Memory5

Wisdom is a matter of both heart and mind

April 7, 2016
Science Daily/University of Waterloo
The fluctuations of your heartbeat may affect your wisdom, according to new research. The study suggests that heart rate variation and thinking process work together to enable wise reasoning about complex social issue

The study suggests that heart rate variation and thinking process work together to enable wise reasoning about complex social issues. The work by Igor Grossmann, professor of psychology at Waterloo, and colleagues based at the Australian Catholic University, appears in the online journal Frontiers in Behavioral Neuroscience.

Their study breaks new ground in wisdom research by identifying conditions under which psychophysiology impacts wise judgment.

"Our research shows that wise reasoning is not exclusively a function of the mind and cognitive ability," says Prof. Grossmann. "We found that people who have greater heart rate variability and who are able to think about social problems from a distanced viewpoint demonstrate a greater capacity for wise reasoning."

The study extends previous work on cognitive underpinnings of wise judgment to include consideration how the heart's functioning impacts the mind.

A growing consensus among philosophers and cognitive scientists defines wise judgment to include the ability to recognize the limits of one's knowledge, to be aware of the varied contexts of life and how they may unfold over time, to acknowledge others' points of view, and to seek reconciliation of opposing viewpoints.

The new study is the first to show that the physiology of the heart, specifically the variability of heart rate during low physical activity, is related to less biased, wiser judgment.

Human heart rate tends to fluctuate, even during steady-state conditions, such as while a person is sitting. Heart rate variability refers to the variation in the time interval between heartbeats and is related to the nervous system's control of organ functions.

The researchers found that people with more varied heart rates were able to reason in a wiser, less biased fashion about societal problems when they were instructed to reflect on a social issue from a third-person perspective. But, when the study's participants were instructed to reason about the issue from a first-person perspective, no relationship between heart rate and wiser judgment emerged.

"We already knew that people with greater variation in their heart rate show superior performance in the brain's executive functioning such as working memory," says Prof. Grossmann. "However, that does not necessarily mean these people are wiser -- in fact, some people may use their cognitive skills to make unwise decisions. To channel their cognitive abilities for wiser judgment, people with greater heart rate variability first need to overcome their egocentric viewpoints."

The study opens the door for further exploration of wise judgment at the intersection of physiological and cognitive research.
Science Daily/SOURCE :https://www.sciencedaily.com/releases/2016/04/160407221449.htm

How even our brains get 'slacker' as we age

October 24, 2016
Science Daily/Newcastle University
Losing the youthful firmness and elasticity in our skin is one of the first outward signs of aging. Now it seems it's not just our skin that starts to sag, but our brains too.

New research from Newcastle University, UK, in collaboration with the Federal University of Rio de Janeiro, investigated the way the human brain folds and how this 'cortical folding' changes with age.

Linking the change in brain folding to the tension on the cerebral cortex -- the outer layer of neural tissue in our brains -- the team found that as we age, the tension on the cortex appears to decrease. This effect was more pronounced in individuals with Alzheimer's disease.

Publishing their findings in the academic journal PNAS, the team say this new research sheds light on the underlying mechanisms which affect brain folding and could be used in the future to help diagnose brain diseases.

Lead author Dr Yujiang Wang, of Newcastle University, explains, "One of the key features of a mammalian brain is the grooves and folds all over the surface -- a bit like a walnut -- but until now no-one has been able to measure this folding in a consistent way.

"By mapping the brain folding of over 1,000 people, we have shown that our brains fold according to a simple universal law. We also show that a parameter of the law, which is interpreted as the tension on the inside of the cortex, decreases with age.

"In Alzheimer's disease, this effect is observed at an earlier age and is more pronounced. The next step will be to see if there is a way to use the changes in folding as an early indicator of disease."

Common in all mammals

The expansion of the cerebral cortex is the most obvious feature of mammalian brain evolution and is generally accompanied by increasing degrees of folding of the cortical surface.

In the average adult brain, for example, if the cortex of one side -- or hemisphere -- was unfolded and flattened out it would have a surface area of about 100,000 mm2, roughly one and a half times the size of a piece of A4 paper.

Previous research has shown that folding of the cortex across mammalian species follows a universal law -- that is, regardless of size and shape, they all fold in the same way.

However, until now there has been no systematic study demonstrating that the same law holds within a species.
 

Tension slackens with age

"Our study has shown that we can use this same law to study changes in the human brain," explains Dr Wang, based in Newcastle University's world-leading School of Computing Science.

