Too much or too little sleep may increase dementia risk

By Brian P. Dunleavy

Getting too much or too little sleep may increase the risk for cognitive decline, or dementia, in older adults, according to a study published Monday by JAMA Network Open.

In an analysis of the sleep habits of more than 20,000 English and Chinese adults age 48 to 75, people who slept for fewer than four hours or more than 10 hours per day showed evidence of declines in cognitive function, including memory and language comprehension, researchers said.

“This study is an observational study and cannot demonstrate a causal relationship,” study co-author Yanjun Ma told UPI, so the findings don’t necessarily prove that lack of sleep or excessive sleep causes a decline in cognitive function.

Observational studies are intended to assess only the effect of an intervention — in this case, sleep — on study participants, without trying to modify it to compare differences.

It’s possible that diminished or excessive sleep is an early sign of cognitive decline or dementia, as opposed to a risk factor, researchers said.

“Future mechanism studies, as well as intervention studies examining the association between sleep duration and cognitive decline are required,” said Ma, of the Peking University Clinical Research Institute in China.

As many as 6 million Americans have some form of dementia, and changes in sleep patterns are common, according to the Alzheimer’s Association.

To date, research has shown that sleep disturbances can result from cognitive impairment, while animal studies have found links between lack of sleep and increased levels of brain proteins that are thought to be signs for Alzheimer’s disease, said Dr. Yue Leng, who authored a commentary on the study findings.

Leng is an assistant professor of psychiatry at the University of California-San Francisco.

For their research, Ma and colleagues analyzed data on sleep behaviors and cognitive function in 20,065 adults from the English Longitudinal Study of Aging and the China Health and Retirement Longitudinal Study, and tracked them for about eight years, on average.

In addition to finding higher levels of cognitive decline among those who slept fewer than four or more than 10 hours per day, the researchers also observed that people with these sleep habits had “faster cognitive decline” than those who slept seven to nine hours per day, Ma said.

“It’s usually believed that sleep deprivation might lead to cognitive decline, but it’s unclear why too much sleep might be bad for cognitive health,” Leng added. “Older adults should pay more attention to their sleep habits, as these might have implications for their cognitive health.”

Why do we sleep? The answer may change right before we turn 3.

By Nicoletta Lanese

Humans spend about a third of our lives sleeping, and scientists have long debated why slumber takes up such a huge slice of our time. Now, a new study hints that our main reason for sleeping starts off as one thing, then changes at a surprisingly specific age.

Two leading theories as to why we sleep focus on the brain: One theory says that the brain uses sleep to reorganize the connections between its cells, building electrical networks that support our memory and ability to learn; the other theory says that the brain needs time to clean up the metabolic waste that accumulates throughout the day. Neuroscientists have quibbled over which of these functions is the main reason for sleep, but the new study reveals that the answer may be different for babies and adults.

In the study, published Sep. 18 in the journal Science Advances, researchers use a mathematical model to show that infants spend most of their sleeping hours in “deep sleep,” also known as random eye movement (REM) sleep, while their brains rapidly build new connections between cells and grow ever larger. Then, just before toddlers reach age 2-and-a-half, their amount of REM sleep dips dramatically as the brain switches into maintenance mode, mostly using sleep time for cleaning and repair.

“It was definitely shocking to us that this transition was so sharp,” from growth mode to maintenance mode, senior author Van Savage, a professor of ecology and evolutionary biology and of computational medicine at the University of California, Los Angeles and the Santa Fe Institute, told Live Science in an email. The researchers also collected data in other mammals — namely rabbits, rats and guinea pigs — and found that their sleep might undergo a similar transformation; however, it’s too soon to tell whether these patterns are consistent across many species.

That said, “I think in actuality, it may not be really so sharp” a transition, said Leila Tarokh, a neuroscientist and Group Leader at the University Hospital of Child and Adolescent Psychiatry and Psychotherapy at the University of Bern, who was not involved in the study. The pace of brain development varies widely between individuals, and the researchers had fairly “sparse” data points between the ages of 2 and 3, she said. If they studied individuals through time as they aged, they might find that the transition is less sudden and more smooth, or the age of transition may vary between individuals, she said.

