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Discussed in the web-based article is the direct link between beta amyloid and Alzheimers. Mice are again the testing experiment, and it proves how vital sleep is to clear the brain of the  harmful waste. The writer even talks about genetically modifying the mice, would this help humans as well?... Our discovery suggests that Alzheimer’s disease starts to manifest long before plaque formation becomes evident,

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Norbert von der Groeben

Carla Shatz led a study that suggests Alzheimer's disease may begin to manifest long before the development of placques that lead to nerve cell death.

Scientists at the Stanford University School of Medicine have shown how a protein fragment known as beta-amyloid, strongly implicated in Alzheimer's disease, begins destroying synapses before it clumps into plaques that lead to nerve cell death.

Key features of Alzheimer's, which affects about 5 million Americans, are wholesale loss of synapses - contact points via which nerve cells relay signals to one another - and a parallel deterioration in brain function, notably in the ability to remember.

"Our discovery suggests that Alzheimer's disease starts to manifest long before plaque formation becomes evident," said Carla Shatz, PhD, professor of neurobiology and of biology and senior author of the study, published Sept. 20 in
Investigators at Harvard University also contributed to the study. The research, conducted in mice and in human brain tissue, may help to explain the failures in recent years of large-scale clinical trials attempting to slow the progression of Alzheimer's by pharmacologically ridding the brain of amyloid plaques. It may also point the way to better treatments at earlier stages of the disease.

Beta-amyloid begins life as a solitary molecule but tends to bunch up - initially into small clusters that are still soluble and can travel freely in the brain, and finally into the plaques that are hallmarks of Alzheimer's. The study showed for the first time that in this clustered form, beta-amyloid can bind strongly to a receptor on nerve cells, setting in motion an intercellular process that erodes their synapses with other nerve cells.

Synapses are the connections between nerve cells. They are essential to storing memories, processing thoughts and emotions, and planning and ordering how we move our bodies. The relative strength of these connections, moreover, can change in response to new experiences.

Using an experimental mouse strain that is highly susceptible to the synaptic and cognitive impairments of Alzheimer's disease, Shatz and her colleagues showed that if these mice lacked a surface protein ordinarily situated very close to synapses, they were resistant to the memory breakdown and synapse loss associated with the disorder. The study demonstrated for the first time that this protein, called PirB, is a high-affinity receptor for beta-amyloid in its "soluble cluster" form, meaning that soluble beta-amyloid clusters stick to PirB quite powerfully. That trips off a cascade of biochemical activities culminating in the destruction of synapses.

Shatz is the Sapp Family Provostial Professor, as well as the director of Bio-X, a large Stanford interdisciplinary consortium drawing on medical, engineering and biology faculty. She has been studying PirB for many years, but in a different context. In earlier work, Shatz explored the role of PirB in the brain using genetically engineered mice that lacked it. She discovered that PirB, previously thought to be used only by cells in the immune system, is also found on nerve cells in the brain, where it impedes the ability of synapses to strengthen as they typically do when they are engaged, and actually promotes their weakening. Such brakes are desirable in the brain because too-easy synaptic strength-shifting could trigger untoward consequences like epilepsy.

In the new study, Shatz's team employed a different genetically engineered mouse strain whose genome contained mutant copies of two separate human genes. Each of these mutations is known to predispose individuals to Alzheimer's disease. When both mutations are present in mice, which ordinarily never develop amyloid plaques, the result is abundant amyloid plaque deposition with advancing age, as well as an eventual decline in performance on various tests of memory.

"I've always found it strange that these mice - and, in fact, all the mouse models for Alzheimer's disease that we and other people study - seem not to have any problems with memory until they get old," Shatz said. "These mice's brains have high levels of beta-amyloid at a very early age."

Shatz found herself wondering if there might be a more sensitive measure of beta-amyloid's early effects on young brains. A study she co-authored in 2012 demonstrated that a particular mouse brain region, whose constituent synapses are normally quite nimble at shifting their relative strengths in response to early-life experiences, showed no such flexibility in young Alzheimer's-prone mice. This suggested that subtle Alzheimer's-related effects might appear far earlier than plaques or memory loss do.

