Researchers at CNRS discovered a mutation that causes dysfunction in a protein which induces migraines. Migraines are related to hyperexcitability in sensory neurons. The researchers found that a mutation in the coding causes a split in the protein with one being inactive and the other targets ion channels at K2P2.1 (a protein in the potasisum channel) which stimulates neural electrical activity causing migraines.
The above picture is from a study performed on mice at the Institut de Biologie Valrose in France. The diagram shows the normal pathway and the mutated pathway of the TRESK gene. In the mice with the TRESK mutation, they exhibit TRESK-MT1 and TRESK-MT2 which in turns cause hyperexcitability instead of the normal TRESK and normal excitability.
I found this discovery very interesting because I am among the 15% of the population that does not respond to migraine medications and treatments. Medications for chronic migraines are typically anti-depressive or anti-epileptic, usually beta-blockers, calcium channel blocker, or serotonin blockers, which both can worsen migraines and cause unwanted side effects. The discovery that a mutation in the potassium channel is related to migraines allows for a further understanding of migraines and can lead to a more effective drug to be developed.
After reading your summary and the article itself, I learned a lot about migraines. When I was younger, I had terrible migraines, however, medicine helped me a lot. The pain is unimaginable and research like this is crucial. It is really interesting to learn that a dysfunctional protein is what is causing migraines. It makes me wonder if a condition like this could possibly be genetic. It's also very shocking that this one protein malfunction causes such a problem in the body unrelated to gene mutations. With research like this, doctors could potentially create a medicine to prevent this separation of the two proteins to occur.
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