An emerging hypothesis

In a previous study, published in 2007 in the journal Proceedings of the National Academy of Sciences, Savage and theoretical physicist Geoffrey West found that an animal’s brain size and brain metabolic rate accurately predict the amount of time the animal sleeps — more so than the animal’s overall body size. In general, big animals with big brains and low brain metabolic rates sleep less than small animals with the opposite features.

This rule holds up across different species and between members of the same species; for instance, mice sleep more than elephants, and newborn babies sleep more than adult humans. However, knowing that sleep time decreases as brains get bigger, the authors wondered how quickly that change occurs in different animals, and whether that relates to the function of sleep over time.

To begin answering these questions, the researchers pooled existing data on how much humans sleep, compiling several hundred data points from newborn babies and children up to age 15. They also gathered data on brain size and metabolic rate, the density of connections between brain cells, body size and metabolic rate, and the ratio of time spent in REM sleep versus non-REM sleep at different ages; the researchers drew these data points from more than 60 studies, overall.

Babies sleep about twice as much as adults, and they spend a larger proportion of their sleep time in REM, but there’s been a long-standing question as to what function that serves, Tarokh noted.

The study authors built a mathematical model to track all these shifting data points through time and see what patterns emerged between them. They found that the metabolic rate of the brain was high during infancy when the organ was building many new connections between cells, and this in turn correlated with more time spent in REM sleep. They concluded that the long hours of REM in infancy support rapid remodeling in the brain, as new networks form and babies pick up new skills. Then, between age 2 and 3, “the connections are not changing nearly as quickly,” and the amount of time spent in REM diminishes, Savage said.

At this time, the metabolic rate of cells in the cerebral cortex — the wrinkled surface of the brain — also changes. In infancy, the metabolic rate is proportional to the number of existing connections between brain cells plus the energy needed to fashion new connections in the network. As the rate of construction slows, the relative metabolic rate slows in turn.

“In the first few years of life, you see that the brain is making tons of new connections … it’s blossoming, and that’s why we see all those skills coming on,” Tarokh said. Developmental psychologists refer to this as a “critical period” of neuroplasticity — the ability of the brain to forge new connections between its cells. “It’s not that plasticity goes away” after that critical period, but the construction of new connections slows significantly, as the new mathematical model suggests, Tarokh said. At the same time, the ratio of non-REM to REM sleep increases, supporting the idea that non-REM is more important to brain maintenance than neuroplasticity.

Looking forward, the authors plan to apply their mathematical model of sleep to other animals, to see whether a similar switch from reorganization to repair occurs early in development, Savage said.

“Humans are known to be unusual in the amount of brain development that occurs after birth,” lead author Junyu Cao, an assistant professor in the Department of Information, Risk, and Operations Management at The University of Texas at Austin, told Live Science in an email. (Cao played a key role in compiling data and performing computations for the report.) “Therefore, it is conceivable that the phase transition described here for humans may occur earlier in other species, possibly even before birth.”

In terms of human sleep, Tarokh noted that different patterns of electrical activity, known as oscillations, occur in REM versus non-REM sleep; future studies could reveal whether and how particular oscillations shape the brain as we age, given that the amount of time spent in REM changes, she said. Theoretically, disruptions in these patterns could contribute to developmental disorders that emerge in infancy and early childhood, she added — but again, that’s just a hypothesis.

Poor Sleep Linked with Future Amyloid-β Build Up

by Abby Olena

There’s evidence in people and animals that short-term sleep deprivation can change the levels of amyloid-β, a peptide that can accumulate in the aging brain and cause Alzheimer’s disease. Scientists now show long-term consequences may also result from sustained poor sleep. In a study published September 3 in Current Biology, researchers found that healthy individuals with lower-quality sleep were more likely to have amyloid-β accumulation in the brain years later. The study could not say whether poor sleep caused amyloid-β accumulation or vice versa, but the authors say that sleep could be an indicator of present and future amyloid-β levels.

