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For white middle class, moderate drinking is linked to cognitive health in old age

August 1, 2017

Science Daily/University of California - San Diego

Older adults who consume alcohol moderately on a regular basis are more likely to live to the age of 85 without dementia or other cognitive impairments than non-drinkers, according to a new study.

 

Previous studies have found a correlation between moderate alcohol intake and longevity. "This study is unique because we considered men and women's cognitive health at late age and found that alcohol consumption is not only associated with reduced mortality, but with greater chances of remaining cognitively healthy into older age," said senior author Linda McEvoy, PhD, an associate professor at UC San Diego School of Medicine.

 

In particular, the researchers found that among men and women 85 and older, individuals who consumed "moderate to heavy" amounts of alcohol five to seven days a week were twice as likely to be cognitively healthy than non-drinkers. Cognitive health was assessed every four years over the course of the 29-year study, using a standard dementia screening test known as the Mini Mental State Examination.

 

Drinking was categorized as moderate, heavy or excessive using gender and age-specific guidelines established by the National Institute on Alcohol Abuse and Alcoholism. By its definition, moderate drinking involves consuming up to one alcoholic beverage a day for adult women of any age and men aged 65 and older; and up to two drinks a day for adult men under age 65. Heavy drinking is defined as up to three alcoholic beverages per day for women of any adult age and men 65 and older; and four drinks a day for adult men under 65. Drinking more than these amounts is categorized as excessive.

 

"It is important to point out that there were very few individuals in our study who drank to excess, so our study does not show how excessive or binge-type drinking may affect longevity and cognitive health in aging," McEvoy said. Long-term excessive alcohol intake is known to cause alcohol-related dementia.

 

The researchers said the study does not suggest drinking is responsible for increased longevity and cognitive health. Alcohol consumption, particularly of wine, is associated with higher incomes and education levels, which in turn are associated with lower rates of smoking, lower rates of mental illness and better access to health care.

 

The UC San Diego School of Medicine research team adjusted the statistical analyses to remove confounding variables, such as smoking or obesity, but noted the study is based only on statistical relationships between different demographic factors, behaviors and health outcomes. There remain on-going debates about whether and how alcohol impacts lifespan or potentially protects against cognitive impairments with age.

 

One of the study's advantages, however, is that the data derive from a relatively homogenous population in a geographically well-defined area. All of the 1,344 older adults (728 women; 616 men) who participated in the study are from Rancho Bernardo, a white-collar, middle-to-upper-middle-class suburb in San Diego County. More than 99 percent of the study participants, tracked from 1984 to 2013, are Caucasian with at least some college education.

 

"This study shows that moderate drinking may be part of a healthy lifestyle to maintain cognitive fitness in aging," said lead author Erin Richard, a graduate student in the Joint San Diego State University/UC San Diego Doctoral Program in Public Health. "However, it is not a recommendation for everyone to drink. Some people have health problems that are made worse by alcohol, and others cannot limit their drinking to only a glass or two per day. For these people, drinking can have negative consequences."

https://www.sciencedaily.com/releases/2017/08/170801131212.htm

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Green tea ingredient may ameliorate memory impairment, brain insulin resistance, and obesity

New research identifies potential therapeutic intervention for memory impairment, neuroinflammation, and brain insulin resistance induced by high-fat, high-fructose diet

July 28, 2017

Science Daily/Federation of American Societies for Experimental Biology

A new study involving mice, suggests that EGCG (epigallocatechin-3-gallate), the most abundant catechin and biologically active component in green tea, could alleviate high-fat and high-fructose (HFFD)-induced insulin resistance and cognitive impairment.

 

"Green tea is the second most consumed beverage in the world after water, and is grown in at least 30 countries," said Xuebo Liu, Ph.D., a researcher at the College of Food Science and Engineering, Northwest A&F University, in Yangling, China. "The ancient habit of drinking green tea may be a more acceptable alternative to medicine when it comes to combatting obesity, insulin resistance, and memory impairment."

 

Liu and colleagues divided 3-month-old male C57BL/6J mice into three groups based on diet:

 

1) a control group fed with a standard diet,

 

2) a group fed with an HFFD diet, and 3) a group fed with an HFFD diet and 2 grams of EGCG per liter of drinking water.