Now, Shatz wondered whether eliminating PirB from the Alzheimer's mouse strain could restore that flexibility. So her team bred the Alzheimer's-genes-carrying strain with the PirB-lacking strain to create hybrids. Experimentation showed that the brains of young "Alzheimer's mice" in which PirB was absent retained as much synaptic-strength-shifting flexibility as those of normal mice. PirB-lacking Alzheimer's mice also performed as well in adulthood as normal mice did on well-established tests of memory, while their otherwise identical PirB-expressing peers suffered substantial synapse and memory loss.

"The PirB-lacking Alzheimer's mice were protected from the beta-amyloid-generating consequences of their mutations," Shatz said. The question now was, why?

Taeho Kim, PhD, a postdoctoral scholar in Shatz's lab and the lead author of the new study, advanced a hypothesis he had cooked up in 2011 while describing his research to a captive audience of one - his then-4-year-old son, whom he was driving to the Monterey Bay Aquarium: Maybe PirB and beta-amyloid were binding. This might cause PirB to stomp on the brakes even more than it usually does, weakening synapses so much they could disappear altogether, taking memories with them.

Further experiments showed that, indeed, beta-amyloid binds strongly to PirB. While PirB is specifically a mouse protein, Kim also identified for the first time an analogous beta-amyloid receptor in the human brain: a protein called LilrB2.

In another experiment, Kim compared proteins in the brains of PirB-lacking Alzheimer's mice to those in the brains of PirB-expressing Alzheimer's mice. The latter showed significantly increased activity on the part of a few workhorse proteins, notably an enzyme called cofilin. Subsequent studies also found that cofilin activity in the brains of autopsied Alzheimer's patients is substantially higher than in the brains of people without the disorder.

Here the plot thickens: Cofilin works by breaking down actin, a building-block protein essential to maintaining synaptic structure. And, as the new study also showed, beta-amyloid's binding to PirB results in biochemical changes to cofilin that revs up its actin-busting, synapse-disassembling activity.

"No actin, no synapse," Shatz said.

Kim's hypothesis appears to have been correct. Beta-amyloid binds to PirB (and, the researchers proved, to its human analog, LilrB2), boosting cofilin activity and busting synapses' structural integrity.

Although there may be other avenues of destruction along which synapses are forced to walk, Shatz doubts there are very many. She said she thinks the direct participation of beta-amyloid - as well as cofilin, so clearly implicated in synaptic breakdown - suggests that this pathway is important. "We looked at human brains in this study, too, and we found that a similar derangement of cofilin activity is present in Alzheimer's brains but not healthy brains," she said.

Shatz suggested that drugs that block beta-amyloid's binding to PirB on nerve-cell surfaces - for example, soluble PirB fragments containing portions of the molecule that could act as decoy - might be able to exert a therapeutic effect. "I hope this finding will be enticing enough to pharmaceutical and biotechnology companies that someone will try pushing this idea forward," she said.

The study was funded by the Ellison Medical Foundation, the National Institutes of Health's National Eye Institute (grants EY02958 and 5T32EY020485) and the G. Harold and Leila Y. Mathers Charitable Foundation. Other Stanford co-authors were Christopher Garcia, PhD, professor of molecular and cellular physiology and of structural biology; research associate Maja Djurisic, PhD; and graduate students George Vidal and Michael Birnbaum.

Information about the medical school's Department of Neurology, which also supported this work, is available at http://neurobiology.stanford.edu.

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Scientists reveal how beta-amyloid may cause Alzheimer's

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Norbert von der Groeben Carla Shatz led a study that suggests Alzheimer's disease may begin to manifest long before the development of placques that lead to nerve cell death. Scientists at the Stanford University School of Medicine have shown how a protein fragment known as beta-amyloid, strongly implicated in Alzheimer's disease, begins destroying synapses before it clumps into plaques that lead to nerve cell death.