“Traditionally, sleep disruptions have been accepted as a symptom of Alzheimer’s disease,” says Ksenia Kastanenka, a neuroscientist at Massachusetts General Hospital who was not involved in the work. Her group showed in 2017 that improving sleep in a mouse model of Alzheimer’s disease, in which the animals’ slow wave sleep is disrupted as it usually is in people with the disease, halted disease progression.

Collectively, the results from these studies and others raise the possibility that “sleep rhythm disruptions are not an artifact of disease progression, but actually are active contributors, if not a cause,” she says, hinting at the prospect of using these sleep measures as a biomarker for Alzheimer’s disease.

As a graduate student at the University of California, Berkeley, Joseph Winer, who is now a postdoc at Stanford University, and his colleagues were interested in whether or not sleep could predict how the brain changes over time. They collaborated with the team behind the Berkeley Aging Cohort Study, which includes a group of 32 cognitively healthy adults averaging about 75 years of age. They participated in a sleep study, then had periodic cognitive assessments and between two and five positron emission tomography (PET) scans to check for the presence of amyloid-β in their brains for an average of about four years after the sleep study.

The researchers found at their baseline PET scan, which happened within six months of their sleep study, that 20 of the 32 participants already had some amyloid-β accumulation, which was not unexpected based on their average age. They also showed that both slow wave sleep, an indicator of depth of sleep, and sleep efficiency, the amount of time sleeping compared to time in bed, were both predictive of the rate of amyloid change several years later. In other words, people with lower levels of slow wave sleep and sleep efficiency were more likely to have faster amyloid build up.

The subjects all remained cognitively healthy over the duration of the study, says Winer. “We do expect that they’re at higher risk for developing Alzheimer’s in their lifetime because of the amyloid plaque.”

The strengths of the study include the well-characterized participants with detailed sleep assessments, as well as cognitive testing and longitudinal amyloid PET imaging, says Brendan Lucey, a sleep neurologist at Washington University in St. Louis who did not participate in the work.

There are still open questions about the link between sleep and amyloid deposition over time. “Amyloid accumulation on PET increases at different rates in amyloid-negative and amyloid-positive individuals, and even within amyloid-positive individuals,” Lucey explains. “Without adjusting for participants’ starting amyloid [levels], we don’t know if some participants would have been more likely to have increased amyloid compared to others, independent of sleep.”

“It is very hard to untangle this question of baselines,” acknowledges Winer. Because the sleep measures the team identified in the study are related to amyloid levels, to actually tease apart the effect of sleep quality on amyloid deposition and vice versa, it’d be necessary to study people starting as early as their fifties, when they’re much less likely to have amyloid accumulation, he says.

This study is “a great start,” David Holtzman, a neurologist and collaborator of Lucey at Washington University in St. Louis who did not participate in the work, tells The Scientist. In addition to controlling for the amount of amyloid deposition that is present in a subject’s brain at the beginning of the study, it would be important to see if the findings bear out in larger numbers of people and what role genetic factors play.

“The most important question down the road is to test the idea in some sort of a treatment paradigm,” Holtzman adds. “You can do something to improve the quality of sleep or increase slow wave sleep, and then determine if it actually slows down the onset of Alzheimer’s disease clinically.”

J.R. Winer et al., “Sleep disturbance forecasts β-amyloid accumulation across subsequent years,” Current Biology, doi:10.1016/j.cub.2020.08.017, 2020.–8BBfH3OsENS0A5GHEfhRVVh3ox2uWli04iEz1JAIpGp_Zeq9dMKwhb5f5X1AeB01d4d07al4rDaOWz_GzA5Ax6TXrGQ&utm_content=95303853&utm_source=hs_email

Children with less sleep experience increased depression and anxiety, and decreased cognitive performance

Shorter sleep duration among children was associated with increased risk for depression, anxiety, impulsive behavior and poor cognitive performance, according to study findings published in Molecular Psychiatry.

