Wednesday, July 19, 2017

Benefits of tumeric

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Salk Institute

Salk Institute's J147 is a derivative of turmeric, a spice used in curry. Learn how it quickly reverses memory deficits and has a host of unexpected anti-aging effects in the lab. 




Salk Institute researchers have found that J147, which is an experimental drug candidate aimed at combating Alzheimer's disease, has a host of unexpected anti-aging effects in animals.

J147, Alzheimer's and Old Age

The Salk team expanded upon their previous development of the drug candidate they labeled J147. It is a derivative of the common spice, turmeric, and takes a different tack by targeting Alzheimer's major risk factor -- old age. In the new work, the team showed that the drug candidate worked well in a mouse model of aging not typically used in Alzheimer's research. When these mice were treated with J147, they had better memory and cognition, healthier blood vessels in the brain and other improved physiological features, as detailed in the journal Aging.

Fighting Alzheimer's By Fighting Aging

"Initially, the impetus was to test this drug in a novel animal model that was more similar to 99 percent of Alzheimer's cases," says Antonio Currais, the lead author and a member of Professor David Schubert's Cellular Neurobiology Laboratory at Salk. "We did not predict we'd see this sort of anti-aging effect, but J147 made old mice look like they were young, based upon a number of physiological parameters."

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Print Friendly Version of this pagePrint Get a PDF version of this webpagePDFAlzheimer's disease is a progressive brain disorder, recently ranked as the third leading cause of death in the United States and affecting more than five million Americans. It is also the most common cause of dementia in older adults, according to the National Institutes of Health.

"While most drugs developed in the past 20 years target the amyloid plaque deposits in the brain (which are a hallmark of the disease), none have proven effective in the clinic," says Schubert, senior author of the study.

Expanding the Fight to More Common Dementias

Several years ago, Schubert and his colleagues began to approach the treatment of the disease from a new angle. Rather than target amyloid, the lab decided to zero in on the major risk factor for the disease--old age. Using cell-based screens against old age-associated brain toxicities, they synthesized J147.

Previously, the team found that J147 could prevent and even reverse memory loss and Alzheimer's pathology in mice that have a version of the inherited form of Alzheimer's, the most commonly used mouse model. However, this form of the disease comprises only about 1 percent of Alzheimer's cases. For everyone else, old age is the primary risk factor, says Schubert. The team wanted to explore the effects of the drug candidate on a breed of mice that age rapidly and experience a version of dementia that more closely resembles the age-related human disorder.

Young Mice, Old Mice and J147-fed Mice

In this latest work, the researchers used a comprehensive set of assays to measure the expression of all genes in the brain, as well as over 500 small molecules involved with metabolism in the brains and blood of three groups of the rapidly aging mice. The three groups of rapidly aging mice included one set that was young, one set that was old and one set that was old but fed J147 as they aged.

7 Benefits

The old mice fed J147 saw the following benefits:
  1. They performed better on memory and other tests for cognition
  2. They displayed more robust motor movements.
  3. They had fewer pathological signs of Alzheimer's in their brains.
  4. J147 prevented the leakage of blood from the microvessels in the brains of old mice. "Damaged blood vessels are a common feature of aging in general, and in Alzheimer's, it is frequently much worse," says Currais.

    Importantly, because of the large amount of data collected on the three groups of mice, it was possible to demonstrate that many aspects of gene expression and metabolism in the old mice fed J147 were very similar to those of the young animals. These included:
  5. markers for increased energy metabolism,
  6. reduced brain inflammation and
  7. reduced levels of oxidized fatty acids in the brain.

Human Clinical Trials

Currais and Schubert note that while these studies represent a new and exciting approach to Alzheimer's drug discovery and animal testing in the context of aging, the only way to demonstrate the clinical relevance of the work is to move J147 into human clinical trials for Alzheimer's disease.

"If proven safe and effective for Alzheimer's, the apparent anti-aging effect of J147 would be a welcome benefit," adds Schubert. The team aims to begin human trials next year.

