Memory

Taking hour-long afternoon naps improves thinking and memory in older Chinese adults

January 5, 2017

American Geriatrics Society

Study participants who took an hour-long nap after lunch did better on the mental tests compared to the people who did not nap. Those who napped for about an hour also did better than people who took shorter or longer rests. People who took no naps, short naps, or longer naps experienced decreases in their mental ability that were about four to six times greater than people who took hour-long naps.

 

Preserving your memory, as well as your ability to think clearly and make decisions, is a key goal for people as they age. Researchers have a growing interest in the role sleep plays in helping older adults maintain their healthy mental function.

 

Recently, researchers examined information provided by nearly 3,000 Chinese adults aged 65 and older to learn whether taking an afternoon nap had any effect on mental health. Their study was published in the Journal of the American Geriatrics Society.

 

Nearly 60 percent of the people in the study said they napped after lunch in the afternoon. They napped between about 30 minutes to more than 90 minutes, with most people taking naps lasting about 63 minutes.

 

The participants took several tests to assess their mental status. They answered simple questions -- such as questions about the date, the season of the year, etc. -- and they did some basic math problems. Participants also were asked to memorize and recall words, and were asked to copy drawings of simple geometric figures. Finally, these older Chinese adults were asked questions about their napping and nighttime sleep habits.

 

According to the study's results, people who took an hour-long nap after lunch did better on the mental tests compared to the people who did not nap. Those who napped for about an hour also did better than people who took shorter or longer rests. People who took no naps, short naps, or longer naps experienced decreases in their mental ability that were about four-to-six times greater than people who took hour-long naps.

 

The people who did not nap, and those who took shorter or longer naps, experienced about the same decline in their mental abilities that a five-year increase in age would be expected to cause.

 

This summary is from "Afternoon Napping and Cognition in Chinese Older Adults: Findings From the China Health and Retirement Longitudinal Study (CHARLS) Baseline Assessment." It appears online ahead of print in the January 2017 issue of the Journal of the American Geriatrics Society. The study authors are Junxin Li, PhD; Pamela Z. Cacchione, PhD; Nancy Hodgson, PhD; Barbara Riegel, PhD; Brendan T. Keenan, MS; Mathew T. Scharf, MD, PhD; Kathy C. Richards, PhD; and Nalaka S. Gooneratne, MD.

https://www.sciencedaily.com/releases/2017/01/170105123148.htm

People learn while they sleep

September 27, 2011

Science Daily/Michigan State University

People may be learning while they're sleeping -- an unconscious form of memory that is still not well understood, according to a new study.

 

The findings are highlighted in the Journal of Experimental Psychology: General.

 

"We speculate that we may be investigating a separate form of memory, distinct from traditional memory systems," said Kimberly Fenn, assistant professor of psychology and lead researcher on the project. "There is substantial evidence that during sleep, your brain is processing information without your awareness and this ability may contribute to memory in a waking state."

 

In the study of more than 250 people, Fenn and Zach Hambrick, associate professor of psychology, suggest people derive vastly different effects from this "sleep memory" ability, with some memories improving dramatically and others not at all. This ability is a new, previously undefined form of memory.

 

"You and I could go to bed at the same time and get the same amount of sleep," Fenn said, "but while your memory may increase substantially, there may be no change in mine." She added that most people showed improvement.

 

Fenn said she believes this potential separate memory ability is not being captured by traditional intelligence tests and aptitude tests such as the SAT and ACT.

 

"This is the first step to investigate whether or not this potential new memory construct is related to outcomes such as classroom learning," she said.

It also reinforces the need for a good night's sleep. According to the National Sleep Foundation, people are sleeping less every year, with 63 percent of Americans saying their sleep needs are not being met during the week.

"Simply improving your sleep could potentially improve your performance in the classroom," Fenn said.

http://www.sciencedaily.com/releases/2011/09/110927124653.htm

 

Sleep And Memory

January 3, 2017

By Anne Foy, Guest Contributor

For some years now, the world appears to have seen sleep as an inconvenience. Sure, we acknowledge that it’s something which needs to happen. We’re even aware of the dire consequences [1] of not getting enough sleep [2]. But we nonetheless try to push it to the margins of our existence. We force ourselves out of bed before we’re fully awake, and, at the other end of the day, bludgeon our exhausted brains into keeping us awake for longer. We stifle sleep with caffeine, or bring it on artificially with pills [3]. We try to make it into our servant, to be called upon at times of our choosing and hidden away when not wanted. Little wonder that so many of us are struggling with sleep disorders. However, poor sleep does a lot more than simply make us feel groggy and slow. Over time, chronic lack of sleep can have a very serious impact upon your cognition. In particular, sleep is associated with good memory function - so much so that disordered sleeping habits are associated with dementia.

More Than Just ‘Recharging’ Time

There is a common misconception that sleep is about ‘switching off’ in order to ‘recharge’. Humans aren’t cellphones, however. We’re far, far more complicated than that. Sleep is in fact the time when your body and mind carries out some of its most complex operations - the kind of thing it doesn’t want your conscious mind and day to day life interrupting. This is why doctors and healthcare providers [4] are eager for patients to sleep well - without good sleep, a lot of these vital health and maintenance operations go undone, leading to myriad health issues down the line. One of these vital operations is the sorting and processing of memories. We’ve known for a long time that sleep plays an incredibly important role in healthy memory, but haven’t been entirely sure precisely what it does or how it does it. Recently, however, a lot of facts about sleep and memory have been discovered [5] - and revealed serious implications about lack of sleep and cognitive decline.

Deep Sleep Neuron Connections

When we’re in deep, ‘slow-wave’ sleep, our brains effectively ‘replay’ what we’ve experienced during the day. As we’re asleep, it’s able to do this without cognitive interruption, and therefore ‘concentrate’ (for want of a better word) on what it’s experienced. During deep sleep, scientists have observed [6] brains making lots of new connections between neurons. New connections forming between neurons is what ‘learning’ looks like from a neurobiological perspective. From a psychological perspective, ‘learning’ involves taking memories, extrapolating from them, and then storing those memories in ‘long-term’. This is the process the scientists observed occurring in the brains of sleeping subjects.

Lack Of Sleep And Dementia

Quite obviously, if your brain uses its deep sleep time to sort through, store, and learn from memories, a lack of deep sleep is going to cause issues with memory. However, it seems to go a lot deeper than the odd spate of simple forgetfulness. Studies show that disturbed sleep patterns can significantly increase one’s chances of developing dementia. As yet, nobody is entirely sure why this should be the case, but the facts are indisputable [7], and many are reasonably sure that it has something to do with sleep’s role in memory formation. Some speculate that lack of usage during deep sleep causes the brain's memory-retention functions to degrade. Others believe that lack of sleep generally puts an inordinate amount of strain on the brain, causing cell death and therefore cognitive decline.All in all, whatever is actually going on inside the skull, if you want to learn more, remember more, and generally maintain good cognitive health, it’s best to sort out your sleep cycle - and quickly!