“Sleep disturbances are common among children and adolescents around the world, with approximately 60% of adolescents in the United States receiving less than 8 hours of sleep on school nights,” Jianfeng Feng, PhD, of the department of computer science at University of Warwick in the UK, told Healio Psychiatry. “An important public health implication is that psychopathology in both children and their parents should be considered in relation to sleep problems in children. Further, we showed that brain structure is associated with sleep problems in children and that this is related to whether the child has depressive problems.”

According to Feng and colleagues, the present study is the first large-scale research effort to analyze sleep duration in children and its impact on psychiatric problems including depression, brain structure and cognition. They analyzed measures related to these areas using data from the Adolescent Brain Cognitive Development Study, which included structural MRI data from 11,067 individuals aged 9 to 11 years.

The researchers found that depression, anxiety and impulsive behavior were negatively correlated with sleep duration. Dimensional psychopathology in participants’ parents was correlated with short sleep duration in the children. Feng and colleagues noted that the orbitofrontal cortex, prefrontal and temporal cortex, precuneus and supramarginal gyrus were brain areas in which higher volume was correlated with longer sleep duration. According to longitudinal data analysis, psychiatric problems, particularly depressive problems, were significantly associated with short sleep duration 1 year later. Moreover, they found that depressive problems significantly mediated these brain regions’ effect on sleep. Higher volume of the prefrontal cortex, temporal cortex and medial orbitofrontal cortex were associated with higher cognitive scores.

“Our findings showed that 53% of children received less than 9 hours of sleep per night,” Feng said. “More importantly, the behavior problems total score for children with less than 7 hours of sleep was 53% higher on average and the cognitive total score was 7.8% lower on average than for children with 9 to 11 hours of sleep. We hope this study attracts public attention to sleep problems in children and provides evidence for governments to develop advice about sleep for children.” – by Joe Gramigna

Scientists Now Know How Sleep Cleans Toxins From the Brain

Laura Lewis and her team of researchers have been putting in late nights in their Boston University lab. Lewis ran tests until around 3:00 in the morning, then ended up sleeping in the next day. It was like she had jet lag, she says, without changing time zones. It’s not that Lewis doesn’t appreciate the merits of a good night’s sleep. She does. But when you’re trying to map what’s happening in a slumbering human’s brain, you end up making some sacrifices. “It’s this great irony of sleep research,” she says. “You’re constrained by when people sleep.”

Her results, published last week in the journal Science, show how our bodies clear toxins out of our brains while we sleep and could open new avenues for treating and preventing neurodegenerative diseases like Alzheimer’s.

When we sleep our brains travel through several phases, from a light slumber to a deep sleep that feels like we’ve fallen unconscious, to rapid eye movement (REM) sleep, when we’re more likely to have dreams. Lewis’ work looks at non-REM sleep, that deep phase which generally happens earlier in the night and which has already been associated with memory retention. One important 2013 study on mice showed that while the rodents slept, toxins like beta amyloid, which can contribute to Alzheimer’s disease, got swept away.

Lewis was curious how those toxins were cleared out and why that process only happened during sleep. She suspected that cerebrospinal fluid, a clear, water-like liquid that flows around the brain, might be involved. But she wasn’t sure what was unique about sleep. So her lab designed a study that measured several different variables at the same time.

Study participants had to lie down and fall asleep inside an MRI machine. To get realistic sleep cycles, the researchers had to run the tests at midnight, and they even asked subjects to stay up late the night before so people would be primed to drift off once the test began.

Lewis outfitted the participants with an EEG cap so she could look at the electrical currents flowing through their brains. Those currents showed her which stage of sleep the person was in. Meanwhile, the MRI measured the blood oxygen levels in their brains and showed how much cerebrospinal fluid was flowing in and out of the brain. “We had a sense each of these metrics was important, but how they change during sleep and how they relate to each other during sleep was uncharted territory for us,” she says.

