Study helps explain why sleep becomes more fragmented with age

Study helps explain why sleep becomes more fragmented with age -

As people age, they often have difficulty falling asleep and staying asleep, and tend to wake up too early. In people with Alzheimer's disease, common and troubling symptom of aging tends to be particularly pronounced, often leading to confusion and nocturnal wandering.

Now, a study led by researchers at Beth Israel Deaconess Medical Center (BIDMC) and the University of Toronto / Sunnybrook Health Sciences Center helps explain why sleep becomes more fragmented with age. Reported online today in the journal brain , the new results demonstrate for the first time a group of inhibitory neurons whose loss leads to sleep disturbance in laboratory animals, are significantly decreased in the elderly and people with Alzheimer's disease, and this, in turn, is accompanied by sleep disruption.

"on average, a person 70 years about an hour less sleep per night than a person in his 20s," says lead author Clifford B. Saper, MD, PhD, Chairman of Neurology at BIDMC and James Jackson Putnam Professor of Neurology at Harvard Medical School. "Loss of sleep and sleep fragmentation is associated with a number of health problems, including cognitive dysfunction, increased blood pressure and vascular disease, and a tendency to develop type 2 diabetes. it now appears that the loss of these neurons may contribute to these various disorders as people age. "

in 1996, Saper laboratory discovered that the nucleus preoptic ventrolateral, a group of key cell inhibitory neurons, functioned as a "sleep switch" rats, turning off the arousal systems of the brain to allow the animals to sleep. "Our experiments on animals have shown that the loss of these neurons deep insomnia products with animals sleeping only about 50 percent more than normal and the rest of their sleep is fragmented and disturbed, "he said.

A group of cells in the human brain, the intermediate core, is located in similar location and has the same inhibitory neurotransmitter, galanin, the vetrolateral preoptic nucleus in the rat. The authors hypothesized that if the intermediate core was important for the human sleep and was homologous to ventrolateral preoptic nucleus of the animal, it can also regulate similarly sleep-wake cycles of humans.

To test this hypothesis, the investigators analyzed data from the Rush Memory and Aging Project, a community-based study of aging and dementia that began in 1997 and followed a group nearly 1,000 subjects who entered the study in healthy 65 and were followed until death, how their brains are donated for research.

"Since 05, most of the subjects in the memory and the project underwent aging actigraphic registration every two years. It consists of wearing them a little wristwatch- the type of device on the arm non- dominant for seven to 10 days, "says first author Andrew Lim MS, MD, of the University of Toronto and Sunnybrook Health Sciences Center and former member of Saper laboratory. The actigraphy device, which is waterproof, is worn 24 hours a day and monitors all movements, large and small, divided into 15 second intervals. "Our previous work had identified these actigraphic records are a good measure of the quantity and sleep quality," adds Lim.

The authors examined the brains of 45 subjects in the study (median age at death, 89.2), ventrolateral preoptic neurons identified by staining brain to neurotransmitter galanin. They then correlated the behavior actigraphic rest-activity of 45 people in the year before their deaths with the number of remaining ventrolateral preoptic neurons at autopsy.

"We found that in older patients who did not Alzheimer's disease, the number of ventrolateral preoptic neurons inversely correlated with the amount of sleep fragmentation," says Saper. " less neurons, more fragmented sleep has become. " The subjects with the highest amount of neurons (more than 6,000) spent 50 percent or more of total sleep time in long periods of non-movement most likely to represent sleep while subjects with fewer neurons ventrolateral preoptic (less than 3000) spent less than 40 percent of total sleep time in extended rest periods. The results also showed that among patients with Alzheimer's, most insufficient sleep appeared to be linked to the ventrolateral preoptic number of neurons that were lost.

"These results provide the first evidence that the ventrolateral preoptic nucleus in humans is likely to play a key role in the onset of sleep, and functions in a similar manner to other species that have been studied, "says Saper. "The loss of these neurons with aging and Alzheimer's disease may be an important reason why the elderly often experience sleep disturbances. These results can therefore lead to new methods to reduce sleep problems in the elderly and prevent cognitive linked to sleep deprivation decline in people with dementia. "