[1] Think!, “Fatigue”, UK Government

[2] Mercola, “How Dangerous Is Sleep Deprivation, Really?”, Mar 2014

[3] Ny Daily News, “CDC: 9 million Americans use prescription sleeping pills”, Aug 2013

[4] Q, "health cover"

[5] James Gallagher, “Sleep’s memory role discovered”, BBC, Jun 2014

[6] Guang Yang, Cora Sau Wan Lai, Joseph Cichon, Lei Ma, Wei Li, Wen-Biao Gan, “Sleep promotes branch-specific formation of dendritic spines after learning”, Science, Jun 2014

[7] Caroline Cassels, “Disturbed Sleep Linked To Increased Dementia Risk”, Medscape, Jul 2014

 

Stress Makes Snails Forgetful

November 6, 2013
Science Daily/University of Exeter
http://images.sciencedaily.com/2013/11/131106202239-large.jpg
New research on pond snails has revealed that high levels of stress can block memory processes. Researchers from the University of Exeter and the University of Calgary trained snails and found that when they were exposed to multiple stressful events they were unable remember what they had learned.

Previous research has shown that stress also affects human ability to remember. This study, published in the journal PLOS ONE, found that experiencing multiple stressful events simultaneously has a cumulative detrimental effect on memory.

Dr Sarah Dalesman, a Leverhulme Trust Early Career Fellow, from the University of Exeter, formally at the University of Calgary, said: "It's really important to study how different forms of stress interact as this is what animals, including people, frequently experience in real life. By training snails, and then observing their behaviour and brain activity following exposure to stressful situations, we found that a single stressful event resulted in some impairment of memory but multiple stressful events prevented any memories from being formed."

The pond snail, Lymnaea stagnalis, has easily observable behaviours linked to memory and large neurons in the brain, both useful benefits when studying memory processes. They also respond to stressful events in a similar way to mammals, making them a useful model species to study learning and memory.

In the study, the pond snails were trained to reduce how often they breathed outside water. Usually pond snails breathe underwater and absorb oxygen through their skin. In water with low oxygen levels the snails emerge and inhale air using a basic lung opened to the air via a breathing hole.

To train the snails not to breathe air they were placed in poorly oxygenated water and their breathing holes were gently poked every time they emerged to breathe. Snail memory was tested by observing how many times the snails attempted to breathe air after they had received their training. Memory was considered to be present if there was a reduction in the number of times they opened their breathing holes. The researchers also assessed memory by monitoring neural activity in the brain.

Immediately before training, the snails were exposed to two different stressful experiences, low calcium -- which is stressful as calcium is necessary for healthy shells -- and overcrowding by other pond snails.

When faced with the stressors individually, the pond snails had reduced ability to form long term memory, but were still able to learn and form short and intermediate term memory lasting from a few minutes to hours. However, when both stressors were experienced at the same time, results showed that they had additive effects on the snails' ability to form memory and all learning and memory processes were blocked.
Science Daily/SOURCE :http://www.sciencedaily.com/releases/2013/11/131106202239.htm

People With Highly Superior Powers of Recall Also Vulnerable to False Memories

November 19, 2013
Science Daily/University of California - Irvine
http://images.sciencedaily.com/2013/11/131119131438-large.jpg
People who can accurately remember details of their daily lives going back decades are as susceptible as everyone else to forming fake memories, UC Irvine psychologists and neurobiologists have found.

"Finding susceptibility to false memories even in people with very strong memory could be important for dissemination to people who are not memory experts. For example, it could help communicate how widespread our basic susceptibility to memory distortions is," said Lawrence Patihis, a graduate student in psychology & social behavior at UC Irvine. "This dissemination could help prevent false memories in the legal and clinical psychology fields, where contamination of memory has had particularly important consequences in the past."

"What I love about the study is how it communicates something that memory distortion researchers have suspected for some time: that perhaps no one is immune to memory distortion," Patihis said. "It will probably make some nonexperts realize, finally, that if even memory prodigies are susceptible, then they probably are too. This teachable moment is almost as important as the scientific merit of the study. It could help educate people -- including those who deal with memory evidence, such as clinical psychologists and legal professionals -- about false memories."

Science Daily/SOURCE :http://www.sciencedaily.com/releases/2013/11/131119131438.htm

Age-Related Cognitive Decline Linked to Synapses in Prefrontal Cortex

December 2, 2013
Science Daily/Mount Sinai Medical Center
Age-related cognitive decline and changes in the nervous system are closely linked, but up until recently, they were thought to result from the loss of neurons in areas such as the prefrontal cortex, the part of the brain important in working memory. A series of papers have shown that the "loss of neurons" concept is simply not true. 

Now, Mount Sinai scientists have begun to look elsewhere, focusing instead on synaptic health in the prefrontal cortex. Their work, published online in the December 2 issue of the peer-reviewed journal Proceedings of the National Academy of Sciences, shows that synaptic health in the brain is closely linked to cognitive decline. Further, the scientists show that estrogen restores synaptic health and also improves working memory.

"We are increasingly convinced that maintenance of synaptic health as we age, rather than rescuing cognition later, is critically important in preventing age-related cognitive decline and Alzheimer's disease," said the study's senior author, John Morrison, PhD, and Dean of Basic Sciences and Professor of the Fishberg Department of Neuroscience and the Friedman Brain Institute, at the Icahn School of Medicine at Mount Sinai.
Science Daily/SOURCE :http://www.sciencedaily.com/releases/2013/12/131202152031.htm

Vitamin B may not reduce risk of memory loss after all

November 12, 2014
Science Daily/American Academy of Neurology (AAN)
Taking vitamin B12 and folic acid supplements may not reduce the risk of memory and thinking problems after all, according to a new study. The study is one of the largest to date to test long-term use of supplements and thinking and memory skills.

The study involved people with high blood levels of homocysteine, an amino acid. High levels of homocysteine have been linked to memory loss and Alzheimer's disease.

"Since homocysteine levels can be lowered with folic acid and vitamin B12 supplements, the hope has been that taking these vitamins could also reduce the risk of memory loss and Alzheimer's disease," said study author Rosalie Dhonukshe-Rutten, PhD, of Wageningen University in Wageningen, the Netherlands.

Early observational studies showed there may be some benefit to thinking and memory skills in taking folic acid and vitamin B12, but the results of later randomized, controlled trials were less convincing.

For the current study, 2,919 people with an average age of 74 took either a tablet with 400 μg of folic acid and 500 μg of vitamin B12 or a placebo every day for two years. Tests of memory and thinking skills were performed at the beginning and end of the study. All of the participants had high blood levels of homocysteine.

"While the homocysteine levels decreased by more in the group taking the B vitamins than in the group taking the placebo, unfortunately there was no difference between the two groups in the scores on the thinking and memory tests," said Dhonukshe-Rutten.
Science Daily/SOURCE :http://www.sciencedaily.com/releases/2014/11/141112161038.htm

Brain training can help in fight against dementia, meta-analysis shows

November 14, 2016


Science Daily/University of Sydney
Engaging in computer-based brain training can improve memory and mood in older adults with mild cognitive impairment, say researchers, but training is no longer effective once a dementia diagnosis has been made, they add.

