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Molecular biology of sleep apnea could lead to new treatments
Date:3/19/2008

pathway to fix itself or one that leads to self destruction. The cell makes that decision based on its initial health.

If a patient has sleep apnea with healthy cells, the cells will take the fix-it path. Then good things happen; the cell activates another molecule called eIF-2alpha, which turns on helpful molecules like anti-oxidants that degrade the misfolded proteins, explains Veasey.

However if cells are unhealthy to begin with, the PERK pathway can also turn on molecules that cause the cell to turn on itself and activate apoptosis or cell death. In this event, we predict that patients with sleep apnea may lose motor neurons, notes Veasey. Eventually sleep apnea could continue to worsen since the few remaining neurons are already stressed when gasping for air during sleep.

A drug called salubrinal does keep the eIF-2alpha path active, thereby preventing vulnerable cells from going down the cell-death path. But salubrinal is a double-edged sword: Just the right amount keeps the cell happy, but too much can shut down all protein synthesis, a highly toxic outcome.

The research team is now working on how to ramp up the eIF-2alpha path with changes in the mouse diet. This paper shows which pathways are important for treating sleep apnea, but well need to come up with therapies other than salubrinal, says Veasey. Ultimately if we can do healthy things that protect the endoplasmic reticula of cells, then sleep apnea wont be such an insult, not only to motor neurons, but neurons involved in cognition and alertness.


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Contact: Karen Kreeger
karen.kreeger@uphs.upenn.edu
215-349-5658
University of Pennsylvania School of Medicine
Source:Eurekalert

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