Related Article:

Curry Derivative J147 Beats Aricept for Alzheimer's

MORE INFORMATION:
  • Other authors on the paper include Oswald Quehenberger of the University of California, San Diego; and Joshua Goldberg, Catherine Farrokhi, Max Chang, Marguerite Prior, Richard Dargusch, Daniel Daugherty and Pamela Maher of the Salk Institute.
  • This study was supported by the Salk Institute Pioneer Fund Postdoctoral Scholar Award and the Salk Nomis Fellowship Award, fellowships from the Hewitt Foundation and Bundy Foundation, and grants from the Burns Foundation and NIH.
SOURCE:

Monday, July 17, 2017

Aging and Alzheimer's risk

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SOURCE:
Washington University School of Medicine’s 2,100 employed and volunteer faculty physicians also are the medical staff of Barnes-Jewish and St. Louis Children’s hospitals. The School of Medicine is one of the leading medical research, teaching and patient-care institutions in the nation, currently ranked sixth in the nation by U.S. News & World Report. Through its affiliations with Barnes-Jewish and St. Louis Children’s hospitals, the School of Medicine is linked to BJC HealthCare

100 VOLUNTEERS IN A STUDY 

The main suspect behind Alzheimer's is a protein called "amyloid-beta". Researchers asked, "Why do older people have more of it?" 



The greatest risk factor for Alzheimer’s disease is advancing age. After 65, the risk doubles every five years. As many as half of the elderly who are over 85 are estimated to be living with some type of dementia, usually Alzheimer's.

A sizable study demonstrated that in our 30s, a healthy brain clears amyloid-beta every four hours. At 80 years old, it takes more than 10 hours. This may explain the link between age and Alzheimer's, as well as what we need to do to fight this disease. Researchers at Washington University School of Medicine in St. Louis have identified some of the key changes in the aging brain that lead to the increased risk. The changes center on amyloid beta 42, a main ingredient of Alzheimer’s brain plaques. The protein, a natural byproduct of brain activity, normally is cleared from the brain before it can clump together into plaques. Scientists long have suspected it is a primary driver of the disease.

Amyloid beta plaque.A new study reveals that the brain's ability to clear the main ingredient of Alzheimer's plaques slows with age (the plaques are red in this image). The findings could help explain why risk of the disease increases with age.
“We found that people in their 30s typically take about four hours to clear half the amyloid beta 42 from the brain,” said senior author Randall J. Bateman, MD, the Charles F. and Joanne Knight Distinguished Professor of Neurology. “In this new study, we show that at over 80 years old, it takes more than 10 hours.”

The slowdown in clearance results in rising levels of amyloid beta 42 in the brain. Higher levels of the protein increase the chances that it will clump together to form Alzheimer’s plaques.

The results appear online in the Annals of Neurology.

For the study, the researchers tested 100 volunteers ages 60 to 87. Half had clinical signs of Alzheimer’s disease, such as memory problems. Plaques had begun to form in the brains of 62 participants.

The subjects were given detailed mental and physical evaluations, including brain scans to check for the presence of plaques. The researchers also studied participants’ cerebrospinal fluids using a technology developed by Bateman and co-author David Holtzman , MD, the Andrew B. and Gretchen P. Jones Professor and head of the Department of Neurology at Washington University. The technology — known as stable isotope-linked kinetics (SILK)— allowed the researchers to monitor the body’s production and clearance of amyloid beta 42 and other proteins.

In patients with evidence of plaques, the researchers observed that amyloid beta 42 appears to be more likely to drop out of the fluid that bathes the brain and clump together into plaques. Reduced clearance rates of amyloid beta 42, such as those seen in older participants, were associated with clinical symptoms of Alzheimer’s disease, such as memory loss, dementia and personality changes.

Scientists believe the brain disposes of amyloid beta in four ways: by moving it into the spine, pushing it across the blood-brain barrier, breaking it down or absorbing it with other proteins, or depositing it into plaques.

“Through additional studies like this, we’re hoping to identify which of the first three channels for amyloid beta disposal are slowing down as the brain ages,” Bateman said. “That may help us in our efforts to develop new treatments.” 


Saturday, July 15, 2017

Light Improves Life with Alzheimer's

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An Alzheimer's trial provided 4 weeks of tailored light therapy. The therapy significantly increased sleep quality, efficiency and total sleep duration. Daytime light therapy also significantly reduced rates of depression and agitation. Learn how. 



A key study offers an easy-to-do care tip. Research suggests that light treatment, tailored to increase circadian stimulation during the day, may improve sleep, depression and agitation in people with Alzheimer's and related dementia. 

Results show that exposure to the tailored light treatment during daytime hours for four weeks significantly increased sleep quality, efficiency and total sleep duration. It also significantly reduced scores for depression and agitation.

"It is a simple, inexpensive, non-pharmacological treatment to improve sleep and behavior in Alzheimer's disease and dementia patients," said principal investigator Mariana Figueiro, PhD, associate professor and Light and Health program director of the Lighting Research Center at Rensselaer Polytechnic Institute in Troy, New York. "The improvements we saw in agitation and depression were very impressive."