The team, comprising researchers from the Brain and Mind Centre, reviewed more than 20 years of research and showed that brain training could lead to improvements in global cognition, memory, learning and attention, as well as psychosocial functioning (mood and self-perceived quality of life) in people with mild cognitive impairment. Conversely, when data from 12 studies of brain training in people with dementia was combined, results were not positive.

The results are published today in the American Journal of Psychiatry.

Mild cognitive impairment involves a decline in memory and other thinking skills despite generally intact daily living skills, and is one of strongest risk factors for dementia. People with mild cognitive impairment are at one-in-10 risk of developing dementia within a year -- and the risk is markedly higher among those with depression.

Brain training is a treatment for enhancing memory and thinking skills by practising mentally challenging computer-based exercises -- which are designed to look and feel like video games.

Dr Amit Lampit from the School of Psychology, who led the study said the results showed brain training could play an important role in helping to prevent dementia.

"Our research shows that brain training can maintain or even improve cognitive skills among older people at very high risk of cognitive decline -- and it's an inexpensive and safe treatment," Dr Lampit said.

To arrive at their conclusions, the team combined outcomes from 17 randomised clinical trials including nearly 700 participants, using a mathematical approach called meta-analysis, widely recognised as the highest level of medical evidence.

The team has used meta-analysis before to show that brain training is useful in other populations, such as healthy older adults and those with Parkinson's disease.

"Taken together, these wide-ranging analyses have provided the necessary evidence to pursue clinical implementation of brain training in the aged-care sector -- while continuing research aimed at improving training effectiveness," Dr Lampit said.

Associate Professor Michael Valenzuela, leader of the Regenerative Neuroscience Group at the Brain and Mind Centre, believes new technology is the key to moving the field forward.

"The great challenges in this area are maintaining training gains over the long term and moving this treatment out of the clinic and into people's homes. " Associate Professor Valenzuela said.

"This is exactly what we are working on right now."

Associate Professor Valenzuela is one of the leaders of the multi-million-dollar Australian Maintain your Brain trial that will test if a tailored program of lifestyle modification, including weekly brain training over four years, can prevent dementia in a group of 18,000 older adults.

Science Daily/SOURCE :https://www.sciencedaily.com/releases/2016/11/161114105531.htm

Unique visual stimulation may be new treatment for Alzheimer's

Noninvasive technique reduces beta amyloid plaques in mouse models of Alzheimer's disease

December 7, 2016

Science Daily/Massachusetts Institute of Technology
Using LED lights flickering at a specific frequency, researchers have shown that they can significantly reduce the beta amyloid plaques seen in Alzheimer's disease in the visual cortex of mice. This treatment appears to work by stimulating brain waves known as gamma oscillations, which the researchers discovered help the brain suppress beta amyloid production and invigorate cells responsible for destroying the plaques.
https://images.sciencedaily.com/2016/12/161207133541_1_540x360.jpg
Professor Li-Huei Tsai, director of MIT's Picower Institute for Learning and Memory, and senior author of the study, which appears in the Dec. 7 online edition of Nature.
Credit: Bryce Vickmark

This treatment appears to work by inducing brain waves known as gamma oscillations, which the researchers discovered help the brain suppress beta amyloid production and invigorate cells responsible for destroying the plaques.

Further research will be needed to determine if a similar approach could help Alzheimer's patients, says Li-Huei Tsai, the Picower Professor of Neuroscience, director of MIT's Picower Institute for Learning and Memory, and senior author of the study, which appears in the Dec. 7 online edition of Nature.

"It's a big 'if,' because so many things have been shown to work in mice, only to fail in humans," Tsai says. "But if humans behave similarly to mice in response to this treatment, I would say the potential is just enormous, because it's so noninvasive, and it's so accessible."

Tsai and Ed Boyden, an associate professor of biological engineering and brain and cognitive sciences at the MIT Media Lab and the McGovern Institute for Brain Research, who is also an author of the Nature paper, have started a company called Cognito Therapeutics to pursue tests in humans. The paper's lead authors are graduate student Hannah Iaccarino and Media Lab research affiliate Annabelle Singer.

"This important announcement may herald a breakthrough in the understanding and treatment of Alzheimer's disease, a terrible affliction affecting millions of people and their families around the world," says Michael Sipser, dean of MIT's School of Science. "Our MIT scientists have opened the door to an entirely new direction of research on this brain disorder and the mechanisms that may cause or prevent it. I find it extremely exciting."

Brain wave stimulation

Alzheimer's disease, which affects more than 5 million people in the United States, is characterized by beta amyloid plaques that are suspected to be harmful to brain cells and to interfere with normal brain function. Previous studies have hinted that Alzheimer's patients also have impaired gamma oscillations. These brain waves, which range from 25 to 80 hertz (cycles per second), are believed to contribute to normal brain functions such as attention, perception, and memory.

In a study of mice that were genetically programmed to develop Alzheimer's but did not yet show any plaque accumulation or behavioral symptoms, Tsai and her colleagues found impaired gamma oscillations during patterns of activity that are essential for learning and memory while running a maze.

Next, the researchers stimulated gamma oscillations at 40 hertz in a brain region called the hippocampus, which is critical in memory formation and retrieval. These initial studies relied on a technique known as optogenetics, co-pioneered by Boyden, which allows scientists to control the activity of genetically modified neurons by shining light on them. Using this approach, the researchers stimulated certain brain cells known as interneurons, which then synchronize the gamma activity of excitatory neurons.

After an hour of stimulation at 40 hertz, the researchers found a 40 to 50 percent reduction in the levels of beta amyloid proteins in the hippocampus. Stimulation at other frequencies, ranging from 20 to 80 hertz, did not produce this decline.

Tsai and colleagues then began to wonder if less-invasive techniques might achieve the same effect. Tsai and Emery Brown, the Edward Hood Taplin Professor of Medical Engineering and Computational Neuroscience, a member of the Picower Institute, and an author of the paper, came up with the idea of using an external stimulus -- in this case, light -- to drive gamma oscillations in the brain. The researchers built a simple device consisting of a strip of LEDs that can be programmed to flicker at different frequencies.

Using this device, the researchers found that an hour of exposure to light flickering at 40 hertz enhanced gamma oscillations and reduced beta amyloid levels by half in the visual cortex of mice in the very early stages of Alzheimer's. However, the proteins returned to their original levels within 24 hours.

The researchers then investigated whether a longer course of treatment could reduce amyloid plaques in mice with more advanced accumulation of amyloid plaques. After treating the mice for an hour a day for seven days, both plaques and free-floating amyloid were markedly reduced. The researchers are now trying to determine how long these effects last.

Furthermore, the researchers found that gamma rhythms also reduced another hallmark of Alzheimer's disease: the abnormally modified Tau protein, which can form tangles in the brain.

Tsai's lab is now studying whether light can drive gamma oscillations in brain regions beyond the visual cortex, and preliminary data suggest that this is possible. They are also investigating whether the reduction in amyloid plaques has any effects on the behavioral symptoms of their Alzheimer's mouse models, and whether this technique could affect other neurological disorders that involve impaired gamma oscillations.