What she discovered was that during non-REM sleep, large, slow waves of cerebrospinal fluid were washing over the brain. The EEG readings helped show why. During non-REM sleep, neurons start to synchronize, turning on and off at the same time. “First you would see this electrical wave where all the neurons would go quiet,” says Lewis. Because the neurons had all momentarily stopped firing, they didn’t need as much oxygen. That meant less blood would flow to the brain. But Lewis’s team also observed that cerebrospinal fluid would then rush in, filling in the space left behind.

“It’s a fantastic paper,” says Maiken Nedergaard, a neuroscientist at the University of Rochester who led the 2013 study that first described how sleep can clear out toxins in mice. “I don’t think anybody in their wildest fantasy has really shown that the brain’s electrical activity is moving fluid. So that’s really exciting.”

One big contribution of the paper is it helps show that the systems Nedergaard has been studying in mice are present and hugely important for humans too. “It’s telling you sleep is not just to relax,” says Nedergaard. “Sleep is actually a very distinct function.” Neurons don’t all turn off at the same time when we’re awake. So brain blood levels don’t drop enough to allow substantial waves of cerebrospinal fluid to circulate around the brain and clear out all the metabolic byproducts that accumulate, like beta amyloid.

The study also could have clinical applications for treating Alzheimer’s. Recent attempts at developing medications have targeted beta amyloid. But drugs that looked promising at first all failed once they got into clinical trials. “This opens a new avenue,” says Nedergaard. Instead of trying to act on one particular molecule, new interventions might instead focus on increasing the amount of cerebrospinal fluid that washes over the brain.

That would help clear out beta amyloid but also could help with other molecules like tau, a protein that gets tangled in Alzheimer’s patients’ brains and harms the connections between neurons. Finding a way to clear out all of that garbage could be much more powerful than just focusing on one piece of the problem. “Aging is not just about one molecule,” says Nedergaard. “Everything fails.”

These discoveries bring along their own set of questions. Lewis didn’t study what happens during other stages of sleep, and she only looked at healthy young adults. But the methods she used were entirely noninvasive—or as noninvasive as having people sleep in an MRI while hooked up to lots of machines can be. She didn’t even inject any dye. That will make it easier to start studying older participants who may be developing neurodegenerative diseases.

Alzheimer’s Directly Kills Brain Cells That Keep You Awake

Brain tissue from deceased patients with Alzheimer’s has more tau protein buildup (brown spots) and fewer neurons (red spots) as compared to healthy brain tissue.

By Yasemin Saplakoglu

Alzheimer’s disease might be attacking the brain cells responsible for keeping people awake, resulting in daytime napping, according to a new study.

Excessive daytime napping might thus be considered an early symptom of Alzheimer’s disease, according to a statement from the University of California, San Francisco (UCSF).

Some previous studies suggested that such sleepiness in patients with Alzheimer’s results directly from poor nighttime sleep due to the disease, while others have suggested that sleep problems might cause the disease to progress. The new study suggests a more direct biological pathway between Alzheimer’s disease and daytime sleepiness.

In the current study, researchers studied the brains of 13 people who’d had Alzheimer’s and died, as well as the brains from seven people who had not had the disease. The researchers specifically examined three parts of the brain that are involved in keeping us awake: the locus coeruleus, the lateral hypothalamic area and the tuberomammillary nucleus. These three parts of the brain work together in a network to keep us awake during the day.

The researchers compared the number of neurons, or brain cells, in these regions in the healthy and diseased brains. They also measured the level of a telltale sign of Alzheimer’s: tau proteins. These proteins build up in the brains of patients with Alzheimer’s and are thought to slowly destroy brain cells and the connections between them.

The brains from patients who had Alzheimer’s in this study had significant levels of tau tangles in these three brain regions, compared to the brains from people without the disease. What’s more, in these three brain regions, people with Alzheimer’s had lost up to 75% of their neurons.

“It’s remarkable because it’s not just a single brain nucleus that’s degenerating, but the whole wakefulness-promoting network,” lead author Jun Oh, a research associate at UCSF, said in the statement. “This means that the brain has no way to compensate, because all of these functionally related cell types are being destroyed at the same time.”

