Posts tagged sleep

September 5, 2012 by Michael C. Purdy

Sleep disruptions may be among the earliest indicators of Alzheimer’s disease, scientists at Washington University School of Medicine in St. Louis report Sept. 5 in Science Translational Medicine.

Working in a mouse model, the researchers found that when the first signs of Alzheimer’s plaques appear in the brain, the normal sleep-wake cycle is significantly disrupted.

“If sleep abnormalities begin this early in the course of human Alzheimer’s disease, those changes could provide us with an easily detectable sign of pathology,” says senior author David M. Holtzman, MD, the Andrew B. and Gretchen P. Jones Professor and head of Washington University’s Department of Neurology. “As we start to treat Alzheimer’s patients before the onset of dementia, the presence or absence of sleep problems may be a rapid indicator of whether the new treatments are succeeding.”

Holtzman’s laboratory was among the first to link sleep problems and Alzheimer’s through studies of sleep in mice genetically altered to develop Alzheimer’s plaques as they age. In a study published in 2009, he showed that brain levels of a primary ingredient of the plaques naturally rise when healthy young mice are awake and drop after they go to sleep. Depriving the mice of sleep disrupted this cycle and accelerated the development of brain plaques.

A similar rising and falling of the plaque component, a protein called amyloid beta, was later detected in the cerebrospinal fluid of healthy humans studied by co-author Randall Bateman, MD, the Charles F. and Joanne Knight Distinguished Professor of Neurology at Washington University.

The new research, led by Jee Hoon Roh, MD, PhD, a neurologist and postdoctoral fellow in Holtzman’s laboratory, shows that when the first indicators of brain plaques appear, the natural fluctuations in amyloid beta levels stop in both mice and humans.

“We suspect that the plaques are pulling in amyloid beta, removing it from the processes that would normally clear it from the brain,” Holtzman says.

Mice are nocturnal animals and normally sleep for 40 minutes during every hour of daylight, but when Alzheimer’s plaques began forming in their brains, their average sleep times dropped to 30 minutes per hour.

To confirm that amyloid beta was directly linked to the changes in sleep, researchers gave a vaccine against amyloid beta to a new group of mice with the same genetic modifications. As these mice grew older, they did not develop brain plaques. Their sleeping patterns remained normal and amyloid beta levels in the brain continued to rise and fall regularly.

Scientists now are evaluating whether sleep problems occur in patients who have markers of Alzheimer’s disease, such as plaques in the brain, but have not yet developed memory or other cognitive problems.

“If these sleep problems exist, we don’t yet know exactly what form they take—reduced sleep overall or trouble staying asleep or something else entirely,” Holtzman says. “But we’re working to find out.”

(Source: news.wustl.edu)

26 August 2012 by Mo Costandi

Subjects trained to sniff pleasant smells while asleep retain the conditioning when they wake up.

It sounds like every student’s dream: research published today in Nature Neuroscience shows that we can learn entirely new information while we snooze.

TIPS/Photoshot

Anat Arzi of the Weizmann Institute of Science in Rehovot, Israel, and her colleagues used a simple form of learning called classical conditioning to teach 55 healthy participants to associate odours with sounds as they slept.

They repeatedly exposed the sleeping participants to pleasant odours, such as deodorant and shampoo, and unpleasant odours such as rotting fish and meat, and played a specific sound to accompany each scent.

It is well known that sleep has an important role in strengthening existing memories, and this conditioning was already known to alter sniffing behaviour in people who are awake. The subjects sniff strongly when they hear a tone associated with a pleasant smell, but only weakly in response to a tone associated with an unpleasant one.

But the latest research shows that the sleep conditioning persists even after they wake up, causing them to sniff strongly or weakly on hearing the relevant tone — even if there was no odour. The participants were completely unaware that they had learned the relationship between smells and sounds. The effect was seen regardless of when the conditioning was done during the sleep cycle. However, the sniffing responses were slightly more pronounced in those participants who learned the association during the rapid eye movement (REM) stage, which typically occurs during the second half of a night’s sleep.

Pillow power

Arzi thinks that we could probably learn more complex information while we sleep. “This does not imply that you can place your homework under the pillow and know it in the morning,” she says. “There will be clear limits on what we can learn in sleep, but I speculate that they will be beyond what we have demonstrated.”

In 2009, Tristan Bekinschtein, a neuroscientist at the UK Medical Research Council’s Cognition and Brain Sciences Unit in Cambridge, and his colleagues reported that some patients who are minimally conscious or in a vegetative state can be classically conditioned to blink in response to air puffed into their eyes. Conditioned responses such as these could eventually help clinicians to diagnose these neurological conditions, and to predict which patients might subsequently recover. “It remains to be seen if the neural networks involved in sleep learning are similar to the ones recruited during wakefulness,” says Bekinschtein.

The findings by Arzi and her colleagues might also be useful for these purposes, and could lead to ‘sleep therapies’ that help to alter behaviour in conditions such as phobia.