Two modes of action

The researchers also performed studies to try to figure out how gamma oscillations exert their effects. They found that after gamma stimulation, the process for beta amyloid generation is less active. Gamma oscillations also improved the brain's ability to clear out beta amyloid proteins, which is normally the job of immune cells known as microglia.

"They take up toxic materials and cell debris, clean up the environment, and keep neurons healthy," Tsai says.

In Alzheimer's patients, microglia cells become very inflammatory and secrete toxic chemicals that make other brain cells more sick. However, when gamma oscillations were boosted in mice, their microglia underwent morphological changes and became more active in clearing away the beta amyloid proteins.

"The bottom line is, enhancing gamma oscillations in the brain can do at least two things to reduced amyloid load. One is to reduce beta amyloid production from neurons. And second is to enhance the clearance of amyloids by microglia," Tsai says.

The researchers also sequenced messenger RNA from the brains of the treated mice and found that hundreds of genes were over- or underexpressed, and they are now investigating the possible impact of those variations on Alzheimer's disease.

Science Daily/SOURCE :https://www.sciencedaily.com/releases/2016/12/161207133541.htm

 

Taking hour-long afternoon naps improves thinking and memory in older Chinese adults

January 5, 2017


Science Daily/American Geriatrics Society
Study participants who took an hour-long nap after lunch did better on the mental tests compared to the people who did not nap. Those who napped for about an hour also did better than people who took shorter or longer rests. People who took no naps, short naps, or longer naps experienced decreases in their mental ability that were about four to six times greater than people who took hour-long naps.

Preserving your memory, as well as your ability to think clearly and make decisions, is a key goal for people as they age. Researchers have a growing interest in the role sleep plays in helping older adults maintain their healthy mental function.

Recently, researchers examined information provided by nearly 3,000 Chinese adults aged 65 and older to learn whether taking an afternoon nap had any effect on mental health. Their study was published in the Journal of the American Geriatrics Society.

Nearly 60 percent of the people in the study said they napped after lunch in the afternoon. They napped between about 30 minutes to more than 90 minutes, with most people taking naps lasting about 63 minutes.

The participants took several tests to assess their mental status. They answered simple questions -- such as questions about the date, the season of the year, etc. -- and they did some basic math problems. Participants also were asked to memorize and recall words, and were asked to copy drawings of simple geometric figures. Finally, these older Chinese adults were asked questions about their napping and nighttime sleep habits.

According to the study's results, people who took an hour-long nap after lunch did better on the mental tests compared to the people who did not nap. Those who napped for about an hour also did better than people who took shorter or longer rests. People who took no naps, short naps, or longer naps experienced decreases in their mental ability that were about four-to-six times greater than people who took hour-long naps.

The people who did not nap, and those who took shorter or longer naps, experienced about the same decline in their mental abilities that a five-year increase in age would be expected to cause.

This summary is from "Afternoon Napping and Cognition in Chinese Older Adults: Findings From the China Health and Retirement Longitudinal Study (CHARLS) Baseline Assessment." It appears online ahead of print in the January 2017 issue of the Journal of the American Geriatrics Society. The study authors are Junxin Li, PhD; Pamela Z. Cacchione, PhD; Nancy Hodgson, PhD; Barbara Riegel, PhD; Brendan T. Keenan, MS; Mathew T. Scharf, MD, PhD; Kathy C. Richards, PhD; and Nalaka S. Gooneratne, MD.

Science Daily/SOURCE :https://www.sciencedaily.com/releases/2017/01/170105123148.htm

Meditation and music may help reverse early memory loss in adults at risk for Alzheimer’s Disease

January 21, 2017


Science Daily/IOS Press
In a recent study of adults with early memory loss, scientists found that practice of a simple meditation or music listening program may have multiple benefits for older adults with preclinical memory loss.

In this randomized controlled trial, 60 older adults with subjective cognitive decline (SCD), a condition that may represent a preclinical stage of Alzheimer's disease, were assigned to either a beginner meditation (Kirtan Kriya) or music listening program and asked to practice 12 minutes/day for 12 weeks. As detailed in a paper recently published by the Journal of Alzheimer's Disease, both the meditation and music groups showed marked and significant improvements in subjective memory function and objective cognitive performance at 3 months. These included domains of cognitive functioning most likely to be affected in preclinical and early stages of dementia (e.g., attention, executive function, processing speed, and subjective memory function). The substantial gains observed in memory and cognition were maintained or further increased at 6 months (3 months post-intervention).

As explained in the research team's previous paper (J Alzheimer's Dis. 52 (4): 1277-1298), both intervention groups also showed improvements in sleep, mood, stress, well-being and quality of life, with gains that were that were particularly pronounced in the meditation group; again, all benefits were sustained or further enhanced at 3 months post-intervention.

The findings of this trial suggest that two simple mind-body practices, Kirtan Kriya meditation and music listening, may not only improve mood, sleep, and quality of life, but also boost cognition and help reverse perceived memory loss in older adults with SCD.

Science Daily/SOURCE :https://www.sciencedaily.com/releases/2017/01/170121190807.htm

Mental activities may protect against mild cognitive impairment

January 30, 2017


Science Daily/Mayo Clinic
Researchers have found that engaging in mentally stimulating activities, even late in life, may protect against new-onset mild cognitive impairment, which is the intermediate stage between normal cognitive aging and dementia. The study found that cognitively normal people 70 or older who engaged in computer use, craft activities, social activities and playing games had a decreased risk of developing mild cognitive impairment.

Mayo Clinic researchers have found that engaging in mentally stimulating activities, even late in life, may protect against new-onset mild cognitive impairment, which is the intermediate stage between normal cognitive aging and dementia. The study found that cognitively normal people 70 or older who engaged in computer use, craft activities, social activities and playing games had a decreased risk of developing mild cognitive impairment. The results are published in the Jan. 30 edition of JAMA Neurology.

Researchers followed 1,929 cognitively normal participants of the population-based Mayo Clinic Study of Aging in Olmsted County, Minn., for an average duration of four years. After adjusting for sex, age and educational level, researchers discovered that the risk of new-onset mild cognitive impairment decreased by 30 percent with computer use, 28 percent with craft activities, 23 percent with social activities, and 22 percent with playing games.

"Our team found that persons who performed these activities at least one to two times per week had less cognitive decline than those who engaged in the same activities only two to three times per month or less," says Yonas Geda, M.D., psychiatrist and behavioral neurologist at Mayo Clinic's Arizona campus and senior author of the study.

Researchers conducted a neurocognitive assessment at the time of enrollment in the study, with evaluations every 15 months. Following the assessment, an expert consensus panel at the Alzheimer Disease Research Center at Mayo Clinic made the classification of normal cognition or mild cognitive impairment for each study participant, based on published criteria.

"Our previous cross-sectional study had found an association between engagement in mentally stimulating activities in late life and decreased odds of mild cognitive impairment," says Dr. Geda. "However, those findings were considered preliminary until confirmed by a prospective cohort study that we are now reporting in JAMA Neurology."

The benefits of being cognitively engaged even were seen among apolipoprotein E (APOE) ?4 carriers. APOE ?4 is a genetic risk factor for mild cognitive impairment and Alzheimer's dementia. However, for APOE ?4 carriers, only computer use and social activities were associated with a decreased risk of mild cognitive impairment.