The researchers also compared the brains from people with Alzheimer’s with tissue samples from seven people who had two other forms of dementia caused by the accumulation of tau: progressive supranuclear palsy and corticobasal disease. Results showed that despite the buildup of tau, these brains did not show damage to the neurons that promote wakefulness.

“It seems that the wakefulness-promoting network is particularly vulnerable in Alzheimer’s disease,” Oh said in the statement. “Understanding why this is the case is something we need to follow up in future research.”

Though amyloid proteins, and the plaques that they form, have been the major target in several clinical trials of potential Alzheimer’s treatments, increasing evidence suggests that tau proteins play a more direct role in promoting symptoms of the disease, according to the statement.

The new findings suggest that “we need to be much more focused on understanding the early stages of tau accumulation in these brain areas in our ongoing search for Alzheimer’s treatments,” senior author Dr. Lea Grinberg, an associate professor of neurology and pathology at the UCSF Memory and Aging Center, said in the statement.

The findings were published Monday (Aug. 12) in Alzheimer’s & Dementia: The Journal of the Alzheimer’s Association.

Checking Your Phone at Night Won’t Necessarily Throw Off Your Internal Clock, Mouse Study Finds

by Ed Cara

People who only occasionally fall down an internet rabbit hole on their smartphones late at night might be able to rest easier—at least according to the results of a new study in mice. Researchers found that short bursts of light exposure at night won’t necessarily disrupt your internal clock, including sleep habits.

The researchers used mice to study the circadian rhythm. In both mice and humans, the circadian rhythm is primarily controlled by the brain’s suprachiasmatic nucleus (SCN), a tiny region found in the hypothalamus. One crucial aspect of the SCN involves regulating our sleep/wake, or light/dark, cycle. It’s long been thought that any kind of light exposure our eyes take in affects the SCN, and thus, can affect our sleep.

“Light information comes into the SCN, and that’s what synchronizes all of the body’s clocks to the light/dark cycle,” said lead author Tiffany Schmidt, a neurogeneticist at Northwestern, in a release from the university. “This one master pacemaker makes sure everything is in sync.”

Schmidt and her team wanted to test this long-held theory that the SCN responds to any light exposure. So they bred mice that had light-sensitive nerve cells in the retina that were only capable of communicating with the SCN. Then they exposed these mice to light for short periods of time.

Because mice, unlike people, are nocturnal, the light should have made them want to fall asleep. But they instead just carried out on with their day, sleeping and waking as normal. Their body temperature, which fluctuates predictably before, during, and after sleep, also followed the same pattern seen in mice with normal circadian rhythms.

What this could mean, according to the authors, is that our brains respond to acute light—meaning brief exposures to light—through a different neural pathway than what’s used for long periods of light exposure, a pathway that doesn’t involve the SCN.

“If these two effects—acute and long-term light exposure—were driven through the same pathway, then every minor light exposure would run the risk of completely shifting our body’s circadian rhythms,” Schmidt said.

The findings will be published this week in the journal eLife.

Mice and their brains aren’t a perfect proxy for people, obviously. And even if the same general principle does apply to us, Schmidt and her team say there’s no clear lead on where these other pathways could exist in the brain. And there’s undoubtedly a point where being exposed to light late at night too long or too often can start to affect our internal clock—even if where that point lies is still a mystery right now. There needs to be a lot much research studying these questions and others.

What is clear, the authors cautioned, is that chronic nighttime light exposure, and the disruptions to our sleep it can cause, can be very bad for health. In other words, don’t use this study as an excuse to start regularly binge-watching Netflix till 4 a.m.

“Light at the wrong time of day is now recognized as a carcinogen,” Schmidt said. “We want people to feel alert while they are exposed to light without getting the health risks that are associated with shifted circadian rhythms, such as diabetes, depression and even cancer.”

The “Price of Wakefulness” Is High, Says DNA Study Revealing Why We Sleep

Birds do it, bees do it, even educated fleas do it: No, they don’t fall in love, they sleep. However, exactly why all animals with a nervous system evolved to sleep has been a longstanding scientific mystery. Slumber certainly feels great, but it doesn’t exactly make sense — why should we spend a third of our lives passed out?