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The TED talk I watched gives visuals and an in depth look at what happens in the brain during the day while you are awake, and at night when sleeping. I wonder if it will ever be possible to have more cerebrospinal fluid enter the brain during times of awakeness

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Jeff Iliff: One more reason to get a good night's sleep

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The brain uses a quarter of the body's entire energy supply, yet only accounts for about two percent of the body's mass. So how does this unique organ receive and, perhaps more importantly, rid itself of vital nutrients? New research suggests it has to do with sleep.

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This essay dives deep into a fluid called beta amyloid, and it's effect on the brain. It also shows the result of a lack on sleep, and the long term effects it has on a humans health. Is there a way to clear this fluid at a faster rate while we are awake? Multiple experts in the field conclude that there is a relationship between the buildup of the beta amyloid fluid and dangerous diseases

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There are two important brain proteins that appear as a result of lack of sleep: beta amyloid and tau. The buildup of these proteins cause almost a 3 times greater chance of having a harmful diseases later in life. People who don't get the required amount of sleep put them self at risk. Does the buildup of these plaques go at a more rapid pace as more is built up, or does it maintain a steady build up pace? No one knows for sure what comes first: Do excess beta-amyl-oid and tau impair sleep, or does impaired sleep lead to a buildup of these proteins? The leading hypothesis is that it goes both ways in a kind of vicious cycle.

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Discovery Service for Diablo Valley College

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Eagleman gives us background knowledge on the brain. He provides countless examples to represent his findings, which makes it easy to read as a reader. His book helped me connect different concepts, especially having to do with the location of where different brain functions take place. “I’m still figuring out which quotes I may want to use.”

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Read 1,725 reviews from the world's largest community for readers. Locked in the silence and darkness of your skull, your brain fashions the rich narrative...

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Scientists found it was possible to reverse the amyloid plaques in mice, which is a huge breakthrough. This is a step towards eventually removing alzheimers. Removal of the beta amyloid plaque buildup allows the brain to better communicate with itself, as well as having cognitive improvement. I know that by not getting enough sleep, the brian starts to breakdown, and causes excess buildup. However, through this article I learned it may be possible to reverse the buildup in humans because it was possible in mice. One of the most concrete ways in which Alzheimer’s is identified in a patient is through an abnormal buildup of beta-amyloid peptide, a protein that can build into the large amyloid plaques in the brain that are a telltale sign of the deadly, and to date incurable disease.

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Future breakthrough?

Researchers were able to reverse the formation of amyloid plaques, which gradually kill neurons in patients with Alzheimer's disease, in the brains of mice - essentially reversing the condition.

Alongside the reduction of plaques that impair communication between brain cells, the mice also experienced cognitive improvement. The team from the Cleveland Clinic Lerner Research Institute in the U.S. detailed the findings in the Journal of Experimental Medicine. The authors achieved the promising set of results by gradually depleting an enzyme that plays a part in the formation of the plaques, known as BACE1.

Proof of concept

One of the most concrete ways in which Alzheimer's is identified in a patient is through an abnormal buildup of beta-amyloid peptide, a protein that can build into the large amyloid plaques in the brain that are a telltale sign of the deadly, and to date incurable disease. BACE1 helps to produce beta-amyloid peptide, and so inhibiting the enzyme with drugs could ultimately open the door to effective Alzheimer's treatments by halting the buildup.

The researchers tested the hypothesis by engineering a group of mice that lose the BACE1 enzyme as they grow older. And while mice that lacked the enzyme altogether were found to suffer severe neurological defects, those who stopped producing it over time remained healthy.

To see how this new genetic makeup performs against Alzheimer's, the researchers then bred their healthy mice with others engineered to develop the disease. They found that while amyloid plaques started building up in the brain of the offspring, they also disappeared as the mice progressively lost the BACE1 enzyme.

Long way ahead

However, the authors explain that such promising results don't come without caveats. First, the experiment has only been performed in a mouse model, so there is no guarantee that comparable results will be achieved in humans. Additionally, BACE1 takes part in many other important processes in the body, and drugs that progressively destroy it could have serious side effects.