"Even for a person who is at genetic risk for cognitive decline, engaging in some activities was beneficial," says Janina Krell-Roesch, Ph.D., the first author of the study and a postdoctoral researcher in Dr. Geda's Translational Neuroscience and Aging Program (TAP). "So I think the signal is there even for APOE ?4 carriers."

Science Daily/SOURCE :https://www.sciencedaily.com/releases/2017/01/170130133315.htm

Mind reader: A consumer EEG device serves up rich new troves of scientific data

January 31, 2017


Science Daily/McMaster University
A wireless brain-sensing headband made to help users focus their thoughts is also generating valuable data for neuroscience researchers, shedding light on what happens to our thinking processes as we age, for example, or how women and men process thoughts differently.

A consumer device designed to help users focus their thoughts is also generating valuable data for neuroscience research.

A team of McMaster and industry researchers is using data collected by a wireless brain-sensing headband called Muse to shed new light on what happens to our thinking processes as we age, for example, or how women and men process thoughts differently. Their work is published in the journal eNeuro.

The device, developed by Toronto's InteraXon, is fitted with four electrodes. It registers and transmits the strength and amplitude of brain waves that reveal, for example, whether thinking is scattered or focused.

Muse shows users real-time information about their brain signals on their tablets or smartphones, creating a real-time feedback loop that they use to train themselves to reach a state of mindfulness and focus.

Users also have the option to share their electroencephalographic (EEG) data for research purposes, on a secure, anonymous basis. The manufacturer makes the resulting database available to qualified researchers, providing scientists an unprecedented snapshot of what is happening in the minds of thousands of people.

Traditional EEG monitoring is cumbersome, laborious and time-consuming. It can take hours to test a single subject in a traditional EEG research lab.

"On a good day, you could run one session of one experiment on maybe three people in the lab. Using Muse, we had a chance to test 6,000 people in multiple sessions. That's a lifetime's work in a normal EEG lab," says co-author Allison Sekuler, a McMaster professor of Psychology, Neuroscience and Behaviour. "The ability to be able test this many people at once, I think, is the future of where science is going. We're merging big data and neuroscience."

"It's taking science outside of the lab and enabling us to look at the brain in the real world," says co-author Ali Hashemi, a McMaster PhD student who works with Sekuler. "The large numbers of participants gave us the power to learn things we couldn't have with traditional lab studies."

The research describes new vistas of information opening with the availability of data from more than 6,000 adults -- a number that has grown by more than 10 times since the research was conducted.

Science Daily/SOURCE :https://www.sciencedaily.com/releases/2017/01/170131133720.htm

Sleep deprivation handicaps the brain's ability to form new memories, mouse study shows

Chemical recalibration of brain cells during sleep is crucial for learning, and sleeping pills may sabotage it

February 2, 2017

Science Daily/SOURCE :https://www.sciencedaily.com/releases/2017/02/170202141916.htm
Science Daily/Johns Hopkins Medicine
Studying mice, scientists have fortified evidence that a key purpose of sleep is to recalibrate the brain cells responsible for learning and memory so the animals can 'solidify' lessons learned and use them when they awaken -- in the case of nocturnal mice, the next evening.
https://images.sciencedaily.com/2017/02/170202141916_1_540x360.jpg
Sleep is crucial for learning.
Credit: © Konstantin Yuganov / Fotolia

The researchers, all of the Johns Hopkins University School of Medicine, also report they have discovered several important molecules that govern the recalibration process, as well as evidence that sleep deprivation, sleep disorders and sleeping pills can interfere with the process.

"Our findings solidly advance the idea that the mouse and presumably the human brain can only store so much information before it needs to recalibrate," says Graham Diering, Ph.D., the postdoctoral fellow who led the study. "Without sleep and the recalibration that goes on during sleep, memories are in danger of being lost."

A summary of their study appears online in the journal Science on Feb. 3.

Diering explains that current scientific understanding of learning suggests that information is "contained" in synapses, the connections among neurons through which they communicate.

On the "sending side" of a synapse, signaling molecules called neurotransmitters are released by a brain cell as it "fires"; on the "receiving side," those molecules are captured by receptor proteins, which pass the "message" along. If a cell receives enough input through its synapses, it fires off its own neurotransmitters.

More specifically, experiments in animals have shown that the synapses on the receiving neuron can be toggled by adding or removing receptor proteins, thereby strengthening or weakening them and allowing the receiving neuron to receive more or less input from nearby signaling neurons.

Scientists believe memories are encoded through these synaptic changes. But there's a hitch in this thinking, Diering says, because while mice and other mammals are awake, the synapses throughout its brain tend to be strengthened, not weakened, pushing the system toward its maximum load. When neurons are "maxed out" and constantly firing, they lose their capacity to convey information, stymying learning and memory.

One possible reason that neurons don't usually max out is a process that has been well-studied in lab-grown neurons but not in living animals, asleep or awake. Known as homeostatic scaling down, it is a process that uniformly weakens synapses in a neural network by a small percentage, leaving their relative strengths intact and allowing learning and memory formation to continue.

To find out if the process does occur in sleeping mammals, Diering focused on the areas of the mouse brain responsible for learning and memory: the hippocampus and the cortex. He purified proteins from receiving synapses in sleeping and awake mice, looking for the same changes seen in lab-grown cells during scaling down.

Results showed a 20 percent drop in receptor protein levels in sleeping mice, indicating an overall weakening of their synapses, compared to mice that were awake.

"That was the first evidence of homeostatic scaling down in live animals," says Richard Huganir, Ph.D., professor of neuroscience, director of the Department of Neuroscience and lead author of the study. "It suggests that synapses are restructured throughout the mouse brain every 12 hours or so, which is quite remarkable."

To learn specifically which molecules were responsible for the phenomenon, the team turned to a protein called Homer1a, discovered in 1997 by Paul Worley, M.D., professor of neuroscience, who was also part of the team conducting the new study. Studies showed that Homer1a -- named for the ancient Greek author and the scientific "odyssey" required to identify it -- is important for the regulation of sleep and wakefulness, and for homeostatic scaling down in lab-grown neurons.

Repeating his previous analysis of synaptic proteins, Diering indeed found much higher levels of Homer1a -- 250 percent more -- in the synapses of sleeping mice than awake mice. And in genetically engineered mice missing Homer1a, the previous decrease of synaptic receptor proteins associated with sleep was no longer present.

To sort out how Homer1a senses when the mice are sleeping or awake, the researchers looked to the neurotransmitter noradrenaline, which drives the brain to arousal and wakefulness. By blocking or enhancing noradrenaline levels, both in lab-grown neurons and in mice, the researchers confirmed that when noradrenaline levels were high, Homer1a stayed away from synapses; when it was low, it collected there.

To directly test whether the location of Homer1a was related to sleep, the team kept mice awake for four extra hours by placing them in an unfamiliar cage. Some then got two and a half hours of "recovery sleep." As predicted, levels of Homer1a in the receiving synapses were much higher in the sleep-deprived mice than in those that got recovery sleep. That suggests, says Diering, that Homer1a is sensitive to an animal's "sleep need," not just what time of day it is.