"From this, we identified a parameter that decreases with age, which we interpret as changing the tension on the cortical surface. It would be similar to the skin. As we age, the tension drops and the skin starts to slacken.

"It has long been known that the size and thickness of the cortex changes with age but the existence of a general law for folding shows us how to combine these quantities into a single measure of folding that can then be compared between genders, age groups and disease states."
 

Women's brains less folded

The team also found that male and female brains differ in size, surface area, and the degree of folding. Indeed, female brains tend to be slightly less folded than male brains of the same age. Despite this, male and female brains are shown to follow exactly the same law.

"This indicates that for the first time, we have a consistent way of quantifying cortical folding in humans," says Dr Wang.

Throughout the lifespan of healthy individuals, cortical folding changes in the same way in both men and women but in those with Alzheimer's disease the change in the brain folding was significantly different.

She adds: "More work is needed in this area but it does suggest that the effect Alzheimer's disease has on the folding of the brain is akin to premature aging of the cortex."
Science Daily/SOURCE :https://www.sciencedaily.com/releases/2016/10/161024161648.htm

Early supplementation may help offset early-life stress on the adult brain

October 26, 2016
Science Daily/Federation of American Societies for Experimental Biology
Early-life stress has been shown to impair learning and memory in later life, but new research suggests that improved nutrition may help offset the negative effects of this stress. Specifically, using mice, scientists focused on essential micronutrients, including methionine, vitamins B6 and B12, and folic acid, none of which are made by the body and need to be ingested through diet. They found that early-life stress reduces the levels of these nutrients in mouse pups, but supplementation prevented the reduction of methionine levels and even prevented some of the lasting negative effects of early-life stress on later learning and memory in adult offspring.

"Today's children are tomorrow's future," said Aniko Korosi, Ph.D., a researcher involved in the work from the Swammerdam Institute for Life Sciences and the Center for Neuroscience at the University of Amsterdam in Amsterdam, The Netherlands. "We hope that this study can contribute to novel nutritional strategies that help prevent lasting consequences of a stressful childhood on later mental health."

To make their discovery, Korosi and colleagues mimicked a stressful early-life environment during the first week after birth (postnatal days 2-9) for newborn mice and their mothers. Control mice and their mothers were housed in a normal environment. During the stress period, half of the mouse mothers (control and early-life stress) received a standard rodent diet, the other half received a diet that was supplemented with essential micronutrients. The lactating mouse mothers ate the diet and thereby developed elevated micronutrient levels in maternal milk and subsequently in the blood and the brains of their pups. After the initial stress period, all mice received a standard diet and environment. Once the mice became 4 months old, their learning and memory skills were tested in various cognitive/behavioral tasks. Mice that were previously exposed to early-life stress performed worse than control animals and demonstrated poor learning and memory skills. However, stress-exposed mice from mothers that received the supplemented diet performed equally well as the control mice did.

"The field of postnatal nutrition has sometimes taken a back seat to research on the maternal-fetal axis, but of course we cannot ever ignore either," said Thoru Pederson, Ph.D., Editor-in-Chief of The FASEB Journal. "Here we see strikingly beneficial cognitive effects of a sound postnatal diet. The nutrients tested were familiar ones, but the results speak for themselves."


Science Daily/SOURCE : https://www.sciencedaily.com/releases/2016/10/161026105215.htm
 

Additional benefit of omega-3 fatty acids for the clearance of metabolites from the brain

October 26, 2016
Science Daily/Federation of American Societies for Experimental Biology
Omega-3 polyunsaturated fatty acids, which are found in fish oil, could improve the function of the glymphatic system, which facilitates the clearance of waste from the brain, and promote the clearance of metabolites including amyloid-? peptides, a primary culprit in Alzheimer's disease, report scientists.

To make this discovery, scientists first used transgenic fat-1 mice, which express high endogenous omega-3 polyunsaturated fatty acids (PUFAs) in the brain, to investigate the effect of omega-3 PUFAs on the clearance function of the glymphatic system. Compared to the wild-type mice, the fat-1 mice with enriched endogenous omega-3 PUFAs significantly promote the clearance function of the lymphatic system, including the Aβ clearance from the brain. Wild-type mice were supplemented with fish oil, which contains high concentrations of omega-3 PUFAs, and found that fish oil-supplemented mice also improved the clearance function of the glymphatic system compared to the control mice without fish oil supplementation. Omega-3 PUFAs help maintain the brain homeostasis, which may provide benefits in a number of neurological diseases, such as Alzheimer's disease, traumatic brain injury, and sleep impairment, among others.

