proteins produced by the body to fight injection – specifically engineered to fight the chemical that causes migraines.

The protein compounds are able to 'mop up' another protein called calcitonin gene-related peptide (CGRP), which triggers the pain, nausea and vomiting associated with a migraine.

Researchers have also discovered a new compound that could potentially treat migraines by blocking light sensors in the eyes, according to a study published in the journal Nature Chemical Biology.

Researchers from the Salk Institute for Biological Studies have found that a series of compounds called opsinamides can block a receptor in the eye called melanopsin – a receptor found in neurons connecting the eyes and the brain.

The researchers discovered 10 years ago that melanopsin is responsible for sensing light on its own, away from normal vision. Continued research found that this receptor is responsible for maintaining sleep cycles and various other sensitivity functions in those with healthy vision.

The receptor was also found to be responsible for constricting the pupil within the eye when it is exposed to bright light, triggering the light-sensitivity that is commonly linked to migraines.

Scientist also found a gene responsible for migraine attacks. The mutation of the KCNK18 gene interferes with the production of a protein called TRESK. TRESK is important in regulating the sensitivity threshold of the brain's pain centers and impacts the K2P (potassium) channels throughout the nervous system, opening possibility to cure migraine through genetic and proteinic therapy.


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