Dying During Sleep Linked to Sleep Apnea
(Ivanhoe Newswire) -- When an otherwise healthy elderly person dies in their sleep, doctors generally say the cause of death is heart failure. But a new study finds that may not be the case after all. Research shows some people die in their sleep because they stop breathing due to a loss of cells in the brain's breathing center.
Obstructive sleep apnea refers to when a person's airway collapses causing them to stop breathing. Central sleep apnea is triggered by something going awry in the brain's breathing command post. The command post is a region in the brainstem called the preBotzinger complex (preBotC). Researchers from UCLA studied in rats what would happen in the brain cells if this complex were destroyed.
Scientists injected rats with a compound to kill more than half of their preBotC neurons. After four to five days they noticed a change. "We were surprised to see that breathing completely stopped when the rat entered REM sleep, forcing the rat to wake up in order to start breathing again," says Leanne Mckay, postdoctoral fellow in neurobiology at UCLA in Calif. "Over time, the breathing lapses increased in severity spreading into non-REM sleep and eventually occurring when the rats were awake, as well."
Study authors say human brains are organized in the same way as rats. The researchers believe humans have thousands of preBotC cells that are slowly lost over a lifetime. Furthermore, they think this may play a role into people suffering the late stages of neurodegenerative disorders, such as Parkinson's disease. "People with these diseases breathe normally when they are awake, but many of them have breathing difficulties during sleep," said Wiktor Janczewski, M.D., Ph.D., assistant researcher in neurobiology at UCLA. "When central sleep apnea strikes, they are already very ill and their sleep-disordered breathing may go unnoticed."
The team is now repeating this research on elderly rats and plan to analyze the brains of people who die from neurodegenerative diseases to see if there is damage in their preBotzinger complexes.
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SOURCE: Nature Neuroscience published online Aug. 7, 2005