In a study published Tuesday in Nature Communications, scientists say they’ve figured out why on the cellular level. The core cellular function of sleep, they explain, is to combat the neuronal DNA damage that accumulates during waking hours. Sleep allows neurons to perform the efficient DNA maintenance that’s essential to a healthy life: Scientists already know that less sleep means greater vulnerability to anxiety, frustration, and ill health, but now they’re closer to understanding exactly why that’s the case.

“We’ve found a causal link between sleep, chromosome dynamics, neuronal activity, and DNA damage and repair with direct physiological relevance to the entire organism,” study lead Lior Appelbaum, Ph.D., said Tuesday. “Sleep gives an opportunity to reduce DNA damage accumulated in the brain during wakefulness.”

Applebaum and his team examined how sleep is linked to nuclear maintenance by examining one of the most frequently used model organisms for genetic and developmental studies: the zebrafish. These transparent zebrafish were genetically engineered so that the chromosomes in their neurons carried colorful chemical tags. While the fish were awake and asleep, the scientists observed the movement of DNA and nuclear proteins inside the fish with a high-resolution microscope, which can be seen in the video above.

They witnessed that when the fish were awake, the chromosomes were relatively inactive, and broken strands of DNA accumulated in the neurons. However, when the fish were asleep the chromosomes became more active, and the DNA damage that had accumulated began to be repaired. Subsequent analysis confirmed that in order to perform nuclear maintenance, single neurons need an animal to go to sleep.

The accumulation of DNA damage, says Appelbaum, is the “price of wakefulness.” During wakefulness, chromosomes are less active, leaving them vulnerable to DNA damage caused by radiation, oxidative stress, and neuronal activity. Sleep kickstarts chromosomal activity and synchronizes nuclear maintenance within individual neurons, allowing the brain to be repaired while it’s not being used to the extent that it is during the day.

“It’s like potholes in the road,” Applebaum says. “Roads accumulate wear and tear, especially during daytime rush hours, and it is most convenient and efficient to fix them at night, when there is light traffic.”

Anecdotally, we know that a good night’s sleep can be restorative. Now it appears that it’s quantifiably restorative for the brain as well, allowing it to naturally mend the damage of the day.


Sleep is essential to all animals with a nervous system. Nevertheless, the core cellular function of sleep is unknown, and there is no conserved molecular marker to define sleep across phylogeny. Time-lapse imaging of chromosomal markers in single cells of live zebrafish revealed that sleep increases chromosome dynamics in individual neurons but not in two other cell types. Manipulation of sleep, chromosome dynamics, neuronal activity, and DNA double-strand breaks (DSBs) showed that chromosome dynamics are low and the number of DSBs accumulates during wakefulness. In turn, sleep increases chromosome dynamics, which are necessary to reduce the amount of DSBs. These results establish chromosome dynamics as a potential marker to define single sleeping cells, and propose that the restorative function of sleep is nuclear maintenance.

A protein in skeletal muscles helps mice recover from sleep deprivation.



The protein Bmal1, which helps regulate the body’s internal clock, is found in especially high levels in the brain and in skeletal muscles. Mice completely deficient in Bmal1 were known to suffer from sleep impairments, but the specifics at play weren’t clear. At the University of California, Los Angeles, Ketema Paul and colleagues looked to these mice for clues about the role Bmal1 plays in sleep regulation.

When Paul’s team restored levels of the Bmal1 protein in the mice’s brains, their ability to rebound from a night of bad sleep remained poor. However, turning on production in skeletal muscles alone enabled mice to sleep longer and more deeply to recover after sleep loss.

For decades, scientists have thought sleep was controlled purely by the brain. But the new study indicates the ability to catch up on one’s sleep after a bout of sleeplessness is locked away in skeletal muscles, not the brain—at least for mice. “I think it’s a real paradigm shift for how we think about sleep,” says John Hogenesch, a chronobiologist at Cincinnati Children’s Hospital Medical Center who discovered the Bmal1 gene but was not involved in this study.