 

For 16 weeks, researchers monitored the mice and found that those fed with HFFD had a higher final body weight than the control mice, and a significantly higher final body weight than the HFFD+EGCG mice. In performing a Morris water maze test, researchers found that mice in the HFFD group took longer to find the platform compared to mice in the control group. The HFFD+EGCG group had a significantly lower escape latency and escape distance than the HFFD group on each test day. When the hidden platform was removed to perform a probe trial, HFFD-treated mice spent less time in the target quadrant when compared with control mice, with fewer platform crossings. The HFFD+EGCG group exhibited a significant increase in the average time spent in the target quadrant and had greater numbers of platform crossings, showing that EGCG could improve HFFD-induced memory impairment.

https://www.sciencedaily.com/releases/2017/07/170728100933.htm

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Is it Alzheimer's disease or another dementia?

New, noninvasive method may help with diagnosis

July 26, 2017

Science Daily/American Academy of Neurology

A new method may help determine whether a person has Alzheimer's disease or frontotemporal dementia, two different types of dementia that often have similar symptoms, according to a preliminary study.

 

"Making the correct diagnosis can be difficult," said study author Barbara Borroni, MD, of the University of Brescia in Brescia, Italy. "Current methods can be expensive brain scans or invasive lumbar punctures involving a needle inserted in the spine, so it's exciting that we may be able to make the diagnosis quickly and easily with this non-invasive procedure."

 

For the technique, called transcranial magnetic stimulation (TMS), a large electromagnetic coil is placed against the scalp. It creates electrical currents that stimulate nerve cells.

 

Once thought to be rare, frontotemporal dementia is now believed to make up 10 to 15 percent of dementia cases. It is often initially misdiagnosed as a psychiatric problem, Alzheimer's disease or Parkinson's disease because of its wide range of symptoms. The disease generally affects people in their mid-40s to mid-60s and is characterized by severe behavior changes and language problems. While there is no cure for frontotemporal dementia, it is important to accurately identify the disease so that doctors can help patients manage their symptoms and avoid unnecessary treatment.

 

For the study, researchers looked at 79 people with probable Alzheimer's disease, 61 people with probable frontotemporal dementia, and 32 people of the same age who did not have any signs of dementia.

 

Using TMS, researchers were able to measure the brain's ability to conduct electrical signals among various circuits in the brain. They found that people with Alzheimer's disease mainly had problems with one type of circuit, while people with frontotemporal dementia had problems with another type of circuit.

 

Researchers were then able to accurately distinguish frontotemporal dementia from Alzheimer's disease with 90 percent accuracy, Alzheimer's disease from healthy brains with 87 percent accuracy and frontotemporal dementia from healthy brains with 86 percent accuracy. The results were almost as good when researchers tested only people with mild forms of the disease. The accuracy of the results for a comparison of the two patient groups was comparable to tests with positron emission tomography (PET) brain scans or through testing spinal fluid through lumbar punctures, Borroni said.

 

Limitations of the study include that those operating the stimulation device were aware when they were conducting the procedure on a healthy person, but they did not know whether the other participants had Alzheimer's disease or frontotemporal dementia. In addition, the dementia diagnoses were not confirmed by autopsy after death.

 

"If our results can be replicated with larger studies, this will be very exciting," Borroni said. "Doctors might soon be able to quickly and easily diagnose frontotemporal dementia with this non-invasive procedure. This disease unfortunately can't be cured, but it can be managed -- especially if it is caught early."

https://www.sciencedaily.com/releases/2017/07/170726161142.htm

 

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How physical exercise prevents dementia

July 21, 2017

Science Daily/Goethe-Universität Frankfurt am Main

Physical exercise seems beneficial in the prevention of cognitive impairment and dementia in old age, numerous studies have shown. Now researchers have explored in one of the first studies worldwide how exercise affects brain metabolism.

 

Numerous studies have shown that physical exercise seems beneficial in the prevention of cognitive impairment and dementia in old age. Now researchers at Goethe University Frankfurt have explored in one of the first studies worldwide how exercise affects brain metabolism.

 

In order to further advance current state of knowledge on the positive influence of physical activity on the brain, gerontologists and sports physicians at Goethe University Frankfurt have examined the effects of regular exercise on brain metabolism and memory of 60 participants aged between 65 and 85 in a randomised controlled trial. Their conclusion: regular physical exercise not only enhances fitness but also has a positive impact on brain metabolism.