"These now-famous fatty acids have been the subject of major studies both in academia and industry. Just when we thought we had heard everything, here is something new, and it is provocative indeed," said Thoru Pederson, Ph.D., Editor-in-Chief of The FASEB Journal. "This study should not turn attention away from the roles of these substances in maintaining vascular health, but neither should they restrict our view. The brain is an extremely vascularized organ, while we might also bear in mind that omega-3 fatty acids may impact neurons, glia, and astrocytes themselves."
Science Daily/SOURCE : https://www.sciencedaily.com/releases/2016/10/161026105336.htm

High blood pressure can impair cognitive function, pose risk for Alzheimer's

October 26, 2016
Science Daily/Loyola University Health System
High blood pressure in middle age can lead to impaired cognition and is a potential risk factor for Alzheimer’s disease, researchers conclude.

Dr. Biller is a member of the multidisciplinary panel of experts that wrote the statement, published in the heart association journal Hypertension. Dr. Biller is chair of the department of neurology of Loyola University Chicago Stritch School of Medicine. The panel is chaired by Constantino Iadecola, MD, of Weill Cornell Medicine and co-chaired by Kristine Yaffe, MD, of the University of California San Francisco.

Dementia affects an estimated 30 to 40 million people worldwide, and the number is expected to triple by 2050 due to an aging population and other factors.

An estimated 80 million people in the United States have hypertension, and the brain is among the organs most affected. Except for age, hypertension is the most important risk factor for vascular problems in the brain that lead to stroke and dementia.

There is consistent evidence that chronic high blood pressure during middle age (40 to 64) is associated with altered cognitive function in both middle age and late life (65 to 84). Cognitive abilities that are affected include memory, speed of processing and executive function (ability to organize thoughts, manage time, make decisions, etc.)

The effect of high blood pressure in late life is less clear. Some studies suggest it's harmful, while other research suggests it may improve cognition. This highlights "the complexities of recommending uniform levels of blood pressure across the life course," the expert panel wrote.

Observational studies have demonstrated that high blood pressure causes atherosclerosis (hardening of the arteries) and other damage to the brain's blood vessels, leading to reduced blood flow to brain cells. But evidence from clinical trials that treating blood pressure improves cognition is not conclusive.

After carefully reviewing available studies, the panel concluded there are not enough data to make evidence-based recommendations. However, judicious treatment of high blood pressure, taking into account goals of care and the patient's individual characteristics, "seems justified to safeguard vascular health and, as a consequence, brain health," the panel concluded.
Science Daily/SOURCE : https://www.sciencedaily.com/releases/2016/10/161026142208.htm

 

Power outage in the brain may be source of Alzheimer's

Restoring damaged genes linked to mitochondrial function may offer strategy for halting disease advance

November 9, 2016
Science Daily/Arizona State University
In a new study, researchers investigate the role of mitochondria in Alzheimer's disease pathology. Mitochondria act as energy centers for cells and are of central importance in health and disease. The study builds on earlier work suggesting gene mutations affecting mitochondrial function may be critical in the development of the disease.

On Nov. 25, 1901, a 51-year-old woman is admitted to a hospital in Frankfurt, Germany, displaying a bizarre constellation of symptoms. Her behavior is erratic. She shows signs of paranoia as well as auditory hallucinations, disorientation and severe memory impairment. Asked to write her own name, she manages "Mrs.," then lingers over the page, unable to remember the rest. "I have lost myself," she tells the attending physician.

Over time, she will withdraw into her own inscrutable universe, before dying on April 9, 1906.

The tragic case of Auguste Deter might have vanished into the recesses of medical history, but for the following fact: Her doctor, Alois Alzheimer, made a thorough examination of her medical condition, including her excised brain, discovering the telltale amyloid plaques and neurofibrillary tangles characteristic of her illness. Auguste Deter was the first person diagnosed with Alzheimer's disease.

Today, society faces an epidemic of Alzheimer's, with some 5 million afflicted in the U.S. alone. The number is projected to swell to 14 million by midcentury, according to the Centers for Disease Control and Prevention. Of the top 10 leading fatal illnesses, Alzheimer's remains the only one that cannot be prevented, treated or cured.

In new research appearing in the journal Alzheimer's and Dementia, Diego Mastroeni, Paul Coleman and their colleagues at the ASU-Banner Neurodegenerative Disease Research Center (NDRC) and the Biodesign Center for Bioenergetics investigate the role of mitochondria in Alzheimer's disease pathology. Mitochondria act as energy centers for cells and are of central importance in health and disease.

The study builds on earlier work suggesting gene mutations affecting mitochondrial function may be critical in the development -- and pitiless progression -- of the disease.