Treating Alzheimer's disease is a difficult and often heartbreaking process, and this research is neither a miracle nor a missed target. This might only be the first step towards realizing such an effective treatment, but given early results it's a worthwhile avenue to pursue.

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Researchers were able to reverse the formation of amyloid plaques, which gradually kill neurons in patients with Alzheimer's disease, in the brains of mice - essentially reversing the condition. Alongside the reduction of plaques that impair communication between brain cells, the mice also experienced cognitive improvement.

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Lack of sleep can cause harmful brain diseases like Alzheimers. Several researchers including Dr. Nedergaard are interviewed and they give their expert opinion on the matter. The excess buildup almost guarantees some health risk later in life, and this is all caused by not sleeping enough. I wonder if the brain can remove plaque buildup on its own, or surgery or something like that is required. I’m curious because I know the process was done in mice but not yet in humans.

That's because one of the waste products removed from the brain during sleep is beta amyloid, the substance that forms sticky plaques associated with the disease.

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While the brain sleeps, it clears out harmful toxins, a process that may reduce the risk of Alzheimer's, researchers say.

During sleep, the flow of cerebrospinal fluid in the brain increases dramatically, washing away harmful waste proteins that build up between brain cells during waking hours, a study of mice found.

"It's like a dishwasher," says Dr. Maiken Nedergaard, a professor of neurosurgery at the University of Rochester and an author of the study in Science.

The results appear to offer the best explanation yet of why animals and people need sleep. If this proves to be true in humans as well, it could help explain a mysterious association between sleep disorders and brain diseases, including Alzheimer's.

Nedergaard and a team of scientists discovered the cleaning process while studying the brains of sleeping mice.

The scientists noticed that during sleep, the system that circulates cerebrospinal fluid through the brain and nervous system was "pumping fluid into the brain and removing fluid from the brain in a very rapid pace," Nedergaard says.

The team discovered that this increased flow was possible in part because when mice went to sleep, their brain cells actually shrank, making it easier for fluid to circulate. When an animal woke up, the brain cells enlarged again and the flow between cells slowed to a trickle. "It's almost like opening and closing a faucet," Nedergaard says. "It's that dramatic."

Nedergaard's team, which is funded by the National Institute of Neurological Disorders and Stroke, had previously shown that this fluid was carrying away waste products that build up in the spaces between brain cells.

The process is important because what's getting washed away during sleep are waste proteins that are toxic to brain cells, Nedergaard says. This could explain why we don't think clearly after a sleepless night and why a prolonged lack of sleep can actually kill an animal or a person, she says.

So why doesn't the brain do this sort of housekeeping all the time? Nedergaard thinks it's because cleaning takes a lot of energy. "It's probably not possible for the brain to both clean itself and at the same time [be] aware of the surroundings and talk and move and so on," she says.

The brain-cleaning process has been observed in rats and baboons, but not yet in humans, Nedergaard says. Even so, it could offer a new way of understanding human brain diseases including Alzheimer's. That's because one of the waste products removed from the brain during sleep is beta amyloid, the substance that forms sticky plaques associated with the disease.

That's probably not a coincidence, Nedergaard says. "Isn't it interesting that Alzheimer's and all other diseases associated with dementia, they are linked to sleep disorders," she says.

Researchers who study Alzheimer's say Nedergaard's research could help explain a number of recent findings related to sleep. One of these involves how sleep affects levels of beta amyloid, says Randall Bateman, a professor of neurology Washington University in St. Louis who wasn't involved in the study.

"Beta amyloid concentrations continue to increase while a person is awake," Bateman says. "And then after people go to sleep that concentration of beta amyloid decreases. This report provides a beautiful mechanism by which this may be happening."

The report also offers a tantalizing hint of a new approach to Alzheimer's prevention, Bateman says. "It does raise the possibility that one might be able to actually control sleep in a way to improve the clearance of beta amyloid and help prevent amyloidosis that we think can lead to Alzheimer's disease."

