An Artificial Retina With the Capacity to Restore Normal Vision

Two researchers at Weill Cornell Medical College have deciphered a mouse's retina's neural code and coupled this information to a novel prosthetic device to restore sight to blind mice. The researchers say they have also cracked the code for a monkey retina -- which is essentially identical to that of a human -- and hope to quickly design and test a device that blind humans can use.

Source: http://commons.wikimedia.org/wiki/File:Amandine_Eyes.jpg

The lead researcher, Dr. Sheila Nirenberg, a computational neuroscientist at Weill Cornell, envisions a day when the blind can choose to wear a visor, similar to the one used on the television show Star Trek. The visor's camera will take in light and use a computer chip to turn it into a code that the brain can translate into an image.The breakthrough, reported in theProceedings of the National Academy of Sciences (PNAS), signals a remarkable advance in longstanding efforts to restore vision. Current prosthetics provide blind users with spots and edges of light to help them navigate. This novel device provides the code to restore normal vision. The code is so accurate that it can allow facial features to be discerned and allow animals to track moving images.

"It's an exciting time. We can make blind mouse retinas see, and we're moving as fast as we can to do the same in humans," says Dr. Nirenberg, a professor in the Department of Physiology and Biophysics and in the Institute for Computational Biomedicine at Weill Cornell. The study's co-author is Dr. Chethan Pandarinath, who was a graduate student with Dr. Nirenberg and is currently a postdoctoral researcher at Stanford University.

This new approach provides hope for the 25 million people worldwide who suffer from blindness due to diseases of the retina. Because drug therapies help only a small fraction of this population, prosthetic devices are their best option for future sight. "This is the first prosthetic that has the potential to provide normal or near-normal vision because it incorporates the code," Dr. Nirenberg explains.

Discovering the Code

Normal vision occurs when light falls on photoreceptors in the surface of the retina. The retinal circuitry then processes the signals from the photoreceptors and converts them into a code of neural impulses. These impulses are then sent up to the brain by the retina's output cells, called ganglion cells. The brain understands this code of neural pulses and can translate it into meaningful images.

Blindness is often caused by diseases of the retina that kill the photoreceptors and destroy the associated circuitry, but typically, in these diseases, the retina's output cells are spared.

Current prosthetics generally work by driving these surviving cells. Electrodes are implanted into a blind patient's eye, and they stimulate the ganglion cells with current. But this only produces rough visual fields.

Many groups are working to improve performance by placing more stimulators into the patient's eye. The hope is that with more stimulators, more ganglion cells in the damaged tissue will be activated, and image quality will improve.

Other research teams are testing use of light-sensitive proteins as an alternate way to stimulate the cells. These proteins are introduced into the retina by gene therapy. Once in the eye, they can target many ganglion cells at once.

But Dr. Nirenberg points out that there's another critical factor. "Not only is it necessary to stimulate large numbers of cells, but they also have to be stimulated with the right code -- the code the retina normally uses to communicate with the brain."

This is what the authors discovered -- and what they incorporated into a novel prosthetic system.

Dr. Nirenberg reasoned that any pattern of light falling on to the retina had to be converted into a general code -- a set of equations -- that turns light patterns into patterns of electrical pulses. "People have been trying to find the code that does this for simple stimuli, but we knew it had to be generalizable, so that it could work for anything -- faces, landscapes, anything that a person sees," Dr. Nirenberg says.

Vision = Chip Plus Gene Therapy

In a eureka moment, while working on the code for a different reason, Dr. Nirenberg realized that what she was doing could be directly applied to a prosthetic. She and her student, Dr. Pandarinath, immediately went to work on it. They implemented the mathematical equations on a "chip" and combined it with a mini-projector. The chip, which she calls the "encoder" converts images that come into the eye into streams of electrical impulses, and the mini-projector then converts the electrical impulses into light impulses. These light pulses then drive the light-sensitive proteins, which have been put in the ganglion cells, to send the code on up to the brain.

The entire approach was tested on the mouse. The researchers built two prosthetic systems -- one with the code and one without. "Incorporating the code had a dramatic impact," Dr. Nirenberg says. "It jumped the system's performance up to near-normal levels -- that is, there was enough information in the system's output to reconstruct images of faces, animals -- basically anything we attempted."