"Age-related neurodegenerative diseases, like Alzheimer's, progress over a long period of time before they become clinically apparent. The earliest physiological and molecular events are largely unknown," said Mastroeni. "Findings from our laboratory have uncovered early expression changes in nuclear-encoded, but not mitochondrial-encoded mRNAs occurring in one's early 30s, giving us a glimpse into what we suspect are some of the earliest cellular changes in the progression of Alzheimer's disease."

Results of the new study show that specific classes of genes associated with mitochondrial cell respiration display reduced expression levels in patients with Alzheimer's disease, compared with normal patients.

The study also examines gene expression in subjects whose brains show an intermediate level of illness known as mild cognitive impairment. Here, the opposite effect is observed, with relevant genes exhibiting increased levels of expression. The authors suggest this observation may point to some kind of compensatory mechanism in the brain attempting to stave off the disease in its earlier stages.

Further, the study proposes that restoring a specific set of damaged genes linked to mitochondrial function and located in the nuclear DNA of cells may offer a promising strategy for halting the disease's advance.

Assault on identity

Alzheimer's -- the most common form of dementia -- is a progressive, degenerative disease of the brain. While commonly associated with elderly individuals, this devastating illness is now believed to have its origins much earlier, infiltrating the nervous system decades before the onset of clinical symptoms. Indeed, the greatest obstacle to successful treatment of Alzheimer's is the fact that the disease is typically not recognized until its progress has irreparably ravaged the brain.

The disease often begins with mild memory loss, which may interfere with normal conversation. While advancing age remains the leading risk factor for Alzheimer's, some individuals are also genetically predisposed. Other risk factors include high cholesterol, heart disease, stroke and high blood pressure. Today, Alzheimer's is the fifth-leading cause of death in adults 65-85 years old.

Despite the increasingly pronounced effects of dementia, a definitive diagnosis of Alzheimer's disease usually requires the post-mortem examination of brain tissue and identification of two stereotypic symptoms, known as plaques and tangles. More recently, new imaging technology has enabled researchers to detect these symptoms in living brains, though Coleman is cautious about their interpretation:

"Although plaques and tangles remain as the definitive neuropathological hallmark of the disease, plaques do not correlate at all with degree of cognitive impairment in [Alzheimer's] and tangles correlate only slightly," he said. "We further know that plaques and tangles are late comers in the cascade of events that cause the dementia of [Alzheimer's]."

Alzheimer's is believed to account for 60-70 percent of dementia cases. As the disease progresses, symptoms become more severe, including erosion of language ability, physical disorientation and behavioral transformations, often involving the withdrawal from family and society. Over time, bodily functions are lost, ultimately leading to death. Life expectancy for Alzheimer's patients varies, but three to nine years following diagnosis is typical.
 

Quick energy

Mitochondria -- membrane-bound organelles found in all eukaryotic organisms -- are often called the powerhouses of the cell. Through a process known as oxidative phosphorylation, they produce most of the cell's chemical energy in the form of adenosine triphosphate or ATP.

In addition to supplying cellular energy, mitochondria are involved in cell signaling, cellular differentiation and cell death, as well as in cellular growth and the maintenance of the cell cycle.

Because mitochondria play such an important role in the cell, mitochondrial dysfunction has been implicated in a broad range of illness, including cardiovascular disease, autism, schizophrenia, bipolar disorder, epilepsy, stroke, Lou Gehrig's disease and diabetes along with forms of dementia including Alzheimer's.

Unsurprisingly, defects in mitochondrial function more severely affect energy-hungry organ systems in the body, particularly muscles, the GI tract and the brain -- an organ making up just 2 percent of a person's weight while consuming 20 percent of the body's total energy budget.

Mitochondria are unique among the cell's organelles, as they possess their own DNA, distinct from the DNA contained within the cell's nucleus. This strange state of affairs is due to mitochondrial evolution. Mitochondria are descended from free-living bacteria that colonized other cells some 2 billion years ago. After being incorporated into nucleated cells, these endosymbionts, as they are known, lost much of their original machinery, yet retained their own complement of DNA.

In addition to the role of mitochondrial dysfunction in disease, the gradual degradation of mitochondrial integrity is believed to play a central role in the normal process of aging.

Broken genes

The current study examines tissue from the hippocampus, a structure critical for memory and one severely impacted by the advance of Alzheimer's. Using microarray technology, the authors examined hippocampal tissue from an aging cohort-44 normal brains from 29-99 years of age, 10 with mild cognitive impairment and 18 with Alzheimer's disease.