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Brains Sweep Themselves Clean Of Toxins During Sleep

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While the brain sleeps, it clears out harmful toxins, a process that may reduce the risk of Alzheimer's, researchers say. During sleep, the flow of cerebrospinal fluid in the brain increases dramatically, washing away harmful waste proteins that build up between brain cells during waking hours, a study of mice found.

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Focusing mainly on the effects of lack of sleep, the article illustrates this through mice. During sleep, the brain is capable of cleaning itself out. But when it is awake, this process is much slower and definitely less effective. 8-10 hours of sleep a night is important in order to get a good night's rest as well as allow the brain time to clean itself. This is important for later in life. In a series of new studies on mice, her team discovered exactly that: When the mouse brain is sleeping or under anesthesia, it’s busy cleaning out the waste that accumulated while it was awake.

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Opinion

Credit... Eiko Ojala

SLEEP seems like a perfectly fine waste of time. Why would our bodies evolve to spend close to one-third of our lives completely out of it, when we could instead be doing something useful or exciting? Something that would, as an added bonus, be less likely to get us killed back when we were sleeping on the savanna?

"Sleep is such a dangerous thing to do, when you're out in the wild," Maiken Nedergaard, a Danish biologist who has been leading research into sleep function at the University of Rochester's medical school, told me. "It has to have a basic evolutional function. Otherwise it would have been eliminated."

We've known for some time that sleep is essential for forming and consolidating memories and that it plays a central role in the formation of new neuronal connections and the pruning of old ones. But that hardly seems enough to risk death-by-leopard-in-the-night. "If sleep was just to remember what you did yesterday, that wouldn't be important enough," Dr. Nedergaard explains.

In a series of new studies, published this fall in the journal Science, the Nedergaard lab may at last be shedding light on just what it is that would be important enough. Sleep, it turns out, may play a crucial role in our brain's physiological maintenance. As your body sleeps, your brain is quite actively playing the part of mental janitor: It's clearing out all of the junk that has accumulated as a result of your daily thinking.

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Credit... Eiko Ojala

Recall what happens to your body during exercise. You start off full of energy, but soon enough your breathing turns uneven, your muscles tire, and your stamina runs its course. What's happening internally is that your body isn't able to deliver oxygen quickly enough to each muscle that needs it and instead creates needed energy anaerobically. And while that process allows you to keep on going, a side effect is the accumulation of toxic byproducts in your muscle cells. Those byproducts are cleared out by the body's lymphatic system, allowing you to resume normal function without any permanent damage.

The lymphatic system serves as the body's custodian: Whenever waste is formed, it sweeps it clean. The brain, however, is outside its reach - despite the fact that your brain uses up about 20 percent of your body's energy. How, then, does its waste - like beta-amyloid, a protein associated with Alzheimer's disease - get cleared? What happens to all the wrappers and leftovers that litter the room after any mental workout?

"Think about a fish tank," says Dr. Nedergaard. "If you have a tank and no filter, the fish will eventually die. So, how do the brain cells get rid of their waste? Where is their filter?"

UNTIL a few years ago, the prevailing model was based on recycling: The brain got rid of its own waste, not only beta-amyloid but other metabolites, by breaking it down and recycling it at an individual cell level. When that process eventually failed, the buildup would result in age-related cognitive decline and diseases like Alzheimer's. That "didn't make sense" to Dr. Nedergaard, who says that "the brain is too busy to recycle" all of its energy. Instead, she proposed a brain equivalent of the lymphatic system, a network of channels that cleared out toxins with watery cerebrospinal fluid. She called it the glymphatic system, a nod to its dependence on glial cells (the supportive cells in the brain that work largely to maintain homeostasis and protect neurons) and its function as a sort of parallel lymphatic system.

She was hardly the first to think in those terms. "It had been proposed about one hundred years ago, but they didn't have the tools to study it properly," she says. Now, however, with advanced microscopes and dyeing techniques, her team discovered that the brain's interstitial space - the fluid-filled area between tissue cells that takes up about 20 percent of the brain's total volume - was mainly dedicated to physically removing the cells' daily waste.