Diering emphasizes that sleep need is controlled by adenosine, a chemical that accumulates in the brain as an animal stays awake, provoking sleepiness. (Caffeine, the world's most widely consumed psychoactive drug, directly interferes with adenosine.) When mice were given a drug during sleep deprivation that blocks adenosine, Homer1a levels no longer increased in their synapses.

"We think that Homer1a is a traffic cop of sorts," says Huganir. "It evaluates the levels of noradrenaline and adenosine to determine when the brain is sufficiently quiet to begin scaling down."

As the final test of their hypothesis that scaling down during sleep is crucial for learning and memory, the researchers tested the mice's ability to learn without scaling down. Individual mice were placed in an unfamiliar arena and given a mild electrical shock, either as they woke up or right before they went to sleep. Some mice then received a drug known to prevent scaling down.

When an undrugged mouse received a shock just before sleep, its brain went through the scaling-down process and formed an association between that arena and the shock. When placed in that same arena, those mice spent about 25 percent of their time motionless, in fear of another shock. When placed in a different unfamiliar arena, they froze sometimes, but only about 9 percent of their time there, probably because they were relatively good a telling the difference between the two unfamiliar arenas.

Expecting that drugged mice that couldn't scale down during sleep would have weaker memories and therefore freeze less than undrugged mice, Diering was surprised that they were motionless longer (40 percent of their time) when returned to the arena where they were shocked. But the drugged mice were also motionless longer (13 percent of their time) when in a new arena. When the shock was given after the mice woke up, the drug made no difference in how long the mice froze in either arena, confirming that scaling down only occurs during sleep.

"We think that the memory of the shock was stronger in the drugged mice because their synapses couldn't undergo scaling down, but all kinds of other memories also remained strong, so the mice were confused and couldn't easily distinguish the two arenas," says Diering. "This demonstrates why 'sleeping on it' can actually clarify your ideas."

"The bottom line," he says, "is that sleep is not really downtime for the brain. It has important work to do then, and we in the developed world are shortchanging ourselves by skimping on it."

Huganir says that sleep is still a big mystery. "In this study, we only examined what goes on in two areas of the brain during sleep. There are probably equally important processes happening in other areas, and throughout the body, for that matter," he adds.

Among the events that require further exploration is how learning and memory are affected by sleep disorders and other diseases known to disrupt sleep in humans, like Alzheimer's disease and autism. Huganir also says that benzodiazapines and other drugs that are commonly prescribed as sedatives, such as muscle relaxants and other sleep aids, are known to prevent homeostatic scaling down and are likely to interfere with learning and memory, though that idea has yet to be tested experimentally.

Science Daily/SOURCE :https://www.sciencedaily.com/releases/2017/02/170202141916.htm

Body and brain timing can be trained

February 20, 2017

Science Daily/Umeå universitet
Good timing is vital in many situations of daily life, but is rarely something we consider. In a new dissertation, a researcher shows that our ability for timing is something that can be trained and it seems to be connected with our cognitive capacity.

Good timing is vital in many situations of daily life, but is rarely something we consider. In a new dissertation from Umeå University in Sweden, Olympia Karampela shows that our ability for timing is something that can be trained and it seems to be connected with our cognitive capacity.

"Understanding the processes revolving our consciousness and how our bodies' time perceptions and movements can be useful, partly in order to improve everyday performance, or when something extra is required. Partly also, it can facilitate treatment for people with certain disorders," says Olympia Karampela.

How things are timed -- that is, happen at the right moment -- is not something people generally consider. But timing is actually more or less fundamental for our existence.

In the big picture, the World is ruled by timing where one revolution around the sun becomes a year, and one rotation around Earth's axis makes up 24 hours. In more detail, microsecond timing is required for everyday situations such as speaking. For example, if the timing is faulty, when air passes through the vocal cords and when the tongue moves, your speech becomes incomprehensible. Even worse would be if we were unable to synchronise chewing and swallowing whilst eating, which could lead to starvation. And if we turned the steering wheel at the wrong moment at a junction, we might crash into an oncoming vehicle.

In relation to the importance of correct timing, the processes behind our brain and body's ability of time perception and movement is relatively unexplored. What we do known is that humans lack a particular centre for timing similar to the brain's centres for eyesight and hearing. That suggests more body parts must be involved.

How well timing is performed can be described using 'timing variability', where a lower value suggests a higher precision. When it comes to Earth's rotation around the sun, a timing variability of a few seconds will hardly have a huge impact for humans. However, for a combat pilot, a time variability of a millisecond may be the difference between life and death when you need to escape a missile.

In her doctoral dissertation, Olympia Karampela has completed three studies with a total of 120 student research participants. The studies aimed to answer some fundamental questions regarding our ability to improve our timing through intense training and to see if there is any connection between motor timing and cognitive capacity. Another aim was to see if we are equally good in performing timing tasks by different body parts. The results showed that students had a noticeably better timing ability after just a few sessions of motor training consisting of performing synchronised drumstick beats to external rhythmic stimuli.

The results show that students had a noticeably better timing ability after just a few sessions of motor training consisting of performing synchronised drumstick beats to external rhythmic stimuli. The biggest improvement, expressed as a reduced timing variability occurred in the first hour of training, whilst other training for up to 3.5 hours did not lead to any improvement.

Even the cognitive ability show positive effects from training in synchronising audiovisual impressions with drumstick beats. When it comes to if timing is similar in all parts of the body, the results vary. A general conclusion is that motor timing is partly controlled by overlapping distributed mechanisms, and that they are connected to systems controlling cognitive processes, such as attention. These results partly explain the well-known relationships between cognitive ability and timing.

"Future research will show if these results can lead to the opportunity to treat people with serious attention deficit disorders using intervention programmes to train motor timing in order to improve their cognitive abilities," says Olympia Karampela.

Link to dissertation: http://umu.diva-portal.org/smash/record.jsf?pid=diva2%3A1069970&dswid=-6414
https://www.sciencedaily.com/releases/2017/02/170220085259.htm

Heart risks in middle age boost dementia risk later in life

February 22, 2017


Science Daily/American Heart Association
Heart disease risk factors in middle age were associated with an increased risk of dementia in later years. Smoking, high blood pressure and diabetes were all dementia risks, with diabetes in middle age raising the risk almost as much as a genetic risk factor for Alzheimer's disease. Some risk factors had a different impact in black and white participants, while genetics and smoking had a greater impact in whites.

People who have heart disease risks in middle age -- such as diabetes, high blood pressure or smoking -- are at higher risk for dementia later in life, according to research presented at the American Stroke Association's International Stroke Conference 2017.

"The health of your vascular system in midlife is really important to the health of your brain when you are older," said Rebecca F. Gottesman, M.D., Ph.D., lead researcher and associate professor of neurology and epidemiology at the Johns Hopkins University in Baltimore.