Gene expression was examined for two sets of genes, 1 encoding mitochondrial DNA and the other, in the nuclear DNA. The two sets of genes both coded for proteins associated with a mitochondrial complex essential for oxidative phosphorylation (OXPHOS), producing energy in the form of ATP for the cell.

Intriguingly, while the mitochondrial genes themselves were largely unaffected, the nuclear genes associated with the OXPHOS complex underwent significant modification, depending on the tissues examined. The microarray data revealed substantial down-regulation of nuclear-encoded OXPHOS genes in Alzheimer's tissue, a finding also found in normally aging brains.

The same genes, however, were up-regulated in the case of mild cognitive impairment, a precursor to Alzheimer's disease. The authors suggest this effect may be due to a compensatory mechanism in the brain in response to early pathology.

The findings are consistent with earlier work establishing that accumulations of amyloid beta (Aβ) in neurons, a hallmark of Alzheimer's, are directly implicated in mitochondrial dysfunction. The pronounced effect on nuclear-encoded but not mitochondrial-encoded OXPHOS genes may point to dysfunctions in the transport of molecules from the cell nucleus to the mitochondria.

"Our work on mitochondria offers the promise of a reliable marker appearing earlier in the course of the disease -- one which more closely correlates with the degree of dementia than the current diagnostic of plaques and tangles," Coleman said.

Precise mechanisms of mitochondrial decline in aging and Alzheimer's have yet to be teased out and will be the focus of continuing research. The study suggests that therapies aimed at restoring function in nuclear-encoded OXPHOS genes may provide an exciting new avenue for treatment of Alzheimer's.
Science Daily/SOURCE :https://www.sciencedaily.com/releases/2016/11/161109175141.htm

New findings on physical activity could shape treatment for mild Alzheimer's disease

November 9, 2016
Science Daily/University of Kansas
For older adults, physical activity is apt to shield against cognitive decline and forms of dementia such as Alzheimer's disease (AD). Yet, as people age and some experience cognitive impairment, they tend to become less physically active.

"Physical activity is very important for brain function," said Amber Watts, assistant professor of clinical psychology at the University of Kansas. "We know that people who are physically active are less likely to develop AD. But we also know that for people already living with AD, physical activity can help them function better, decline more slowly and help them with symptoms like agitation, wandering and sleeplessness."

According to Watts, too little is known about patterns of activity for people experiencing the early stages of AD. For instance, researchers have lacked useful data about how the progression of the disease itself plays a role in diminishing day-to-day physical activity.

"Part of the issue is they're a difficult population to study," she said. "It's mostly assumed that they're not active, that they don't engage in physical activity, but our research showed people in early stages of AD are capable of being active -- they just need assistance."

Watts, who researches health behaviors, prevention strategies and bio-behavioral processes tied to cognitive decline and dementia, wanted to know if there were differences in physical activity between the two groups.

She recently co-authored research appearing in the peer-reviewed Journal of Alzheimer's Disease that used state-of-the-art accelerometers to track daily physical activity of healthy people and those in the early stage of AD.

"In researching physical activity, people in the past have collected data using body-worn devices like Fitbit and accelerometers that collect data every second," Watts said. "But instead of using all the data, they've summed it into one score over the entire time the person was wearing the device. What we've done is look at variability in physical activity over course of the entire day. This may help us to customize interventions, and it may help us to understand disrupted sleep cycles as well."

With colleague Vijay R. Varma of the National Institute on Aging, Watts analyzed daily physical activity of 92 volunteers with and without AD at KU's Alzheimer's Disease Center in Kansas City. Participants wore Actigraph GT3X+ accelerometers for a week.

"We found people with AD have different daily patterns of activity than people without AD," Watts said. "They spend less time in moderate-intensity activity. But it has to do with time of day. They're a lot less active in the morning, when most people are at the peak of activity -- and that may influence caregivers and people who are trying to help people with dementia."

The KU researcher said understanding this different daily pattern in physical activity could be key to designing interventions and improving sleep for people with early AD, perhaps by targeting more physical activity in morning.

Watts said the kinds of physical activity found to be helpful to people with AD might be as simple as finding time to walk around the neighborhood. Her past research includes studies on the benefits of walkable communities for older adults.

"Walking is actually the best thing," she said. "It's low risk, it's safe, anyone can do it, it doesn't require specific equipment, it can be done anywhere. There are other light-intensity activities like stretching, tai chi, household chores, gardening, walking around the mall -- those are also beneficial. People with AD don't have to go to the gym, they just need to do something that keeps them moving and keeps them from sitting continuously."