When members of Dr. Nedergaard's team injected small fluorescent tracers into the cerebrospinal fluid of anesthetized mice, they found that the tracers quickly entered the brain - and, eventually, exited it - via specific, predictable routes.

The next step was to see how and when, exactly, the glymphatic system did its work. "We thought this cleaning process would require tremendous energy," Dr. Nedergaard says. "And so we asked, maybe this is something we do when we're sleeping, when the brain is really not processing information."

In a series of new studies on mice, her team discovered exactly that: When the mouse brain is sleeping or under anesthesia, it's busy cleaning out the waste that accumulated while it was awake.

In a mouse brain, the interstitial space takes up less room than it does in ours, approximately 14 percent of the total volume. Dr. Nedergaard found that when the mice slept, it swelled to over 20 percent. As a result, the cerebrospinal fluid could not only flow more freely but it could also reach further into the brain. In an awake brain, it would flow only along the brain's surface. Indeed, the awake flow was a mere 5 percent of the sleep flow. In a sleeping brain, waste was being cleared two times faster. "We saw almost no inflow of cerebrospinal fluid into the brain when the mice were awake, but then when we anesthetized them, it started flowing. It's such a big difference I kept being afraid something was wrong," says Dr. Nedergaard.

Similar work in humans is still in the future. Dr. Nedergaard is currently awaiting board approval to begin the equivalent study in adult brains in collaboration with the anesthesiologist Helene Benveniste at Stony Brook University.

So far the glymphatic system has been identified as the neural housekeeper in baboons, dogs and goats. "If anything," Dr. Nedergaard says, "it's more needed in a bigger brain."

MODERN society is increasingly ill equipped to provide our brains with the requisite cleaning time. The figures are stark. Some 80 percent of working adults suffer to some extent from sleep deprivation. According to the National Sleep Foundation, adults should sleep seven to nine hours. On average, we're getting one to two hours less sleep a night than we did 50 to 100 years ago and 38 minutes less on weeknights than we did as little as 10 years ago. Between 50 and 70 million people in the United States suffer from some form of chronic sleep disorder. When our sleep is disturbed, whatever the cause, our cleaning system breaks down. At the University of Pennsylvania's Center for Sleep and Circadian Neurobiology, Sigrid Veasey has been focusing on precisely how restless nights disturb the brain's normal metabolism. What happens to our cognitive function when the trash piles up?

At the extreme end, the result could be the acceleration of neurodegenerative diseases like Alzheimer's and Parkinson's. While we don't know whether sleep loss causes the disease, or the disease itself leads to sleep loss - what Dr. Veasey calls a "classic chicken-and-egg" problem - we do know that the two are closely connected. Along with the sleep disturbances that characterize neurodegenerative diseases, there is a buildup of the types of proteins that the glymphatic system normally clears out during regular sleep, like beta-amyloids and tau, both associated with Alzheimer's and other types of dementia.

"To me," says Dr. Veasey, "that's the most compelling part of the Nedergaard research. That the clearance for these is dramatically reduced from prolonged wakefulness." If we don't sleep well, we may be allowing the very things that cause neural degeneration to pile up unchecked.

Even at the relatively more benign end - the all-nighter or the extra-stressful week when you caught only a few hours a night - sleep deprivation, as everyone who has experienced it knows, impedes our ability to concentrate, to pay attention to our environment and to analyze information creatively. "When we're sleep-deprived, we can't integrate or put together facts," as Dr. Veasey puts it.

But there is a difference between the kind of fleeting sleep loss we sometimes experience and the chronic deprivation that comes from shift work, insomnia and the like. In one set of studies, soon to be published in The Journal of Neuroscience, the Veasey lab found that while our brains can recover quite readily from short-term sleep loss, chronic prolonged wakefulness and sleep disruption stresses the brain's metabolism. The result is the degeneration of key neurons involved in alertness and proper cortical function and a buildup of proteins associated with aging and neural degeneration.