Therapy lights are easy to find. Check out:
The research abstract was published recently in an online supplement of the journal Sleep and was presented in Minneapolis, Minnesota, at the 28th annual meeting of the Associated Professional Sleep Societies LLC.

The pilot study involved 14 nursing home patients with Alzheimer's disease and related dementia. A light source producing low levels of 300 to 400 lux of a bluish-white light with a color temperature of more than 9000 K was installed in the residents' rooms. Light exposure occurred during daytime hours for a period of four weeks. Light-dark and activity-rest patterns were collected using a calibrated instrument prior to and after the lighting intervention. Measures of sleep quality, depression and agitation also were collected using standardized questionnaires.

Figueiro added that the improvement in sleep quality also was associated with other noticeable behavioral changes.

"Subjective reports by the nursing staff were that the patients were calmer, eating better and their overall behavior was more manageable," she said.

More Information:
The research was supported by funding from the National Institute on Aging (NIA) within the National Institutes of Health (NIH).
Established in 1975, the American Academy of Sleep Medicine (AASM) improves sleep health and promotes high quality patient centered care through advocacy, education, strategic research, and practice standards. With about 9,000 members, the AASM is the largest professional membership society for physicians, scientists and other health care providers dedicated to sleep medicine. For more information, visit http://www.aasmnet.org.





Thursday, July 13, 2017

The Link Between Sleep and Alzheimer’s

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Summary: A new study published in brain reveals that just one night of sleep disruption causes an increase in amyloid beta in the brains of healthy, middle aged people. A full week of sleep disturbances leads to a build up of Tau, another protein associated with Alzheimer’s and other neurodegenerative diseases. The study sheds light on why poor sleep has previously been associated with the development of Alzheimer’s and other dementias.
Source: WUSTL.
Poor sleep leads to increase in Alzheimer’s proteins associated with cognitive decline.
A good night’s sleep refreshes body and mind, but a poor night’s sleep can do just the opposite. A study from Washington University School of Medicine in St. Louis, Radboud University Medical Centre in the Netherlands, and Stanford University has shown that disrupting just one night of sleep in healthy, middle-aged adults causes an increase in amyloid beta, a brain protein associated with Alzheimer’s disease. And a week of tossing and turning leads to an increase in another brain protein, tau, which has been linked to brain damage in Alzheimer’s and other neurological diseases.
“We showed that poor sleep is associated with higher levels of two Alzheimer’s-associated proteins,” said David M. Holtzman, MD, the Andrew B. and Gretchen P. Jones Professor, head of the Department of Neurology and the study’s senior author. “We think that perhaps chronic poor sleep during middle age may increase the risk of Alzheimer’s later in life.”
These findings, published July 10 in the journal Brain, may help explain why poor sleep has been associated with the development of dementias such as Alzheimer’s.
More than 5 million Americans are living with Alzheimer’s disease, which is characterized by gradual memory loss and cognitive decline. The brains of people with Alzheimer’s are dotted with plaques of amyloid beta protein and tangles of tau protein, which together cause brain tissue to atrophy and die. There are no therapies that have been proven to prevent, slow or reverse the course of the disease.
Previous studies by Holtzman, co-first author Yo-El Ju, MD, an assistant professor of neurology, and others have shown that poor sleep increases the risk of cognitive problems. People with sleep apnea, for example, a condition in which people repeatedly stop breathing at night, are at risk for developing mild cognitive impairment an average of 10 years earlier than people without the sleep disorder. Mild cognitive impairment is an early warning sign for Alzheimer’s disease.
But it wasn’t clear how poor sleep damages the brain. To find out, the researchers — Holtzman; Ju; co-first author and graduate student Sharon Ooms of Radboud; Jurgen Claassen, MD, PhD, of Radboud; Emmanuel Mignot, MD, PhD, of Stanford; and colleagues — studied 17 healthy adults ages 35 to 65 with no sleep problems or cognitive impairments. Each participant wore an activity monitor on the wrist for up to two weeks that measured how much time they spent sleeping each night.
After five or more successive nights of wearing the monitor, each participant came to the School of Medicine to spend a night in a specially designed sleep room. The room is dark, soundproof, climate-controlled and just big enough for one; a perfect place for sleeping, even as the participants wore headphones over the ears and electrodes on the scalp to monitor brain waves.
Half the participants were randomly assigned to have their sleep disrupted during the night they spent in the sleep room. Every time their brain signals settled into the slow-wave pattern characteristic of deep, dreamless sleep, the researchers sent a series of beeps through the headphones, gradually getting louder, until the participants’ slow-wave patterns dissipated and they entered shallower sleep.
The next morning, the participants who had been beeped out of slow-wave sleep reported feeling tired and unrefreshed, even though they had slept just as long as usual and rarely recalled being awakened during the night. Each underwent a spinal tap so the researchers could measure the levels of amyloid beta and tau in the fluid surrounding the brain and spinal cord.
A month or more later, the process was repeated, except that those who had their sleep disrupted the first time were allowed to sleep through the night undisturbed, and those who had slept uninterrupted the first time were disturbed by beeps when they began to enter slow-wave sleep.
The researchers compared each participant’s amyloid beta and tau levels after the disrupted night to the levels after the uninterrupted night, and found a 10 percent increase in amyloid beta levels after a single night of interrupted sleep, but no corresponding increase in tau levels. However, participants whose activity monitors showed they had slept poorly at home for the week before the spinal tap showed a spike in levels of tau.
“We were not surprised to find that tau levels didn’t budge after just one night of disrupted sleep while amyloid levels did, because amyloid levels normally change more quickly than tau levels,” Ju said. “But we could see, when the participants had several bad nights in a row at home, that their tau levels had risen.”
Slow-wave sleep is the deep sleep that people need to wake up feeling rested. Sleep apnea disrupts slow-wave sleep, so people with the disorder often wake up feeling unrefreshed, even after a full eight hours of shut-eye.
Slow-wave sleep is also the time when neurons rest and the brain clears away the molecular byproducts of mental activity that accumulate during the day, when the brain is busily thinking and working.
Ju thinks it is unlikely that a single night or even a week of poor sleep, miserable though it may be, has much effect on overall risk of developing Alzheimer’s disease. Amyloid beta and tau levels probably go back down the next time the person has a good night’s sleep, she said.