 

As the researchers report in the current issue of the medical journal Translational Psychiatry, they thoroughly examined all the participants in the SMART study (Sport and Metabolism in Older Persons, an MRT Study) by assessing movement-related parameters, cardiopulmonary fitness and cognitive performance. In addition, magnetic resonance tomography (MRT) and magnetic resonance spectroscopy (MRS) were used to measure brain metabolism and brain structure. Following this examination, the participants mounted an exercise bike three times a week over a period of 12 weeks. The 30-minute training sessions were individually adapted to each participant's performance level. The participants were examined again after the end of the programme in order to document the effects of this physical activity on brain metabolism, cognitive performance and brain structure. The researchers also investigated to what extent exercise had led to an improvement in the participants' physical fitness. The study was conducted by the Gerontology Department of the Institute of General Medicine (headed by Professor Johannes Pantel) and the Department of Sports Medicine (led by Professor Winfried Banzer).

 

As expected, physical activity had influenced brain metabolism: it prevented an increase in choline. The concentration of this metabolite often rises as a result of the increased loss of nerve cells, which typically occurs in the case of Alzheimer's disease. Physical exercise led to stable cerebral choline concentrations in the training group, whereas choline levels increased in the control group. The participants' physical fitness also improved: they showed increased cardiac efficiency after the training period. Overall, these findings suggest that physical exercise not only improves physical fitness but also protects cells.

https://www.sciencedaily.com/releases/2017/07/170721090107.htm

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Sleep disorders may increase cognitive problems particularly in those at risk for Alzheimer's

July 21, 2017

Science Daily/American Thoracic Society

People who carry a genetic susceptibility to Alzheimer's disease appear to be at greater risk of diminished cognition from sleep-disordered breathing than those without the susceptibility, according to new research.

 

In "Greater Cognitive Deficits with Sleep-Disordered Breathing among Individuals with Genetic Susceptibility to Alzheimer's Disease: The Multi-Ethnic Study of Atherosclerosis," researchers report that study participants carrying the apolipoprotein ?-4 (APOE-?4) allele showed greater cognitive deficits with the various indices of sleep-disordered breathing compared to those without the allele.

 

APOE is a major cholesterol carrier that supports injury repair in the brain. Other studies have shown that those carrying the alternate form of the gene, ?4 allele, are at increased risk of Alzheimer's disease. Estimates are that 20 percent of the population carries the ?4 allele.

 

"Previous studies have shown inconsistent findings between sleep-disordered breathing and cognition, which may be due to the different tests used," said lead study author Dayna A. Johnson, PhD, MPH, MS, MSW, instructor of medicine at Brigham and Women's Hospital and Harvard Medical School.

 

Dr. Johnson and colleagues investigated the association in a diverse sample using several indicators of sleep-disordered breathing and cognition. They also evaluated whether the presence of the APOE-?4 allele, which is known to increase risk of Alzheimer's disease, influenced the link between sleep-disordered breathing and cognition.

 

The authors analyzed data from 1,752 participants (average age 68) in the Multi-Ethnic Study of Atherosclerosis (MESA) who underwent an in-home polysomnography (sleep) study, completed standardized sleep questions, and a battery of tests to measure their cognition. The authors defined sleep-disordered breathing as an apnea-hypopnea index (AHI), which measures the number of stopped or shallow breaths per hour, as AHI > 15, and sleep apnea syndrome as AHI > 5 (below 5 is normal) plus self-reported sleepiness (based on a standardized scale).

https://www.sciencedaily.com/releases/2017/07/170721084704.htm

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Bacteria found in Alzheimer's brains

Brains from patients with Alzheimer's disease show changes in bacterial populations compared with healthy brains

July 17, 2017

Science Daily/Frontiers

Researchers have used DNA sequencing to examine bacteria in post-mortem brains from patients with Alzheimer's disease. Their findings suggest increased bacterial populations and different proportions of specific bacteria in Alzheimer's, compared with healthy brains. The findings may support evidence that bacterial infection and inflammation in the brain could contribute to Alzheimer's disease.

 

Alzheimer's disease is a neurodegenerative disease that results in cognitive decline, and eventually death. In the brain, the disease causes neurons to die and break down, and involves high levels of a peptide called amyloid and aggregations of a protein called tau. However, scientists are coming to appreciate that inflammation may also play a role.