In an ongoing study that began in 1987 and enrolled 15,744 people in four U.S. communities, the risk of dementia increased as people got older. That was no surprise, but heart disease risks detected at the start of the study, when participants were between 45-64 years of age, also had a significant impact on later dementia, researchers noted. Dementia developed in 1,516 people during the study, and the researchers found that the risk of dementia later in life was:

41 percent higher in midlife smokers than in non-smokers or former smokers;
39 percent higher in people with high blood pressure (?140/90 mmHg) in middle age, and 31 percent higher in those with pre-hypertension (between 120/80 mmHg and 139/89 mmHg) compared to those with normal blood pressure; and
77 percent higher in people with diabetes in middle age than in non-diabetics.
"Diabetes raises the risk almost as much as the most important known genetic risk factor for Alzheimer's disease," Gottesman said.

Overall, the risk of dementia was 11 percent lower in women. The risk was highest in individuals who were black, had less than a high school education, were older, carried the gene known to increase Alzheimer's risk, or had high blood pressure, diabetes or were current smokers at the time of initial evaluation.

Smoking and carrying the gene known to increase the chance of Alzheimer's were stronger risk factors in whites than in blacks, the researchers noted.

"If you knew you carried the gene increasing Alzheimer's risk, you would know you were predisposed to dementia, but people don't necessarily think of heart disease risks in the same way. If you want to protect your brain as you get older, stop smoking, watch your weight, and go to the doctor so diabetes and high blood pressure can be detected and treated," said Gottesman.

Because Atherosclerosis Risk in Communities is an observational study, the current study could not test whether treating heart risk factors will result in a lessened dementia risk later in life.

"The benefit is that this is a long-term study and we know a lot about these people. Data like these may supplement data from clinical trials that look at the impact of treatment for heart disease risks," Gottesman said.

Science Daily/SOURCE :https://www.sciencedaily.com/releases/2017/02/170222152749.htm

Sugar's 'tipping point' link to Alzheimer's disease revealed

February 23, 2017


Science Daily/University of Bath
For the first time a "tipping point" molecular link between the blood sugar glucose and Alzheimer's disease has been established by scientists, who have shown that excess glucose damages a vital enzyme involved with inflammation response to the early stages of Alzheimer's.

Abnormally high blood sugar levels, or hyperglycaemia, is well-known as a characteristic of diabetes and obesity, but its link to Alzheimer's disease is less familiar.

Diabetes patients have an increased risk of developing Alzheimer's disease compared to healthy individuals. In Alzheimer's disease abnormal proteins aggregate to form plaques and tangles in the brain which progressively damage the brain and lead to severe cognitive decline.

Scientists already knew that glucose and its break-down products can damage proteins in cells via a reaction called glycation but the specific molecular link between glucose and Alzheimer's was not understood.

But now scientists from the University of Bath Departments of Biology and Biochemistry, Chemistry and Pharmacy and Pharmacology, working with colleagues at the Wolfson Centre for Age Related Diseases, King's College London, have unraveled that link.

By studying brain samples from people with and without Alzheimer's using a sensitive technique to detect glycation, the team discovered that in the early stages of Alzheimer's glycation damages an enzyme called MIF (macrophage migration inhibitory factor) which plays a role in immune response and insulin regulation.

MIF is involved in the response of brain cells called glia to the build-up of abnormal proteins in the brain during Alzheimer's disease, and the researchers believe that inhibition and reduction of MIF activity caused by glycation could be the 'tipping point' in disease progression. It appears that as Alzheimer's progresses, glycation of these enzymes increases.

The study is published in the journal Scientific Reports.

Professor Jean van den Elsen, from the University of Bath Department of Biology and Biochemistry, said: "We've shown that this enzyme is already modified by glucose in the brains of individuals at the early stages of Alzheimer's disease. We are now investigating if we can detect similar changes in blood.

"Normally MIF would be part of the immune response to the build-up of abnormal proteins in the brain, and we think that because sugar damage reduces some MIF functions and completely inhibits others that this could be a tipping point that allows Alzheimer's to develop.

Dr Rob Williams, also from the Department of Biology and Biochemistry, added: "Knowing this will be vital to developing a chronology of how Alzheimer's progresses and we hope will help us identify those at risk of Alzheimer's and lead to new treatments or ways to prevent the disease.

Dr Omar Kassaar, from the University of Bath, added: "Excess sugar is well known to be bad for us when it comes to diabetes and obesity, but this potential link with Alzheimer's disease is yet another reason that we should be controlling our sugar intake in our diets."

Globally there are around 50 million people with Alzheimer's disease, and this figure is predicted to rise to more than 125 million by 2050. The global social cost of the disease runs into the hundreds of billions of dollars as alongside medical care patients require social care because of the cognitive effects of the disease.

The study was funded by the Dunhill Medical Trust. Human brain tissue for this study was provided through Brains for Dementia Research, a joint initiative between Alzheimer's Society and Alzheimer's Research UK in association with the Medical Research Council.

Science Daily/SOURCE :https://www.sciencedaily.com/releases/2017/02/170223124253.htm

Blueberry concentrate improves brain function in older people

March 7, 2017


Science Daily/University of Exeter
Drinking concentrated blueberry juice improves brain function in older people, according to new research.
https://images.sciencedaily.com/2017/03/170307100356_1_540x360.jpg
Blueberries. The study gave people a daily drink of blueberry concentrate, providing the equivalent of 230g of blueberries.
Credit: © Tim UR / Fotolia

In the study, healthy people aged 65-77 who drank concentrated blueberry juice every day showed improvements in cognitive function, blood flow to the brain and activation of the brain while carrying out cognitive tests.

There was also evidence suggesting improvement in working memory.

Blueberries are rich in flavonoids, which possess antioxidant and anti-inflammatory properties.

Dr Joanna Bowtell, head of Sport and Health Sciences at the University of Exeter, said: "Our cognitive function tends to decline as we get older, but previous research has shown that cognitive function is better preserved in healthy older adults with a diet rich in plant-based foods.

"In this study we have shown that with just 12 weeks of consuming 30ml of concentrated blueberry juice every day, brain blood flow, brain activation and some aspects of working memory were improved in this group of healthy older adults."

Of the 26 healthy adults in the study, 12 were given concentrated blueberry juice -- providing the equivalent of 230g of blueberries -- once a day, while 14 received a placebo.

Before and after the 12-week period, participants took a range of cognitive tests while an MRI scanner monitored their brain function and resting brain blood flow was measured.

Compared to the placebo group, those who took the blueberry supplement showed significant increases in brain activity in brain areas related to the tests.

The study excluded anyone who said they consumed more than five portions of fruit and vegetables per day, and all participants were told to stick to their normal diet throughout.

Previous research has shown that risk of dementia is reduced by higher fruit and vegetable intake, and cognitive function is better preserved in healthy older adults with a diet rich in plant-based foods.

Flavonoids, which are abundant in plants, are likely to be an important component in causing these effects.