Research from Washington University School of Medicine in St. Louis, Radboud University Medical Centre in the Netherlands, and Stanford University shows that disrupting just one night of sleep in healthy, middle-aged adults causes an increase in a brain protein associated with Alzheimer’s disease. Further, a week of poor sleep leads to an increase in another brain protein that has been linked to brain damage in Alzheimer’s and other neurological diseases. Shown are brain waves during slow-wave sleep, measured as a study participant slept. NeuroscienceNews.com image is credited to Yo-El Ju.
“The main concern is people who have chronic sleep problems,” Ju said. “I think that may lead to chronically elevated amyloid levels, which animal studies have shown lead to increased risk of amyloid plaques and Alzheimer’s.”
Ju emphasized that her study was not designed to determine whether sleeping more or sleeping better reduce risk of Alzheimer’s but, she said, neither can hurt.
“Many, many Americans are chronically sleep-deprived, and it negatively affects their health in many ways,” Ju said. “At this point, we can’t say whether improving sleep will reduce your risk of developing Alzheimer’s. All we can really say is that bad sleep increases levels of some proteins that are associated with Alzheimer’s disease. But a good night’s sleep is something you want to be striving for anyway.”
ABOUT THIS NEUROSCIENCE RESEARCH ARTICLE
Funding: Funding provided by National Institutes of Health, J.P.B Foundation, Alzheimer Nederland, Washington University Institute of Clinical and Translational Sciences, National Center for Advancing Translational Sciences.
Source: Judy Martin Finch – WUSTL
Image Source: NeuroscienceNews.com image is credited to Yo-El Ju.
Original Research: Full open access research for “Slow wave sleep disruption increases cerebrospinal fluid amyloid-β levels” by Yo-El S. Ju, Sharon J. Ooms, Courtney Sutphen, Shannon L. Macauley, Margaret A. Zangrilli, Gina Jerome, Anne M. Fagan, Emmanuel Mignot, John M. Zempel, Jurgen A.H.R. Claassen, and David M. Holtzman in Brain. Published online July 10 2017 

