Discover a new mechanism responsible for migraine


Although it affects 15% of the entire population, to date the genetic, environmental and hormonal causes of migraine are unknown. Now a team of scientists has now discovered a mutation in a gene that would cause increased neuronal activity and induce migraine pain.

Episodes of migraine are related to increased electrical excitability of sensory neurons, the researchers found. (Reference Image)Pixabay

Migraine causes recurrent and severe episodes of headache and, in some cases, also nausea, vomiting and photophobia. 80% of cases are considered migraine without aura, and the remaining 20% ​​are episodes in which the headache is preceded by transient neurological symptoms that are usually visual (migraine with aura). (You may be interested: They approve medication to prevent migraines)

Despite the high prevalence of this type of headache, "most of the genetic causes and pathophysiological mechanisms involved are still unknown, making it difficult to find effective treatments," says Xavier Gasull. (In addition: migraine surgery confronts surgeons and neurologists in Colombia)

A new paper published in the journal Neuron concludes now that a mutation in the gene that encodes the TRESK ion channel -Implication in the control of the excitability of the neurons – causes the dysfunction of some proteins that they increase neuronal activity and induce migraine pain.

The specialists Xavier Gasull and Alba Andrés-Bilbé, from the Faculty of Medicine and Health Sciences, the Institute of Neurosciences of the University of Barcelona (UBNeuro) and the Group of Research in Neurophysiology of IDIBAPS participate in the study.

The control of neuronal excitability

The episodes of Migraine is related to increased electrical excitability of sensory neurons. The electrical activity is controlled by proteins – the ion channels – responsible for facilitating or inhibiting the activation of neurons. The study, in particular, focuses on the TRESK and TREK ion channels, which are found in sensory neurons and delay excessive neuronal activation.

According to the findings, a mutation in the gene encoding the TRESK ion channel leads to a dysfunctional protein, which alters the channel's ability to reduce electrical activity. In parallel, this mutation also generates another altered protein that affects the physiological function of other ion channels, such as TREK1. The discovery of a mechanism by which a mutation generates two dysfunctional proteins – a process perhaps shared with other genetic pathologies – also opens up new perspectives that will have to be explored in the future.

"Paradoxically, other mutations that also eliminated the TRESK protein, but did not cause migraine, have been described so far." In the new study, we found that the combination of the two factors is necessary for greater electrical activation of the sensory neurons, which causes the pain characteristic of migraine, "says Xavier Gasull.

The work, coordinated by researcher Guillaume Sandoz, of the University of Nice and the National Center for Scientific Research of France (CNRS), will open new ways of designing future therapeutic strategies against migraine, and it is a very significant advance to know in detail the mechanisms that cause episodes of migraine with aura, unknown until now.


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