Challenges for people with AD to getting physically active include changes to what researchers call "motor planning" that come along with typical symptoms of mild AD, even though gross motor function is largely preserved.

"That's the ability to plan out what movements they will do," Watts said. "There's an interaction between cognitive features and motor features. If you have difficulty with cognition, you have trouble with motor function. For instance, if you want to walk, but fear getting lost, you are reluctant because you need cognition to guide motor behavior. In early stages of AD, people are still high functioning physically, but they perceive it's more difficult to get physically active."

Watts will present her latest findings to the annual meeting of the Gerontological Society of America in New Orleans on Nov. 16.

She's following up the research with a larger study of volunteers from KU's Alzheimer's Disease Center, which is headed by colleague Jeffrey Burns.

"There will be hundreds who wear accelerometers for two weeks at a time, collecting data, and we'll look at both sleep and physical activity," Watts said. "So we're continuing this line of research to find out more. We're especially interested in how nighttime sleep and daytime activity levels interact and influence one another."
Science Daily/SOURCE :https://www.sciencedaily.com/releases/2016/11/161109114243.htm

Healthy living means better brain function

November 9, 2016
Science Daily/Frontiers
A feedback loop exists between greater executive function and healthy behavior, scientists report. Specifically, individuals with poor executive function showed subsequent decreases in their rates of participation in physical activity and older adults who engaged in sports and other physical activities tended to retain high levels of executive function over time.

But new research suggests living a healthier lifestyle could also increase executive function, which is the ability to exert self-control, set and meet goals, resist temptation and solve problems. In effect, the study suggests a feedback loop exists where greater executive function enables people to lead a healthier lifestyle, which in turn, improves their executive function.

"It seems that physical activity and EF are synergistic -- they improve one another," according to the study, titled "A Bidirectional Relationship between Executive Function and Health Behaviors."

The study, published by researchers at the University of Aberdeen, the University of Stirling and the University College Dublin, used data collected from 4,555 adults through the English Longitudinal Study of Aging. Researchers analyzed the relationship between physical activity and executive function, adjusting for other variables such as age, gender, education, wealth and illness and found evidence that the relationship between the two is bidirectional. It is the first study of its kind to look at whether the effects are bidirectional and has expanded the understanding of such relationships.

Specifically, individuals with poor executive function showed subsequent decreases in their rates of participation in physical activity and older adults who engaged in sports and other physical activities tended to retain high levels of executive function over time.

Researchers noted that while the study focused on physical activity and its relationship to executive function, it's likely a positive feedback loop also exists between executive function and eating nutritious foods.

Similarly, it is likely that negative feedback loops also exist, in that unhealthy behaviors such as smoking or drinking too much alcohol will be both a result of and a predictor of declining executive function. This has implications, according to the study, for aging.

The older one gets, the more likely executive function is to decline, the study notes. Older people, then, may become more likely to engage in unhealthy behaviors like remaining sedentary and less likely to maintain healthy but effortful behaviors like taking prescribed medication regularly. Conversely, the longer one can maintain high executive function, the longer and more easily that person can stave off behavior that will be detrimental to their health.

Dr. Julia Allan suggests that "people who make a change to their health behavior, like participating in physical activity, eating less processed food, or consuming more fruits and vegetables, can see an improvement in their brain function over time and increase their chances of remaining healthy as they age."

That may be why, researchers opined, those with higher executive function tend to avoid chronic illnesses and live longer after a chronic diagnosis than those who have weaker executive function. With the world's population of elderly folks to hit 1.5 billion by 2050, as the study notes, the research could have major implications for the future of health care.
Science Daily/SOURCE :https://www.sciencedaily.com/releases/2016/11/161109113054.htm

Alzheimer's disease found to be a diabetic disorder of the brain

November 9, 2016
Science Daily/Tohoku University
A promising treatment for Alzheimer's disease has been found by researchers who noticed a similarity in the way insulin signaling works in the brain and in the pancreas of diabetic patients.

"In the pancreas, the Kir6.2 channel blockade increases the insulin signaling, and insulin signaling decreases the blood glucose levels," says Dr. Shigeki Moriguchi. "In the brain, insulin signaling increases the acquisition of memory through CaM kinase II activation by Kir6.2 channel blockade."

The research group, led by Dr. Moriguchi and Professor Kohji Fukunaga of the Graduate School of Pharmaceutical Sciences, thus concluded that Alzheimer's disease can be described as a diabetic disorder of the brain.

