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[News] Molecule Could Lead to Better Sleep Apnea Treatments
#1
Molecule Could Lead to Better Sleep Apnea Treatments
Discovery of Vital Molecule That Regulates Breathing Could Lead to Better Sleep Apnea Treatments

Published on February 7, 2017

Respiratory conditions could be better targeted and treated, thanks to the discovery of the vital molecule which regulates breathing. This is according to research by the University of Warwick.

Nicholas Dale PhD, professor at the School of Life Sciences has identified Connexin26 (Cx26) as a key molecule that reacts to CO2 in our bodies and activates breathing.

Cx26 molecules detect levels of CO2 in the bloodstream, and when levels reach a certain point, they tell our bodies to excrete the CO2 and take in oxygen—the vital life-preserving process that allows us to breathe, and creates blood flow to the brain.

Without this essential molecular function, harmful levels of CO2 would remain in the bloodstream, making breathing difficult or impossible.


[Image: Cx26molecule.jpg]

Mutations in Cx26 are directly connected to a number of serious conditions—ranging from congenital deafness, to respiratory conditions, and serious syndromes that affect skin, vision, and hearing. As Cx26 is vital to breathing well, people carrying these mutations may be at risk of sleep apnea.
Identifying these mutations and working out how to restore the molecule to its normal function could lead to effective, targeted, personalized treatments to mitigate these risks and improve quality of life.

Different animals have varying levels of sensitivity to CO2. Dale’s group exploited this idea to see whether the properties of Cx26 matched the physiological requirements of: birds, which fly at high-altitude and can tolerate low levels of CO2; humans and rats, which are broadly similar at an intermediate level; and mole rats, which live exclusively underground and tolerate very high levels of CO2.

The researchers found that the CO2 binding properties matched the sensitivities of these different animals. Evolutionary natural selection has thus modified the CO2-binding properties of Cx26—showing that this molecule is a universally important sensor of CO2 in warm-blooded animals.

In a release, Dale comments on the significance of the research: “Important molecules with universal physiological functions are shaped by evolution. We have exploited this simple fact to show that the CO2-binding characteristics of Cx26 are important in our bodies too. This is likely to open up new ways to identify and treat people at risk of sleep apneas.”


Fair Use from:
http://www.sleepreviewmag.com/2017/02/di...reatments/
The above post may contain copyrighted material the use of which has not always been specifically authorized by the copyright owner. The material available is intended to advance the understanding of Sleep Apnea treatment and to advance the educational level of Sleep Apnea patients with regard to their health. Sometimes included is the full text of articles and documents rather than a simple link because outside links frequently "go bad" or change over time. This constitutes a "fair use" of any such copyrighted material as provided for in section 107 of the US Copyright Law. In accordance with Title 17 U.S.C. Section 107, the material in this post is distributed without fee or payment of any kind for research and educational purposes. If you wish to use copyrighted material from this post for purposes of your own that go beyond "fair use", you must obtain permission from the copyright owner.
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#2
RE: Molecule Could Lead to Better Sleep Apnea Treatments
Interesting. This could in the long term provide a pharmaceutical treatment for central apnea, but I don't see how it could help obstructive apnea which is basically a mechanical condition.
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#3
RE: Molecule Could Lead to Better Sleep Apnea Treatments
This discovery is probably one of several steps in a feedback loop or even an additional feedback loop that communicates blood CO2 levels with the brain.  Currently it is believed that the primary stimulus to breathing is blood pH.  CO2 in the blood becomes Carbonic Acid.  The Carbonic Acid in turn lowers pH which is measured by sensors in locations such as the Carotid Body and other locations.  The sensors then signal the brain to stimulate respiration which washes out excess CO2 raising the pH.  There is an enzyme called Carbonic Anhydrase which is instrumental in converting Carbonic Acid back into CO2.  The Carbonic Anhydrase can be inhibited by a medication known as Diamox or acetazolemide.  The reduction in Carbonic Anhydrase lowers the blood pH and stimulates respiration.  So far this is one of the few medications used to treat Central Apnea not associated with heart disease.  It is going to take a lot of study to figure out how Cx26 actually works and if medications can be formulated that utilize its function.  

Rich
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