It's like the difference between a snowstorm's disrupting a single day of trash pickup and a prolonged strike. No longer quite as easy to fix, and even when the strike is over, there's likely to be some stray debris floating around for quite some time yet. "Recovery from sleep loss is slower than we'd thought," Dr. Veasey notes. "We used to think that after a bit of recovery sleep, you should be fine. But this work shows you're not."

If you put her own research together with the findings from the Nedergaard lab, Dr. Veasey says, it "very clearly shows that there's impaired clearance in the awake brain. We're really starting to realize that when we skip sleep, we may be doing irreparable damage to the brain, prematurely aging it or setting it up for heightened vulnerability to other insults."

In a society that is not only chronically sleep-deprived but also rapidly aging, that's bad news. "It's unlikely that poor sleep as a child would actually cause Alzheimer's or Parkinson's," says Dr. Veasey, "but it's more likely that you may shift one of those diseases by a decade or so. That has profound health and economic implications."

It's a pernicious cycle. We work longer hours, become more stressed, sleep less, impair our brain's ability to clean up after all that hard work, and become even less able to sleep soundly. And if we reach for a sleeping pill to help us along? While work on the effects of sleeping aids on the glymphatic system remains to be done, the sleep researchers I spoke with agree that there's no evidence that aided sleep is as effective as natural sleep.

There is, however, reason to hope. If the main function of sleep is to take out our neural trash, that insight could eventually enable a new understanding of both neurodegenerative diseases and regular, age-related cognitive decline. By developing a diagnostic test to measure how well the glymphatic system functions, we could move one step closer to predicting someone's risk of developing conditions like Alzheimer's or other forms of dementia: The faster the fluids clear the decks, the more effectively the brain's metabolism is functioning.

"Such a test could also be used in the emergency room after traumatic brain injury," Dr. Nedergaard says, "to see who is at risk of developing decline in cognitive function."

We can also focus on developing earlier, more effective interventions to prevent cognitive decline. One approach would be to enable individuals who suffer from sleep loss to sleep more soundly - but how? Dr. Nedergaard's mice were able to clear their brain's waste almost as effectively under anesthesia as under normal sleeping conditions. "That's really fascinating," says Dr. Veasey. Though current sleeping aids may not quite do the trick, and anesthetics are too dangerous for daily use, the results suggest that there may be better ways of improving sleep pharmacologically.

Now that we have a better understanding of why sleep is so important, a new generation of drug makers can work to create the best possible environment for the trash pickup to occur in the first place - to make certain that our brain's sleeping metabolism is as efficient as it can possibly be.

A second approach would take the opposite tack, by seeking to mimic the cleanup-promoting actions of sleep in the awake brain, which could make a full night of sound sleep less necessary. To date, the brain's metabolic process hasn't been targeted as such by the pharmaceutical industry. There simply wasn't enough evidence of its importance. In response to the evolving data, however, future drug interventions could focus directly on the glymphatic system, to promote the enhanced cleaning power of the sleeping brain in a brain that is fully awake. One day, scientists might be able to successfully mimic the expansion of the interstitial space that does the mental janitorial work so that we can achieve maximally efficient round-the-clock brain trash pickup.

If that day comes, they would be on their way to discovering that all-time miracle drug: one that, in Dr. Veasey's joking words, "could mean we never have to sleep at all."

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Opinion SLEEP seems like a perfectly fine waste of time. Why would our bodies evolve to spend close to one-third of our lives completely out of it, when we could instead be doing something useful or exciting? Something that would, as an added bonus, be less likely to get us killed back when we were sleeping on the savanna?

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The article goes more into depth about why teens/young adults can’t get enough sleep, and what happens to their brains as a result. They become more tired and less able to concentrate when they get less than 8-10 hours of sleep a night. This is also important to prevent the breakup of the beta amyloid fluid in the brain. This buildup can cause harmful diseases later in life. I also know that my own choices of going to hang with friends or working out cause me sleep deprivation. To be at your best, you need between 8 and 10 hours of sleep every day. While you might not always be able to get this much, it’s important to try and get as much as you can.

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Tired of always feeling sleepy?

Having trouble staying awake in class?

Find it hard to get out of bed for school in the morning?