Paul’s group also found that having too much of the Bmal1 protein in their muscles not only made mice vigilant but also invulnerable to the effects of sleep loss, so that they remained alert even when sleep-deprived and slept fewer hours to regain lost sleep. “To me, that presents a potential target where you could treat sleep disorders,” says Paul, noting that an inability to recover from sleep loss can make us more susceptible to diseases.

The paper
J.C. Ehlen et al., “Bmal1 function in skeletal muscle regulates sleep,” eLife, 6:e26557, 2017.–EaFM3BB6i_l04LL2zbvjlEHCWVwrSrks2D9Aksml-wGa9f88gfOwPhtiPCXEMJRqzu6WG53_vzEvHht0oAGylLgMANQ&_hsmi=66141129

Growing number of McSleepers in Hong Kong

he number of people sleeping in McDonald’s outlets has increased six-fold over the past five years, a trend partly driven by rising rents and substandard housing that makes life especially unbearable in the city’s baking weather, a study has found.

The survey, organised by Junior Chamber International’s Tai Ping Shan branch and conducted in June by volunteers, found 334 people had slept in a McDonald’s outlet nightly over at least the past three months. Of the 110 branches that operate 24 hours in the city, 84 had seen overnight sleepers.

This is a six-fold increase from a similar study in 2013, which found only 57 such people, popularly dubbed McRefugees or McSleepers.

A branch in Tsuen Wan hosted more than 30 sleepers, the highest among all branches, according to the latest study.

Researchers were able to interview 53 McRefugees aged between 19 and 79 in depth, and found 57 per cent of them had a job and 71 per cent of them had flats that they rented or owned, contrary to the common belief that these people tended to be jobless and homeless.

Saving on air conditioning costs, as well as comfort and security, topped a list of reasons given by these interviewees, followed by high rents, conflict with family members, the ability to develop social relations at the chain and substandard housing.

Other reasons included saving on transport costs and time to work, and seeking temporary shelter while waiting for low-rent public housing.

“Family is the basic unit in a society,” Tai Ping Shan publication commission chairwoman Jennifer Hung Sin-yu said. “Even one person who has a home but cannot return is too many. This phenomenon is worth our attention.”

Hung said the reasons given by interviewees showed that unaffordable housing had forced the poor into inferior living conditions such as subdivided flats, which subsequently drove them into McDonald’s for comfort and security.

One McRefugee renting a subdivided flat in To Kwa Wan, Hung said, told volunteers that her landlord charged her HK$16 for a unit of electricity, compared to about HK$1.10 charged by the city’s two main power suppliers.

Hung said the woman’s flat did not have any windows, which made the city’s humid and hot summer even more unbearable without air conditioning.

“She told us sometimes she couldn’t even feel the flow of the air,” Hung said.

Hong Kong is consistently ranked the world’s least affordable property market. As of the end of March, there were 270,000 applicants on the waiting list for public rental housing; the average waiting time for families or single elderly applicants was five years and one month.

Subdivided housing is the main option for these families while they wait, but it is affordable only because of the small sizes – often around 100 sq ft – of these units, which entail fire risks, poor ventilation and poor hygiene.

Besides inadequate housing, family problems are another main issue, Hung said.

One of the cases, a 19-year-old referred to in the study as Ah Lung, was a construction worker who ate, played mobile phone games and slept at a McDonald’s branch in Mong Kok. He did not want to go home due to a bad relationship with his parents, while his income enabled him to live away from home.

A 60-year-old woman was observed by volunteers as “without the unique characteristics of street sleepers”. She was well dressed, with her diamond wedding ring still on her finger. She also had a flat in the New Territories, but had nobody to share the home with her.

She and her late husband did not have any children and she felt lonely in her home and eating by herself, which was why she spent most of her time at the fast-food chain, where there were many people coming and going.

Project consultant Lee Ho-ey said the government should allocate more resources to non-governmental organisations to reach out to McRefugees, providing them with counselling and help.

Thanks to Kebmodee for bringing this to the It’s Interesting community.