Tuesday, July 11, 2017

Drug Restores Cells and Memories in Alzheimer’s: Mouse Study

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Summary: A new drug has proven effective at restoring memories and neural connections in mouse models of Alzheimer’s disease. The new drug was originally developed as a treatment for Schizophrenia. While the drug does not destroy amyloid plaques associated with Alzheimer’s, it does allow the plaques to co-exist with neurons.
Source: Yale.
A new drug can restore memories and connections between brain cells in mice with a model of Alzheimer’s disease, a new Yale-led study suggests.
“The drug completely erased evidence of Alzheimer’s synapse damage and memory loss in mouse models of the disease,” said Stephen Strittmatter, the Vincent Coates Professor of Neurology and senior author of the study appearing July 5 in the journal Cell Reports.
Researchers such as Strittmatter have made significant inroads into understanding the biology of Alzheimer’s disease, but identifying effective and safe treatments has been difficult. It is known that amyloid-beta peptides, the hallmark of Alzheimer’s, couple with prion protein at the surface of brain cells and transmit damaging instructions to the interior of the cell. Yale researchers had previously identified a protein on the cell membrane — metabotropic glutamate receptor 5 or mGluR5 — as the gateway that helps transmit damage from the coupling.
Previous attempts had been made to target mGluR5, but most drugs also disrupt signaling of glutamate, the most common neurotransmitter in the human brain. The new compound, Silent Allosteric Modulation or SAM (BMS 984923), was created by Bristol Myers Squibb as part of its effort to treat schizophrenia. The drug does not restrict neurotransmitter signaling in culture tissue or living mice, the study found. After four weeks of treatment, memory and synapses linking brain cells had been restored in mice with a model of Alzheimer’s.
“The drug does not destroy plaques associated with Alzheimer’s, but allows them to co-exist with neurons,” Strittmatter said.
Image shows cortical tissue.
Cortical tissue with plaques stained in blue, and astrocytes responding to drug treatment in red. NeuroscienceNews.com image is credited to the researchers.
Yale researchers say the next step is to prepare for preliminary trials of the drug’s effects on humans.
Primary funding for the research comes from the National Institutes of Health.
ABOUT THIS NEUROSCIENCE RESEARCH ARTICLE
Yale’s Laura T. Haas is lead author of the study. Researchers from Bristol-Myers Squibb Research and Development also contributed to the paper.
Source: Bill Hathaway – Yale

Sunday, July 9, 2017

Sleep Problems May Be An Early Sign of Alzheimer’s

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Summary: A new study links sleep problems with increased biomarkers for Alzheimer’s disease. Researchers discovered those who report low sleep quality, daytime sleepiness and other sleep problems had elevated levels of Alzheimer’s related biomarkers in their spinal fluid than those who reported no sleep problems. However, no abnormalities were found in the spinal fluid of people with obstructive sleep apnea.
Source: AAN.
Poor sleep may be a sign that people who are otherwise healthy may be more at risk of developing Alzheimer’s disease later in life than people who do not have sleep problems, according to a study published in the July 6, 2017, online issue of Neurology. Researchers have found a link between sleep disturbances and biological markers for Alzheimer’s disease found in the spinal fluid.
“Previous evidence has shown that sleep may influence the development or progression of Alzheimer’s disease in various ways,” said study author Barbara B. Bendlin, PhD, of the University of Wisconsin-Madison. “For example, disrupted sleep or lack of sleep may lead to amyloid plaque buildup because the brain’s clearance system kicks into action during sleep. Our study looked not only for amyloid but for other biological markers in the spinal fluid as well.”
Amyloid is a protein that can fold and form into plaques. Tau is a protein that forms into tangles. These plaques and tangles are found in the brains of people with Alzheimer’s disease.
For the study, researchers recruited 101 people with an average age of 63 who had normal thinking and memory skills but who were considered at risk of developing Alzheimer’s, either having a parent with the disease or being a carrier of a gene that increases the risk for Alzheimer’s disease called apolipoprotein E or APOE. Participants were surveyed about sleep quality. They also provided spinal fluid samples that were tested for biological markers of Alzheimer’s disease.
Researchers found that people who reported worse sleep quality, more sleep problems and daytime sleepiness had more biological markers for Alzheimer’s disease in their spinal fluid than people who did not have sleep problems. Those biological markers included signs of amyloid, tau and brain cell damage and inflammation.
“It’s important to identify modifiable risk factors for Alzheimer’s given that estimates suggest that delaying the onset of Alzheimer’s disease in people by a mere five years could reduce the number of cases we see in the next 30 years by 6.7 million and save $367 billion in health care spending,” said Bendlin.
While some of these relationships were strong when looking at everyone as a group, not everyone with sleep problems has abnormalities in their spinal fluid. For example, there was no link between biological markers in the spinal fluid and obstructive sleep apnea.
The results remained the same when researchers adjusted for other factors such as use of medications for sleep problems, amount of education, depression symptoms or body mass index.
an alarm clock
While some of these relationships were strong when looking at everyone as a group, not everyone with sleep problems has abnormalities in their spinal fluid. For example, there was no link between biological markers in the spinal fluid and obstructive sleep apnea. NeuroscienceNews.com image is for illustrative purposes only.
“It’s still unclear if sleep may affect the development of the disease or if the disease affects the quality of sleep,” said Bendlin. “More research is needed to further define the relationship between sleep and these biomarkers.”
Bendlin added, “There are already many effective ways to improve sleep. It may be possible that early intervention for people at risk of Alzheimer’s disease may prevent or delay the onset of the disease.”
One limitation of the study was that sleep problems were self-reported. Monitoring of sleep patterns by health professionals may be beneficial in future studies.
ABOUT THIS NEUROSCIENCE RESEARCH ARTICLE
Funding: The study was supported by the National Institute on Aging and the National Institutes of Health National Center for Advancing Translational Sciences.
Source: Renee Tessman – AAN
Image Source: NeuroscienceNews.com image is in the public domain.
Original Research: The study will appear in Neurology.

