You should not stay up all night worrying, but a new study has found a link between lack of sleep and a biomolecule thought to be important in the development of the disease Alzheimer.
in humans and mice, the levels of a peptide called amyloid-β place during working hours and declining waking during sleep, the researchers found. They also report that the sleep-deprived mice are more likely to develop amyloid-β deposits, called plaques, like those found in the brains of Alzheimer's patients. Although far from proven, the finding suggests that sleep disturbances may be a risk factor for Alzheimer's disease. On a brighter note, he also alluded to new treatment avenues.
Numerous evidence suggests that naturally occurring amyloid-β in the brain built over many years in people who develop Alzheimer's disease, beginning long before people show signs of loss memory. But very little is known about the factors that may influence peptide levels in the brain, says David Holtzman, a neurologist at Washington University in St. Louis, Missouri.
To study, Holtzman and colleagues conducted a series of experiments with mice in which a small tube is inserted into the brain to take samples of the fluid flowing through the space between the cells. Sampling of the hippocampus, a crucial memory region which is one of the first to be ravaged by Alzheimer's disease, the researchers found that levels of amyloid-β peaked when the animals were awake and fell during sleep. They found a similar pattern in 10 healthy people who agreed to lumbar punctures to allow researchers to sample their cerebrospinal fluid.
The researchers also probed the effects of chronic sleep deprivation in mice that are genetically prone to developing amyloid plaques. To keep awake mice, the researchers placed each on a small platform surrounded by water, which gave them no room to lie down and doze. Mice that stayed awake for 20 hours a day for 3 weeks developed more amyloid plaques than their well-rested peers, the researchers found. Moreover, a drug that blocks orexin receptors, a hormone that promotes wakefulness, reduced plaque formation in the same strain of mice, reports online today in team Science .
The results suggest that people who are chronically sleep deprived may have higher levels of amyloid-β that make them more susceptible to Alzheimer's disease, Holtzman said. He said the team spoke with researchers who do clinical studies of sleep about combing their databases for any signs that people with sleep disorders history are more prone to Alzheimer's disease. "No one has ever studied it," he said. The team will also investigate the use of drugs that interfere with orexin to thwart Alzheimer's disease.
"I find it really cool that sleep is a modulator of the amyloid-β production, "says Sam Sisodia, molecular neurobiologist at the University of Chicago in Illinois. This represents further evidence that amyloid ß rises and falls with levels of synaptic activity, Sisodia said. But the cutting-edge treatments for Alzheimer's disease are far away, he says. "There is another vision, another glimmer of hope."
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