Memantine, a drug widely used to treat Alzheimer's disease, is a well known inhibitor of the N-methyl-D-aspartate (NMDA) receptors that prevent excessive glutamate transmission in the brain. Researchers have now found that memantine also inhibits the ATP-sensitive potassium channel (Kir6.2 channel), improving insulin signal dysfunction in the brain.

In their experiment with mice, the researchers found that memantine treatment improved impaired hippocampal long-term potentiation (LTP) and memory-related behaviors in the mice through the inhibition of KATP channel Kir6.2.

"Since KATP channels Kir6.1 or Kir6.2 are critical components of sulfonylurea receptors (SURs) which is downstream insulin receptor signaling, the KATP channel inhibition by Memantine mediates the anti-diabetic drug action in peripheral tissues," says Dr. Moriguchi. "And this leads to improved cognitive functions and improved memory retention among Alzheimer's patients."

The researchers now hope that results of their study and the parallels drawn with diabetes, will lead to new treatments for Alzheimer's disease, using the inhibition of Kir6.2 channel.

Science Daily/SOURCE : https://www.sciencedaily.com/releases/2016/11/161109111922.htm

Researchers reveal how neurodegenerative diseases spread through the brain

November 9, 2016
Science Daily/VIB - Flanders Interuniversity Institute for Biotechnology
Synapses, the place where brain cells contact one another, play a pivotal role in the transmission of toxic proteins. This allows neurodegenerative diseases such as Alzheimer’s to spread through the brain, scientists conclude. If the spreading of these toxic proteins could be prevented, the progression of neurodegenerative diseases might be slowed down substantially.

During neurodegenerative disease, including Alzheimer's, toxic proteins are known to spread throughout the brain. As the disease progresses, more and more brain areas are affected.

Prof. Patrik Verstreken (VIB-KU Leuven): "You can compare it to a drop of ink that falls into a glass of water: gradually, the toxic proteins diffuse through the brain. We knew that the disease follows the existing brain paths but so far it wasn't clear which processes enabled the spread itself."

Genetic risk factors

The researchers now offer proof that synapses are critical to mediate the transmission of toxic protein species and reveal the mechanisms behind this process. They show that the toxic proteins cross from one brain cell to the next by being engulfed by 'vesicles', small bubbles in the receiving brain cell. There the vesicles burst and release the toxic proteins.

Prof. Patrik Verstreken (VIB-KU Leuven): "We also show how familial history has an impact on this process. There are known genetic factors in the human population that increase the risk to develop Alzheimer's and we show that one of the more common genetic variants, dubbed 'BIN1', directly affects the transmission of toxic proteins at synapses. BIN1 'improves' the transmission at synapses but in doing so, it enables the spread of toxic proteins."
 

Next steps

These findings open new perspectives for the treatment of neurodegenerative diseases. By understanding how toxic proteins are passed on between brain cells, researchers may also be able to identify therapeutic avenues to block this process or to shuttle the toxic proteins to the cellular "waste bins."

Dr. Dieder Moechars (Scientific Director at Janssen Research & Development): "Our work is based on in vitro experiments, so it will now be critical to put our models to the test in in vivo models of Alzheimer's disease. Knowing the mechanism of spreading, we now need to devise clever ways to interfere with it."
 

Science Daily/SOURCE :https://www.sciencedaily.com/releases/2016/11/161109085807.htm

 

Who has the better memory, men or women?

November 9, 2016
Science Daily/The North American Menopause Society (NAMS)
Middle-aged women may remember more than men, but their memory fades as estrogen levels decline, report researchers.

In the battle of the sexes, women have long claimed that they can remember things better and longer than men can. A new study proves that middle-aged women outperform age-matched men on all memory measures, although memory does decline as women enter postmenopause. The study is being published online in Menopause, the journal of The North American Menopause Society (NAMS).

Memory loss, unfortunately, is a well-documented consequence of the aging process. Epidemiological estimates suggest that approximately 75% of older adults report memory-related problems. Women report increased forgetfulness and "brain fog" during the menopause transition. In addition, women are disproportionately at risk for memory impairment and dementia compared with men. Despite these conditions working against them, middle-aged women still outscore their similarly aged male counterparts on all memory measures, according to the study.

The cross-sectional study of 212 men and women aged 45 to 55 years assessed episodic memory, executive function, semantic processing, and estimated verbal intelligence through cognitive testing. Associative memory and episodic verbal memory were assessed using a Face-Name Associative Memory Exam and Selective Reminding Test.