Have an overwhelming need for a nap as soon as you get home from school?

If you answered yes to any of these questions, you are not alone. Many teenagers feel that they are always tired.

Why do teens need more sleep?

Sleep helps to fuel your brain and your body. Teens need more sleep because their bodies and minds are growing quickly.

Scientific research shows that many teens do not get enough sleep. To be at your best, you need between 8 and 10 hours of sleep every day. While you might not always be able to get this much, it's important to try and get as much as you can.

Why is it important to get enough sleep?

Although getting enough sleep may not seem that big a deal, teens who don't get enough sleep and are overtired are more likely to:

struggle in school,

have trouble with memory, concentration and motivation (the desire to accomplish a goal),

be involved in car crashes and other accidents. Sleepiness (the feeling of wanting or needing to sleep in places and at times when you shouldn't) affects reaction times, or

feel depressed, which can become a serious medical condition.

What causes my sleepiness?

Often the reason is obvious, such as too many late nights in a row. Although there are some medical causes of sleepiness, most sleepy teens just aren't getting enough sleep.

How do I know if I'm getting enough sleep?

Signs that you need more sleep can include:

difficulty waking up in the morning,

trouble concentrating throughout the day,

falling asleep during classes, and

feeling moody or even depressed.

Why is it so hard to get enough sleep?

There are many reasons. Some you may be able to control and some you may not.

You probably have a very busy life, but you still need "downtime" to relax, unwind and spend time with friends. This usually happens at the expense of sleeping. Many teens also crave the quiet privacy of a late night after parents have gone to bed.

When you think about all the other things you need to do (homework, socializing, sports, chores, part-time jobs, etc.), getting to bed early enough to get 8 to 10 hours of sleep can seem pretty hard.

Here are some suggestions:

Have a relaxing bedtime routine. Have a light snack (such as a glass of milk) before bed. Try to go to bed at about the same time every night. Keep your room cool, dark and quiet but open the curtains or turn on the lights as soon as you get up in the morning.

Always fall asleep in your bed. Use your bed for sleeping only. Avoid doing homework, using a smartphone or tablet, or playing video games while in bed. Try to be in your bed with the lights out for at least 8 hours every night.

Napping during the day can make it difficult to fall asleep. If you want to nap, keep it short (less than 30 minutes). Definitely don't nap after dinner.

Get exercise every day, but avoid very hard exercise in the evening.

Avoid caffeine (coffee, tea, pop, energy drinks), especially after mid-afternoon. Don't use any products to help you sleep such as alcohol, herbal products or over-the-counter sleep aids.

Limit screen time before bed. Using electronic media and being exposed to the screen's light before trying to sleep can make it harder to fall asleep.

On weekends, no matter how late you go to bed, try to get up within 2 hours to 4 hours of your usual wake time. This is especially important if you have trouble falling asleep on Sunday nights.

Make sure you are not trying to do too much. Do you still have some time for fun and to get enough sleep? If you are having trouble sleeping because you have too much on your mind, try keeping a diary or to-do lists. If you write things down before sleep, you may feel less worried or stressed.

See your doctor if you:

have trouble falling asleep at night despite trying the tips in this document.

wake up through the night or early in the morning and cannot get back to sleep.

continue to feel like you have no energy despite getting enough sleep.

are having trouble meeting your responsibilities - such as not being able to go to school, get to work on time, or spend time with your friends.

have feelings of sadness that don't seem to go away.

have worried feelings that make it hard to focus on other things.

often feel sick in other ways (such as headaches, loss of appetite or other symptoms you can't explain).

More information from the CPS:

Additional resources:

Reviewed by the following CPS committees:

Adolescent Health Committee

Community Paediatrics Committee

Public Education Advisory Committee

Last Updated: May 2018

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Teens and sleep: Why you need it and how to get enough

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Tired of always feeling sleepy? Having trouble staying awake in class? Find it hard to get out of bed for school in the morning? Have an overwhelming need for a nap as soon as you get home from school? If you answered yes to any of these questions, you are not alone.