Science Daily/SOURCE :https://www.sciencedaily.com/releases/2017/03/170307100356.htm

Caffeine boosts enzyme that could protect against dementia

New analysis reveals 24 compounds that can help reduce impact of harmful proteins in the brain

March 7, 2017

Science Daily/Indiana University
Researchers have identified 24 compounds -- including caffeine -- with the potential to boost an enzyme in the brain shown to protect against dementia.

https://images.sciencedaily.com/2017/03/170307130903_1_540x360.jpg
Indiana University scientists have identified 24 compounds that increase the brain's production of the enzyme NMNAT2, which helps prevent the formation of these tangles associated with neurodegenerative disorders such as Alzheimer's disease.
Credit: Image courtesy of the National Institute on Aging/National Institutes of Health

The protective effect of the enzyme, called NMNAT2, was discovered last year through research conducted at IU Bloomington. The new study appears today in the journal Scientific Reports.

"This work could help advance efforts to develop drugs that increase levels of this enzyme in the brain, creating a chemical 'blockade' against the debilitating effects of neurodegenerative disorders," said Hui-Chen Lu, who led the study. Lu is a Gill Professor in the Linda and Jack Gill Center for Biomolecular Science and the Department of Psychological and Brain Sciences, a part of the IU Bloomington College of Arts and Sciences.

Previously, Lu and colleagues found that NMNAT2 plays two roles in the brain: a protective function to guard neurons from stress and a "chaperone function" to combat misfolded proteins called tau, which accumulate in the brain as "plaques" due to aging. The study was the first to reveal the "chaperone function" in the enzyme.

Misfolded proteins have been linked to neurodegenerative disorders such as Alzheimer's, Parkinson's and Huntington's diseases, as well as amyotrophic lateral sclerosis, also known as ALS or Lou Gehrig's disease. Alzheimer's disease, the most common form of these disorders, affects over 5.4 million Americans, with numbers expected to rise as the population ages.

To identify substances with the potential to affect the production of the NMNAT2 enzyme in the brain, Lu's team screened over 1,280 compounds, including existing drugs, using a method developed in her lab. A total of 24 compounds were identified as having potential to increase the production of NMNAT2 in the brain.

One of the substances shown to increase production of the enzyme was caffeine, which also has been shown to improve memory function in mice genetically modified to produce high levels of misfolded tau proteins.

Lu's earlier research found that mice altered to produce misfolded tau also produced lower levels of NMNAT2.

To confirm the effect of caffeine, IU researchers administered caffeine to mice modified to produce lower levels of NMNAT2. As a result, the mice began to produce the same levels of the enzyme as normal mice.

Another compound found to strongly boost NMNAT2 production in the brain was rolipram, an "orphaned drug" whose development as an antidepressant was discontinued in the mid-1990s. The compound remains of interest to brain researchers due to several other studies also showing evidence it could reduce the impact of tangled proteins in the brain.

Other compounds shown by the study to increase the production of NMNAT2 in the brain -- although not as strongly as caffeine or rolipram -- were ziprasidone, cantharidin, wortmannin and retinoic acid. The effect of retinoic acid could be significant since the compound derives from vitamin A, Lu said.

An additional 13 compounds were identified as having potential to lower the production of NMNAT2. Lu said these compounds are also important because understanding their role in the body could lead to new insights into how they may contribute to dementia.

"Increasing our knowledge about the pathways in the brain that appear to naturally cause the decline of this necessary protein is equally as important as identifying compounds that could play a role in future treatment of these debilitating mental disorders," she said.

Science Daily/SOURCE :https://www.sciencedaily.com/releases/2017/03/170307130903.htm

Sound waves boost older adults' memory, deep sleep

Pink noise synced to brain waves deepens sleep and triples memory scores in older adults

March 8, 2017

Science Daily/Northwestern University
Gentle sound stimulation -- such as the rush of a waterfall -- synchronized to the rhythm of brain waves significantly enhanced deep sleep in older adults and tripled their ability to recall words, reports a new study. The goal is to make the new technology available for home use.
https://images.sciencedaily.com/2017/03/170308081024_1_540x360.jpg
Deep sleep is critical for memory consolidation. But beginning in middle age, deep sleep decreases substantially, which scientists believe contributes to memory loss in aging.
Credit: © WavebreakMediaMicro / Fotolia

Deep sleep is critical for memory consolidation. But beginning in middle age, deep sleep decreases substantially, which scientists believe contributes to memory loss in aging.

The sound stimulation significantly enhanced deep sleep in participants and their scores on a memory test.

"This is an innovative, simple and safe non-medication approach that may help improve brain health," said senior author Dr. Phyllis Zee, professor of neurology at Northwestern University Feinberg School of Medicine and a Northwestern Medicine sleep specialist. "This is a potential tool for enhancing memory in older populations and attenuating normal age-related memory decline."

The study will be published March 8 in Frontiers in Human Neuroscience.

In the study, 13 participants 60 and older received one night of acoustic stimulation and one night of sham stimulation. The sham stimulation procedure was identical to the acoustic one, but participants did not hear any noise during sleep. For both the sham and acoustic stimulation sessions, the individuals took a memory test at night and again the next morning. Recall ability after the sham stimulation generally improved on the morning test by a few percent. However, the average improvement was three times larger after pink-noise stimulation.

The older adults were recruited from the Cognitive Neurology and Alzheimer's Disease Center at Northwestern.

The degree of slow wave sleep enhancement was related to the degree of memory improvement, suggesting slow wave sleep remains important for memory, even in old age.

Although the Northwestern scientists have not yet studied the effect of repeated nights of stimulation, this method could be a viable intervention for longer-term use in the home, Zee said.

Previous research showed acoustic simulation played during deep sleep could improve memory consolidation in young people. But it has not been tested in older adults.

The new study targeted older individuals -- who have much more to gain memory-wise from enhanced deep sleep -- and used a novel sound system that increased the effectiveness of the sound stimulation in older populations.

The study used a new approach, which reads an individual's brain waves in real time and locks in the gentle sound stimulation during a precise moment of neuron communication during deep sleep, which varies for each person.

During deep sleep, each brain wave or oscillation slows to about one per second compared to 10 oscillations per second during wakefulness.

Giovanni Santostasi, a study coauthor, developed an algorithm that delivers the sound during the rising portion of slow wave oscillations. This stimulation enhances synchronization of the neurons' activity.

After the sound stimulation, the older participants' slow waves increased during sleep.

Larger studies are needed to confirm the efficacy of this method and then "the idea is to be able to offer this for people to use at home," said first author Nelly Papalambros, a Ph.D. student in neuroscience working in Zee's lab. "We want to move this to long-term, at-home studies."

Northwestern scientists, under the direction of Dr. Roneil Malkani, assistant professor of neurology at Feinberg and a Northwestern Medicine sleep specialist, are currently testing the acoustic stimulation in overnight sleep studies in patients with memory complaints. The goal is to determine whether acoustic stimulation can enhance memory in adults with mild cognitive impairment.

Previous studies conducted in individuals with mild cognitive impairment in collaboration with Ken Paller, professor of psychology at the Weinberg College of Arts and Sciences at Northwestern, have demonstrated a possible link between their sleep and their memory impairments.

Science Daily/SOURCE :https://www.sciencedaily.com/releases/2017/03/170308081024.htm

Member Login
Welcome, (First Name)!

Forgot? Show
Log In
Enter Member Area
My Profile Not a member? Sign up. Log Out