Sleep Reinforces Learning: Children’s Brains Transform Subconsciously

During sleep, our brains store what we have learned during the day a process even more effective in children than in adults. 

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During sleep, our brains store what we have learned during the day ‒ a process even more effective in children than in adults, new research shows.

It is important for children to get enough sleep. Children's brains transform subconsciously learned material into active knowledge while they sleep -- even more effectively than adult brains do, according to a study by Dr. Ines Wilhelm of the University of Tübingen's Institute for Medical Psychology and Behavioral Neurobiology. Dr Wilhelm and her Swiss and German colleagues have published their results in Nature Neuroscience.

Studies of adults have shown that sleeping after learning supports the long-term storage of the material learned, says Dr Wilhelm. During sleep, memory is turned into a form that makes future learning easier; implicit knowledge becomes explicit and therefore becomes more easily transferred to other areas.

Children sleep longer and deeper, and they must take on enormous amounts of information every day. In the current study, the researchers examined the ability to form explicit knowledge via an implicitly-learned motor task.

Children between 8 and 11, and young adults, learned to guess the predetermined series of actions -- without being aware of the existence of the series itself. Following a night of sleep or a day awake, the subjects' memories were tested.

The result: after a night's sleep, both age groups could remember a larger number of elements from the row of numbers than those who had remained awake in the interim. And the children were much better at it than the adults.

"In children, much more efficient explicit knowledge is generated during sleep from a previously learned implicit task, says Wilhelm. And the children's extraordinary ability is linked with the large amount of deep sleep they get at night.

"The formation of explicit knowledge appears to be a very specific ability of childhood sleep, since children typically benefit as much or less than adults from sleep when it comes to other types of memory tasks."

The Human body's Circadian biological clock: Scientists redraw the blueprint

The discovery of a major gear in the biological clock that tells the body when to sleep and metabolize food may lead to new drugs to treat sleep problems and metabolic disorders, including diabetes.

Scientists at the Salk Institute for Biological Studies, led by Ronald M. Evans, a professor in Salk's Gene Expression Laboratory, showed that two cellular switches found on the nucleus of mouse cells, known as REV-ERBα and REV-ERBβ, are essential for maintaining normal sleeping and eating cycles and for metabolism of nutrients from food.

The findings, reported March 29 in Nature, describe a powerful link between circadian rhythms and metabolism and suggest a new avenue for treating disorders of both systems, including jet lag, sleep disorders, obesity and diabetes.

"This fundamentally changes our knowledge about the workings of the circadian clock and how it orchestrates our sleep-wake cycles, when we eat and even the times our bodies metabolize nutrients," says Evans.

"Nuclear receptors can be targeted with drugs, which suggests we might be able to target REV-ERBα and β to treat disorders of sleep and metabolism."

Nurses, emergency personnel and others who work shifts that alter the normal 24-hour cycle of waking and sleeping are at much higher risk for a number of diseases, including metabolic disorders such as diabetes.

To address this, scientists are trying to understand precisely how the biological clock works and uncover possible targets for drugs that could adjust the circadian rhythm in people with sleep disorders and circadian-associated metabolic disorders.

In mammals, the circadian timing system is orchestrated by a central clock in the brain and subsidiary clocks in most other organs.

The master clock in the brain is set by light and determines the overall diurnal or nocturnal preference of an animal, including sleep-wake cycles and feeding behaviour.

Scientists knew that two genes, BMAL1 and CLOCK, worked together at the core of the clock's molecular machinery to activate the network of circadian genes.

In this way, BMAL1 acts like the accelerator on a car, activating genes to rev up our physiology each morning so that we are alert, hungry and physically active.

Prior to this work REV-ERBα and β were thought to play only a minor role in these cycles, possibly working together to slow CLOCK-BMAL1 activity to make minor adjustments to keep the clock running on time.

However, genetic studies of two genes with similar functions can be very difficult and thus the real importance of REV-ERBα and β remained mysterious.

The Salk scientists got around this hurdle by developing mice in which both genes could be turned off in the liver at any point by giving them an estrogen derivative called tamoxifen.

Now mice could develop normally to adulthood, at which point the scientists could turn off REV-ERBα and REV-ERBβ in their livers, an organ crucial to maintaining the correct balance of sugar and fat in blood, to see what effects it had on circadian rhythms and metabolism.

"When we turned off both receptors, the animal's biological clocks went haywire," says Han Cho, first author on the paper and a postdoctoral researcher in Evan's Salk laboratory.

"The mice started running on their exercise wheels when they should have been resting. This suggested REV-ERBα and REV-ERBβ aren't an auxiliary system that makes minor adjustments, but an integral part of the clock's core mechanism. Without them, the clock can't function properly."

Digging more deeply into the clockworks, the Salk scientists mapped out the genes that the REV-ERBs control to keep the body operating on the right schedule, finding that they overlap with hundreds of the same genes controlled by CLOCK and BMAL1.

This and other findings suggested that the REV-ERBs, act as a break on the genes BMAL1 activates.

"We thought that the core of the clock was an accelerator, and that all REV-ERBα and REV-ERBβ did was to pull the foot off that pedal," says Evans.

"What we've shown is that these receptors act directly as a break to slow clock activity. Now we've got a accelerator and a break, each equally important in creating the daily rhythm of the clock."

The scientists also found that the REV-ERBs control the activity of hundreds of genes involved metabolism, including those responsible for controlling levels of fats and bile.

The mice in which REV-ERBα and REV-ERBβ were turned off had high levels of fat and sugar in their blood, common problems in people with metabolic disorders.