 

"Alzheimer's brains usually contain evidence of neuroinflammation, and researchers increasingly think that this could be a possible driver of the disease, by causing neurons in the brain to degenerate," says David Emery, a researcher from the University of Bristol, and an author on the study, which was recently published in Frontiers in Aging Neuroscience.

 

So, what's causing this inflammation? Some genetic risk-factors for Alzheimer's disease can have effects on the inflammatory response, but infection may also play a role. "Neuroinflammation in the brain may be a reaction to the presence of bacteria," says Emery. The brain is normally sealed behind specialized blood vessels that make it very difficult for things like bacteria in the blood to enter. However, at least one of the genetic risk-factors for Alzheimer's disease may cause these blood vessels to lose some of their integrity, which could allow bacteria to enter and colonize the brain.

 

The research team set out to discover if there were any differences in the types of bacteria present in brains from Alzheimer's disease patients and healthy brains. "Previous studies looking at bacteria in the Alzheimer's brain have primarily investigated specific bacterial species," explains Shelley Allen, another researcher involved in the study. "We wanted to use an unbiased method to obtain the fullest overview possible of the entire bacterial population in the Alzheimer's brain, and compare these results with those from a healthy aged brain."

 

The researchers analyzed eight Alzheimer's and six healthy brain samples from a brain bank, where people donate their brains after death for medical research. They used a technique called next generation sequencing (NGS) to detect specific bacterial genes. "NGS technology allows millions of these DNA molecules to be sequenced at the same time, providing an unbiased overview of a complex bacterial population," explains Allen.

 

They found that the Alzheimer's brains contained different proportions of specific bacteria compared with the healthy brains. "Comparing the bacterial populations showed at least a tenfold higher ratio overall of Actinobacteria (mostly P. acnes) to Proteobacteria in the Alzheimer's brain compared with the healthy brain," says Emery.

 

However, the researchers were surprised to find that there also appeared to be more bacteria in the Alzheimer's brains. "Unexpectedly, Alzheimer's brains gave on average an apparent 7-fold increase in bacterial sequences above that seen in the healthy brain," says Allen. "The healthy brains yielded only low levels of bacterial sequences, consistent with either a background signal or normal levels present in the blood stream in brain tissue."

 

The team caution that the NGS method does not directly indicate actual bacterial numbers, and further work will be required to confirm that bacteria play an active role in Alzheimer's disease. "We need quantitative studies on the bacterial presence in the brain," says Allen. "Larger numbers of brain samples are required, and future studies should also investigate if bacteria are involved in other neurodegenerative diseases involving neuroinflammation."

https://www.sciencedaily.com/releases/2017/07/170717100425.htm

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Sleep, Alzheimer's link explained

July 10, 2017

Science Daily/Washington University in St. Louis

Disrupting just one night of sleep in healthy, middle-aged adults causes an increase in a brain protein associated with Alzheimer's disease, research shows. 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.

 

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.

 

"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."

https://www.sciencedaily.com/releases/2017/07/170710161442.htm

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Sleep problems may be early sign of Alzheimer's

July 5, 2017

Science Daily/American Academy of Neurology

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. 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 5.7 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.

 

"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.

https://www.sciencedaily.com/releases/2017/07/170705164548.htm

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Sleep after learning strengthens connections between brain cells and memory

June 5, 2014

Science Daily/NYU Langone Medical Center / New York University School of Medicine

Researchers show for the first time that sleep after learning encourages the growth of dendritic spines, the tiny protrusions from brain cells that connect to other brain cells and facilitate the passage of information across synapses, the junctions at which brain cells meet.

The findings, in mice, provide important physical evidence in support of the hypothesis that sleep helps consolidate and strengthen new memories, and show for the first time how learning and sleep cause physical changes in the motor cortex, a brain region responsible for voluntary movements.

"We've known for a long time that sleep plays an important role in learning and memory. If you don't sleep well you won't learn well," says senior investigator Wen-Biao Gan, PhD, professor of neuroscience and physiology and a member of the Skirball Institute of Biomolecular Medicine at NYU Langone Medical Center. "But what's the underlying physical mechanism responsible for this phenomenon? Here we've shown how sleep helps neurons form very specific connections on dendritic branches that may facilitate long-term memory. We also show how different types of learning form synapses on different branches of the same neurons, suggesting that learning causes very specific structural changes in the brain."