In a rigorous series of experiments, the researchers found that the patterns produced by the blind retinas in mice closely matched those produced by normal mouse retinas.

"The reason this system works is two-fold," Dr. Nirenberg says. "The encoder -- the set of equations -- is able to mimic retinal transformations for a broad range of stimuli, including natural scenes, and thus produce normal patterns of electrical pulses, and the stimulator (the light sensitive protein) is able to send those pulses on up to the brain."

"What these findings show is that the critical ingredients for building a highly-effective retinal prosthetic -- the retina's code and a high resolution stimulating method -- are now, to a large extent, in place," reports Dr. Nirenberg.

Dr. Nirenberg says her retinal prosthetic will need to undergo human clinical trials, especially to test safety of the gene therapy component, which delivers the light-sensitive protein. But she anticipates it will be safe since similar gene therapy vectors have been successfully tested for other retinal diseases.

"This has all been thrilling," Dr. Nirenberg says. "I can't wait to get started on bringing this approach to patients."

The study was funded by grants from the National Institutes of Health and Cornell University's Institute for Computational Biomedicine.

Both Drs. Nirenberg and Pandarinath have a patent application for the prosthetic system filed through Cornell University.

Source: Weill Cornell Medical College (2012, August 14). An artificial retina with the capacity to restore normal vision. ScienceDaily. Retrieved April 23, 2013, from http://www.sciencedaily.com­/releases/2012/08/120814213326.htm

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Half of Inhaled Soot Particles from Diesel Exhaust, Fires Gets Stuck in the Lungs

The exhaust from diesel-fueled vehicles, wood fires and coal-driven power stations contains small particles of soot that flow out into the atmosphere. The soot is a scourge for the climate but also for human health. Now for the first time, researchers have studied in detail how diesel soot gets stuck in the lungs. The results show that more than half of all inhaled soot particles remain in the body. (Credit: © Imagenatural / Fotolia)

The figure is higher than for most other types of particles. For example "only" 20 per cent of another type of particle from wood smoke and other biomass combustion gets stuck in the lungs. One explanation is that diesel soot is made up of smaller particles and can therefore penetrate deeper into the lungs, where it is deposited. The study was made on diesel particles (which mainly consist of soot) and was recently published in the Journal of Aerosol Science. Ten healthy people volunteered for the the study.

"Findings of this kind can be extremely useful both for researchers to determine what doses of soot we get into our lungs out of the amount we are exposed to, and to enable public authorities to establish well-founded limits for soot particles in outdoor air," says Jenny Rissler, researcher in aerosol technology at Lund University's Faculty of Engineering and responsible for publishing the study.

In population studies, other researchers have been able to observe that people who live in areas with high concentrations of particulates are more affected by both respiratory and cardiovascular diseases. But since there is no conclusive evidence that it is precisely the soot that is to blame, the authorities have so far not taken any decisions on guidelines.

"Currently there is no specific limit for soot particles in the air, despite the fact that soot in the air is linked to both lung cancer and other diseases," says Jenny Rissler.

But Jenny Rissler thinks that in the future, limits on soot levels will also be set, with reference to the WHO's recent reclassification of diesel exhaust from "probably carcinogenic" to "carcinogenic."

Soot particles are not only connected to effects on health but may also contribute to a warmer climate. Paradoxically, other types of aerosol particles can partly be desirable, insofar as they have a cooling effect on the climate and thereby mitigate the warming effect of carbon dioxide.

"Soot particles are black and absorbs light, thus producing a warming effect. So it could be a double advantage to reduce it," she observes.

Jenny Rissler will next be studying individual variations in lung deposition and exposing cells to soot. She is also in the process of further developing methods to measure the surface area of the particles, as this has shown to be an important indicator of their harmfulness.

Background: Every time we breathe, we inhale tiny airborne particles, so-called aerosol particles. Some occur naturally, while others are the result of human activity. Soot mainly belongs in the latter category, as a by-product of combustion from power stations to small-scale wood fires and decorative candles. Another common source of soot is the exhaust from diesel engines, even though modern diesel cars have considerably reduced emissions thanks to efficient filters.

The EU will be tightening rules on emissions for heavy duty diesel vehicles in 2014.