"This explains how our cellular metabolism is tied to daylight cycles determined by the movements of the sun and the earth," says Satchidananda Panda, an associate professor in Salk's Regulatory Biology Laboratory and co-author on the paper.

"Now we want to find ways of leveraging this mechanism to fix a person's metabolic rhythms when they are disrupted by travel, shift work or sleep disorders."

Provided by Salk Institute

Genetic study links body clock receptor to diabetes

A study published in Nature Genetics today has found new evidence for a link between the body clock hormone melatonin and type 2 diabetes.

The study found that people who carry rare genetic mutations in the receptor for melatonin have a much higher risk of type 2 diabetes.

The findings should help scientists to more accurately assess personal diabetes risk and could lead to the development of personalised treatments.

Previous research has found that people who work night shifts have a higher risk of type 2 diabetes and heart disease. Studies have also found that if volunteers have their sleep disrupted repeatedly for three days, they temporarily develop symptoms of diabetes.

The body's sleep-wake cycle is controlled by the hormone melatonin, which has effects including drowsiness and lowering body temperature.

In 2008, a genetic study led by Imperial College London discovered that people with common variations in the gene for MT2, a receptor for melatonin, have a slightly higher risk of type 2 diabetes.

The new study reveals that carrying any of four rare mutations in the MT2 gene increases a person's risk of developing type 2 diabetes six times.

The release of insulin, which regulates blood sugar levels, is known to be regulated by melatonin. The researchers suggest that mutations in the MT2 gene may disrupt the link between the body clock and insulin release, leading to abnormal control of blood sugar.


Professor Philippe Froguel, from the School of Public Health at Imperial College London, who led the study, said: "Blood sugar control is one of the many processes regulated by the body's biological clock.

This study adds to our understanding of how the gene that carries the blueprint for a key component in the clock can influence people's risk of diabetes.

"We found very rare variants of the MT2 gene that have a much larger effect than more common variants discovered before. Although each mutation is rare, they are common in the sense that everyone has a lot of very rare mutations in their DNA. Cataloguing these mutations will enable us to much more accurately assess a person's risk of disease based on their genetics."

In the study, the Imperial team and their collaborators at several institutions in the UK and France examined the MT2 gene in 7,632 people to look for more unusual variants that have a bigger effect on disease risk.

They found 40 variants associated with type 2 diabetes, four of which were very rare and rendered the receptor completely incapable of responding to melatonin. The scientists then confirmed the link with these four variants in an additional sample of 11,854 people.

Professor Froguel and his team analysed each mutation by testing what effect they have on the MT2 receptor in human cells in the lab. The mutations that completely prevented the receptor from working proved to have a very big effect on diabetes risk, suggesting that there is a direct link between MT2 and the disease.

More information: A. Bonnefond et al. 'Rare MTNR1B variants impairing melatonin receptor 1B function contribute to type 2 diabetes' Nature Genetics, published online 29 January 2012.

UFO Alien Encounters are Only Dreams?

American researchers are claiming that supposed human encounters with aliens and unidentified flying objects (UFO) may just be dreams based on results of a sleep experiment.

The researchers from the Out-Of-Body Experience Research Center in Los Angeles made the findings after subjecting 20 volunteers to out-of-body experiences when they are half-awake at night and asking them to meet aliens during that dream-like state.

Out of those volunteers, more than half were able to achieve out-of-body experiences with seven or 35 percent dreaming of alien or UFO encounters at their home as instructed, according to lead researcher Michael Raduga.

Raduga has a theory that people claiming to encounter aliens or see UFOs are just dreaming, so he conducted the study to prove it.

"When people experience alien abductions in the night, they usually don't know they are actually in REM sleep and having an out-of-body experience," Raduga told Life's Little Mysteries.

The volunteers had varying response to the instructions. Raduga said there were some who needed more attempts to separate from their sleeping bodies while others failed to do so out of fear.

There were also some who never proceeded to looking for aliens while dreaming also due to fear.

Those who encountered aliens described their dreams to the researchers. One described the aliens as resembling the creatures from the movie "The Thing."

The volunteered told Raduga the three aliens that appeared before him scared him so much that he regained consciousness.

The Cause and Effect of Headaches?

Lack of sleep linked to Alzheimer's disease

Lack of sleep linked to Alzheimer's - health - 24 September 2009 - New Scientist

A lack of sleep could help toxic plaques develop in the brain, accelerating the progression of Alzheimer's disease.

David Holtzman looked at how sleep affected the levels of beta-amyloid protein in mice and humans. This protein causes plaques to build up in the brain, which some think cause Alzheimer's disease by killing cells.

Holtzman's group found that beta-amyloid levels were higher in mouse brains when the mice were awake than when they were sleeping.

Lack of sleep also had an effect on plaque levels: when the mice were sleep-deprived – forced to stay awake for 20 hours of the day – they developed more plaques in their brains.
Sleep therapy

Holtzman also tried sending the mice to sleep with a drug that is being trialled for insomnia, called Almorexant. This reduced the amount of plaque-forming protein.

He suggests that sleeping for longer could limit the formation of plaques, and perhaps block it altogether.

The group also measured levels of beta-amyloid in the cerebrospinal fluid of 10 healthy men, both at night and during the day. Levels were lower at night, suggesting that sleep might also help keep levels of the plaque protein low in humans.

Holtzman reckons that when we're awake, our brains are more active, and that this may cause us to produce more beta-amyloid protein.