“We are now trying to implement helpful behavioural modification through sleep-learning,” says Arzi. “We also want to investigate the brain mechanisms involved, and the type of learning we use in other states of altered consciousness, such as vegetative state and coma.”

Source: Nature

21 August 2012 by Lois Rogers

Thousands of otherwise healthy people put up with a level of sleep deprivation that would drive the rest of us insane. But they are not the usual candidates for insomnia, such as shift workers or those with severe mental illness. Instead, they belong to a newly identified group of people born without the ‘comfort’ genes needed for easy sleep.

This means they are immune to the feeling of warmth and relaxation which sends an average person off to sleep within 15 minutes. Their genes are designed instead to maintain a state of mental alertness. This makes normal, prolonged sleep impossible so they sleep fitfully, in only short bursts. Even then, their lack of ‘comfort’ genes may mean they struggle to get comfortable, fussing about the bedding or finding their sleeping position.

There are other so-called insomnia genes — some cause repeated periods of wakefulness in the small hours of the night or at the slightest disturbance, or drive an affected person to leap out of bed raring to start the day at 4am, but leave them exhausted by 4pm. Until recently, insomnia was considered a purely psychological complaint triggered by stress, grief, or sleep disruption as a result of shift work or jet lag.

But doctors are now unravelling the genetic explanation of why at least one-third of us have intermittent or constant sleep problems. Even so, it’s already thought there could be six or more different types of insomnia linked to genes. This means it will be possible to develop drugs to block the effect of the chemical signals they produce.

(Source: Daily Mail)

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Aug. 20, 2012 by Quinn Eastman

People with Parkinson’s disease performed markedly better on a test of working memory after a night’s sleep, and sleep disorders can interfere with that benefit, researchers have shown.

The ability of sleep to improve scores on a test of working memory specifically depends on how much slow wave sleep Parkinson’s patients obtain, researchers have found.

While the classic symptoms of Parkinson’s disease include tremors and slow movements, Parkinson’s can also affect someone’s memory, including “working memory.” Working memory is defined as the ability to temporarily store and manipulate information, rather than simply repeat it. The use of working memory is important in planning, problem solving and independent living.

The findings underline the importance of addressing sleep disorders in the care of patients with Parkinson’s, and indicate that working memory capacity in patients with Parkinson’s potentially can be improved with training. The results also have implications for the biology of sleep and memory.

The results were published this week in the journal Brain.

"It was known already that sleep is beneficial for memory, but here, we’ve been able to analyze what aspects of sleep are required for the improvements in working memory performance," says postdoctoral fellow Michael Scullin, who is the first author of the paper. The senior author is Donald Bliwise, professor of neurology at Emory University School of Medicine.

The performance boost from sleep was linked with the amount of slow wave sleep, or the deepest stage of sleep. Several research groups have reported that slow wave sleep is important for synaptic plasticity, the ability of brain cells to reorganize and make new connections.

Sleep apnea, the disruption of sleep caused by obstruction of the airway, interfered with sleep’s effects on memory. Study participants who showed signs of sleep apnea, if it was severe enough to lower their blood oxygen levels for more than five minutes, did not see a working memory test boost.

In this study, participants took a “digit span test,” in which they had to repeat a list of numbers forward and backward. The test was conducted in an escalating fashion: the list grows incrementally until someone makes a mistake. Participants took the digit span test eight times during a 48-hour period, four during the first day and four during the second. In between, they slept.

Repeating numbers in the original order is a test of short-term memory, while repeating the numbers in reverse order is a test of working memory.

"Repeating the list in reverse order requires some effort to manipulate the numbers, not just spit them back out again," Scullin says. "It’s also a purely verbal test, which is important when working with a population that may have motor impairments."

54 study participants had Parkinson’s disease, and 10 had dementia with Lewy bodies: a more advanced condition, where patients may have hallucinations or fluctuating cognition as well as motor symptoms. Those who had dementia with Lewy bodies saw no working memory boost from the night’s rest. As expected, their  baseline level of performance was lower than the Parkinson’s group.

Participants with Parkinson’s who were taking dopamine-enhancing medications saw their performance on the digit span test jump up between the fourth and fifth test. On average, they could remember one more number backwards. The ability to repeat numbers backward improved, even though the ability to repeat numbers forward did not.

Patients needed to be taking dopamine-enhancing medications to see the most performance benefit from sleep. Patients not taking dopamine medications, even though they had generally had Parkinson’s for less time, did not experience as much of a performance benefit. This may reflect a role for dopamine, an important neurotransmitter, in memory.

Scullin and Bliwise are planning an expanded study of sleep and working memory, in healthy elderly people as well as patients with neurodegenerative diseases.

"Many elderly people go through a decline in how much slow wave sleep they experience, and this may be a significant contributor to working memory difficulties," Scullin says.

Source: Emory