In addition to comparing sex differences, the study also found that premenopausal and perimenopausal women outperformed postmenopausal women in a number of key memory areas. Declines in estradiol levels in postmenopausal women were specifically associated with lower rates of initial learning and retrieval of previously recalled information, while memory storage and consolidation were maintained.

"Brain fog and complaints of memory issues should be taken seriously," says Dr. JoAnn Pinkerton, NAMS executive director. "This study and others have shown that these complaints are associated with memory deficits."
Science Daily/SOURCE : https://www.sciencedaily.com/releases/2016/11/161109112447.htm

Probiotics improve cognition in Alzheimer's patients

November 10, 2016
Science Daily/Frontiers
For the first time, scientists have shown that probiotics -- beneficial live bacteria and yeasts taken as dietary supplements -- can improve cognitive function in humans. In a new clinical trial, scientists show that a daily dose of probiotic Lactobacillus and Bifidobacterium bacteria taken over a period of just 12 weeks is enough to yield a moderate but significant improvement in the score of elderly Alzheimer's patients on the Mini-Mental State Examination (MMSE) scale, a standard measure of cognitive impairment.

Probiotics are known to give partial protection against certain infectious diarrheas, irritable bowel syndrome, inflammatory bowel disease, eczema, allergies, colds, tooth decay, and periodontal disease. But scientists have long hypothesized that probiotics might also boost cognition, as there is continuous two-way communication between the intestinal microflora, the gastrointestinal tract, and the brain through the nervous system, the immune system, and hormones (along the so-called "microbiota-gut-brain axis"). In mice, probiotics have indeed been shown to improve learning and memory, and reduce anxiety and depression- and OCD-like symptoms. But prior to the present study there was very limited evidence of any cognitive benefits in humans.

Here, the researchers, from Kashan University of Medical Sciences, Kashan, and Islamic Azad University, Tehran, Iran, present results from a randomized, double-blind, controlled clinical trial on a total of 52 women and men with Alzheimer's between 60 and 95 years of age. Half of the patients daily received 200 ml milk enriched with four probiotic bacteria Lactobacillus acidophilus, L. casei, L. fermentum, and Bifidobacterium bifidum (approximately 400 billion bacteria per species), while the other half received untreated milk.

At the beginning and the end of the 12-week experimental period, the scientists took blood samples for biochemical analyses and tested the cognitive function of the subjects with the MMSE questionnaire, which includes tasks like giving the current date, counting backwards from 100 by sevens, naming objects, repeating a phrase, and copying a picture.

Over the course of the study, the average score on the MMSE questionnaire significantly increased (from 8.7 to 10.6, out of a maximum of 30) in the group receiving probiotics, but not in the control group (from 8.5 to 8.0). Even though this increase is moderate, and all patients remained severely cognitively impaired, these results are important because they are the first to show that probiotics can improve human cognition. Future research, on more patients and over longer time-scales, is necessary to test if the beneficial effects of probiotics become stronger after longer treatment.

"In a previous study, we showed that probiotic treatment improves the impaired spatial learning and memory in diabetic rats, but this is the first time that probiotic supplementation has been shown to benefit cognition in cognitively impaired humans," says Professor Mahmoud Salami from Kashan University, the senior author of the study.

Treatment with probiotics also resulted in lower levels of triglycerides, Very Low Density Lipoprotein (VLDL), high-sensitivity C-Reactive Protein (hs-CRP) in the blood of the Alzheimer patients, and likewise a reduction in two common measures (called "Homeostatic Model Assessment," HOMA-IR and HOMA-B) of insulin resistance and the activity of the insulin-producing cells in the pancreas.

"These findings indicate that change in the metabolic adjustments might be a mechanism by which probiotics affect Alzheimer's and possibly other neurological disorders," says Salami. "We plan to look at these mechanisms in greater detail in our next study."

Walter Lukiw, Professor of Neurology, Neuroscience and Ophthalmology and Bollinger Professor of Alzheimer's disease at Louisiana State University, who reviewed the study but was not involved in the research, said: "This early study is interesting and important because it provides evidence for gastrointestinal (GI) tract microbiome components playing a role in neurological function, and indicates that probiotics can in principle improve human cognition. This is in line with some of our recent studies which indicate that the GI tract microbiome in Alzheimer's is significantly altered in composition when compared to age-matched controls, and that both the GI tract and blood-brain barriersbecome significantly more leaky with aging, thus allowing GI tract microbial exudates (e.g. amyloids, lipopolysaccharides, endotoxins and small non-coding RNAs) to access Central Nervous System compartments."


Science Daily/SOURCE : https://www.sciencedaily.com/releases/2016/11/161110162840.htm

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