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The above story is reprinted from materials provided byLund University.

Jenny Rissler, Erik Swietlicki, Agneta Bengtsson, Christoffer Boman, Joakim Pagels, Thomas Sandström, Anders Blomberg, Jakob Löndahl. Experimental determination of deposition of diesel exhaust particles in the human respiratory tract. Journal of Aerosol Science, 2012; 48: 18 DOI: 10.1016/j.jaerosci.2012.01.005

Lund University (2012, June 27). Half of inhaled soot particles from diesel exhaust, fires gets stuck in the lungs. ScienceDaily. Retrieved April 15, 2013, from http://www.sciencedaily.com­/releases/2012/06/120627092016.htm

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How stress can boost the immune system

The study's findings provide a thorough overview of how a triad of stress hormones affects the main cell subpopulations of the immune system. They also offer the prospect of, someday, being able to manipulate stress-hormone levels to improve patients' recovery from surgery or wounds or their responses to vaccines.

You've heard it a thousand times: Stress is bad for you. And it's certainly true that chronic stress, lasting weeks and months, has deleterious effects including, notably, suppression of the immune response. But short-term stress -- the fight-or-flight response, a mobilization of bodily resources lasting minutes or hours in response to immediate threats -- stimulates immune activity, said lead author Firdaus Dhabhar, PhD, an associate professor of psychiatry and behavioral sciences and member of the Stanford Institute for Immunity, Transplantation and Infection.

And that's a good thing. The immune system is crucial for wound healing and preventing or fighting infection, and both wounds and infections are common risks during chases, escapes and combat.

Working with colleagues at Stanford and two other universities in a study published online June 22 inPsychoneuroendocrinology, Dhabhar showed that subjecting laboratory rats to mild stress caused a massive mobilization of several key types of immune cells into the bloodstream and then onto destinations including the skin and other tissues. This large-scale migration of immune cells, which took place over a time course of two hours, was comparable to the mustering of troops in a crisis, Dhabhar said. He and colleagues had previously shown that a similar immune-cell redistribution in patients experiencing the short-term stress of surgery predicts enhanced postoperative recovery.

In the new study, the investigators were able to show that the massive redistribution of immune cells throughout the body was orchestrated by three hormones released by the adrenal glands, in different amounts and at different times, in response to the stress-inducing event. These hormones are the brain's call-to-arms to the rest of the body, Dhabhar said.

"Mother Nature gave us the fight-or-flight stress response to help us, not to kill us," said Dhabhar, who has been conducting experiments for well over a decade on the effects of the major stress hormones on the immune system. Last summer, Dhabhar received the International Society for Psychoneuroendocrinology's Curt. P. Richter Award for his work in this area, culminating in the new study.

The findings paint a clearer picture of exactly how the mind influences immune activity. "An impala's immune system has no way of knowing that a lion is lurking in the grass and is about to pounce, but its brain does," Dhabhar said. In such situations, it benefits lion and impala alike when pathogen-fighting immune cells are in positions of readiness in such places as the skin and mucous membranes, which are at high risk for damage and consequent infection.

So it makes perfect evolutionary sense that predator/prey activity and other situations in nature, such as dominance challenges and sexual approaches, trigger stress hormones. "You don't want to keep your immune system on high alert at all times," Dhabhar said. "So nature uses the brain, the organ most capable of detecting an approaching challenge, to signal that detection to the rest of the body by directing the release of stress hormones. Without them, a lion couldn't kill, and an impala couldn't escape." The stress hormones not only energize the animals' bodies -- they can run faster, jump higher, bite harder -- but, it turns out, also mobilize the immune troops to prepare for looming trouble.

The response occurs across the animal kingdom, he added. You see pretty much the same pattern of hormone release in a fish that has been picked up out of the water.

The experiments in this study were performed on rats, which Dhabhar subjected to mild stress by confining them (gently, and with full ventilation) in transparent Plexiglas enclosures to induce stress. He drew blood several times over a two-hour period and, for each time point, measured levels of three major hormones -- norepinephrine, epinephrine and corticosterone (the rat analog of cortisol in humans) -- as well as of several distinct immune-cell types in the blood.