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The Dementia Caregiver's Little Book of Hope [Kindle Edition

Friday, July 7, 2017

Sleep clears Alzheimers

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Beta-amyloid (also known as "plaque") is the main suspect behind Alzheimer's. Sleep cleared it TWICE as quickly as normal in the lab. Find out how sleep doubles the clearance of this dangerous Alzheimer's molecule. 



A mouse study suggests that sleep helps restore the brain by flushing out toxins that build up during waking hours. The results point to a potential new role for sleep in health and disease.



Scientists watched dye flow through the glymphatic system, a brain "plumbing" system, of a mouse when it was asleep (left) and then, later, when it was awake (right). More dye flowed into the brain during sleep. Results from this study suggest the brain may flush out toxic molecules associated with neurodegenerative disorders during sleep. Courtesy of Nedergaard Lab, University of Rochester Medical Center.

Scientists and philosophers have long wondered why people sleep and how it affects the brain. Sleep is important for storing memories. It also has a restorative function. Lack of sleep impairs reasoning, problem-solving, and attention to detail, among other effects. However, the mechanisms behind these sleep benefits have been unknown.

Dr. Maiken Nedergaard and her colleagues at the University of Rochester Medical Center recently discovered a system that drains waste products from the brain. Cerebrospinal fluid, a clear liquid surrounding the brain and spinal cord, moves through the brain along a series of channels that surround blood vessels. The system is managed by the brain’s glial cells, and so the researchers called it the glymphatic system.

The scientists also reported that the glymphatic system can help remove a toxic protein called beta-amyloid from brain tissue. Beta-amyloid is renowned for accumulating in the brains of patients with Alzheimer's disease. Other research has shown that brain levels of beta-amyloid decrease during sleep. In their new study, the team tested the idea that sleep might affect beta-amyloid clearance by regulating the glymphatic system. The work was funded by NIH’s National Institute of Neurological Disorders and Stroke (NINDS).

The researchers first injected dye into the cerebrospinal fluid of mice and monitored electrical brain activity as they tracked the dye flow through the animals’ brains. As reported in the October 18, 2013, edition of Science, the dye barely flowed when the mice were awake. In contrast, when the mice were unconscious—asleep or anesthetized—it flowed rapidly.

Changes in the way fluid moves through the brain between conscious and unconscious states may reflect differences in the space available for movement. To test the idea, the team used a method that measures the volume of the space outside brain cells. They found that this “extracellular” volume increased by 60% in the brain’s cortex when the mice were asleep or anesthetized.

The researchers next injected mice with labeled beta-amyloid and measured how long it lasted in their brains when they were asleep and awake. Beta-amyloid disappeared twice as quickly in the brains of mice that were asleep.

Glial cells control flow through the glymphatic system by shrinking and swelling. The hormone noradrenaline, which increases alertness, is known to cause cells to swell. The researchers thus tested whether the hormone might affect the glymphatic system. Treating mice with drugs that block noradrenaline induced a sleep-like state and increased brain fluid flow and extracellular brain volume. This result suggests a molecular connection between the sleep-wake cycle and the brain’s cleaning system.

The study raises the possibility that certain neurological disorders might be prevented or treated by manipulating the glymphatic system. “These findings have significant implications for treating ‘dirty brain’ diseases like Alzheimer’s,” Nedergaard says. “Understanding precisely how and when the brain activates the glymphatic system and clears waste is a critical first step in efforts to potentially modulate this system and make it work more efficiently.”

Fitness is important in dementia prevention. Click below for more info