On the cellular level, sleep is anything but restful: Brain cells that spark as we digest new information during waking hours replay during deep sleep, also known as slow-wave sleep, when brain waves slow down and rapid-eye movement, as well as dreaming, stops. Scientists have long believed that this nocturnal replay helps us form and recall new memories, yet the structural changes underpinning this process have remained poorly understood.

To shed light on this process, Dr. Gan and colleagues employed mice genetically engineered to express a fluorescent protein in neurons. Using a special laser-scanning microscope that illuminates the glowing fluorescent proteins in the motor cortex, the scientists were then able to track and image the growth of dendritic spines along individual branches of dendrites before and after mice learned to balance on a spin rod. Over time mice learned how to balance on the rod as it gradually spun faster. "It's like learning to ride a bike," says Dr. Gan. "Once you learn it, you never forget."

After documenting that mice, in fact, sprout new spines along dendritic branches, within six hours after training on the spinning rod, the researchers set out to understand how sleep would impact this physical growth. They trained two sets of mice: one trained on the spinning rod for an hour and then slept for 7 hours; the second trained for the same period of time on the rod but stayed awake for 7 hours. The scientists found that the sleep-deprived mice experienced significantly less dendritic spine growth than the well-rested mice. Furthermore, they found that the type of task learned determined which dendritic branches spines would grow.

Running forward on the spinning rod, for instance, produced spine growth on different dendritic branches than running backward on the rod, suggesting that learning specific tasks causes specific structural changes in the brain.

"Now we know that when we learn something new, a neuron will grow new connections on a specific branch," says Dr. Gan. "Imagine a tree that grows leaves (spines) on one branch but not another branch. When we learn something new, it's like we're sprouting leaves on a specific branch."

Finally, the scientists showed that brain cells in the motor cortex that activate when mice learn a task reactivate during slow-wave deep sleep. Disrupting this process, they found, prevents dendritic spine growth. Their findings offer an important insight into the functional role of neuronal replay -- the process by which the sleeping brain rehearses tasks learned during the day -- observed in the motor cortex.

"Our data suggest that neuronal reactivation during sleep is quite important for growing specific connections within the motor cortex," Dr. Gan adds.

http://www.sciencedaily.com/releases/2014/06/140605141849.htm

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Short and long sleep, and sleep disturbances associated with increased risk of dementia and lung cancer

May 24, 2017

Science Daily/University of Eastern Finland

Difficulties in initiating or maintaining sleep at middle-age are associated with an increased risk of dementia, according to a new study. The 20-year follow-up study was conducted among 2,682 men participating the Kuopio Ischaemic Heart Disease Study. Shorter or longer sleep than 7–7.5 hours related independently with an increased risk of lung cancer after health behavior, such as smoking, was taken account of. Additionally, a relationship between higher serum copper levels and short sleep duration was observed.

uring sleep, the body's energy is allocated to cellular repair, immune functions, neuronal plasticity of the brain, and memory consolidation. The need of sleep is individual and differs during the lifespan. For adults, the recommended sleep duration is 7 to 9 hours. Insufficient sleep, sleep-disordered breathing, insomnia or disruptions in the sleep-wake rhythm can lead to excessive daytime tiredness. Acute effects of poor sleep include difficulties in cognitive tasks, increased need for energy, increased cellular stress, as well as lower heart rate and body temperature. Long-term sleep disturbances both precede and co-occur with chronic diseases, such as cardiovascular diseases, cancer and dementia. Furthermore, an increased mortality risk is observed in individuals with short or long sleep duration.

The underlying factors regarding the association between sleep duration and an increased risk of lung cancer concern low-grade inflammation and disruptions in melatonin secretion. These factors contribute to the pathogenesis of cancer and acceleration of tumour growth. Low-grade inflammation is associated with sleep duration and zinc and copper levels, which contribute to pro-oxidative processes and thereby may increase the risk of cardiovascular diseases and cancer. An association between sleep disturbances and dementia may result from structural changes in the brain, low-grade inflammation, and disruptions of neurogenesis.

Science Daily/SOURCE :https://www.sciencedaily.com/releases/2017/05/170524084505.htm

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