What he saw was a pattern of carefully choreographed changes in blood levels of the three hormones along with the movement of many different subsets of immune cells from reservoirs such as the spleen and bone marrow into the blood and, finally, to various "front line" organs.

To show that specific hormones were responsible for movements of specific cell types, Dhabhar administered the three hormones, separately or in various combinations, to rats whose adrenal glands had been removed so they couldn't generate their own stress hormones. When the researchers mimicked the pattern of stress-hormone release previously observed in the confined rats, the same immune-cell migration patterns emerged in the rats without adrenal glands. Placebo treatment produced no such effect.

The general pattern, Dhabhar said, was that norepinephrine is released early and is primarily involved in mobilizing all major immune-cell types -- monocytes, neutrophils and lymphocytes -- into the blood. Epinephrine, also released early, mobilized monocytes and neutrophils into the blood, while nudging lymphocytes out into "battlefield" destinations such as skin. And corticosterone, released somewhat later, caused virtually all immune cell types to head out of circulation to the "battlefields."

The overall effect of these movements is to bolster immune readiness. A study published by Dhabhar and his colleagues in 2009 in the Journal of Bone and Joint Surgery assessed patients' recovery from surgery as a function of their immune-cell redistribution patterns during the stress of the operation. Those patients in whom the stress of surgery mobilized immune-cell redistributions similar to those seen in the confined rats in the new study did significantly better afterward than patients whose stress hormones less adequately guided immune cells to appropriate destinations.

The mechanisms Dhabhar has delineated could lead to medical applications, such as administering low doses of stress hormones or drugs that mimic or antagonize them in order to optimize patients' immune readiness for procedures such as surgery or vaccination. "More study will be required including in human subjects, which we hope to conduct, before these applications can be attempted," Dhabhar said. Closer at hand is the monitoring of patients' stress-hormone levels and immune-cell distribution patterns during surgery to assess their surgical prognosis, or during immunization to predict vaccine effectiveness.

The study was funded by the John D. & Catherine T. MacArthur Foundation, the Dana Foundation, the DeWitt Wallace Foundation, the Carl & Elizabeth Naumann Fund and the National Institutes of Health. The medical school's Department of Psychiatry and Behavioral Sciences also supported this work. Dhabhar's co-authors were statistician Eric Neri at Stanford, and neuroendocrinologists at Ohio State University and Rockefeller University.

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The above story is reprinted from materials provided byStanford University Medical Center. The original article was written by Bruce Goldman.

Stanford University Medical Center (2012, June 21). How stress can boost immune system.ScienceDaily. Retrieved April 15, 2013, from http://www.sciencedaily.com­/releases/2012/06/120621223525.htm

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Keep aging brains sharp

Exercising, eating a healthy diet and playing brain games may help you keep your wits about you well into your 80s and even 90s, advises a new book by researchers at George Mason University. 

"These are all cheap, easy things to do," says Pamela Greenwood, an associate professor in the Department of Psychology on Mason's Fairfax, Va. campus. "We should all be doing them anyway. You should do them for your heart and health, so why not do them for your brain as well?" 

For the past 20 years, Greenwood and Raja Parasuraman, University Professor of Psychology, have studied how the mind and brain age, focusing on Alzheimer's disease. Their book, "Nurturing the Older Brain and Mind" published by MIT Press, came out in March. The cognitive neuroscientists geared the book to middle-aged readers who want to keep their mental snap. 

"We know that if we can put off dementing illnesses even by a year or two through lifestyle changes, that will reduce the number of people with Alzheimer's disease, which is reaching epidemic proportions," Parasuraman says. 

Not everyone's brain declines when retirement age hits. "You can look at a group of 65-year-olds — some are in nursing homes, and some are running the world," Greenwood says. 

Now that more workers are staying on the job longer for economic reasons and because countries are upping the retirement age, keeping the mind agile becomes paramount, Parasuraman says. 

For the book, Parasuraman and Greenwood examined only scientific studies, theirs and others, ranging from neurological to physiological. A few surprises leaped out of the data. 

"Several old dogmas were overturned," Parasuraman says. "There's the tired old joke that we're losing brain cells as we age — maybe starting as young as 20 or 30 — and it's all downhill after that." 

Not so, new research reveals. Not only are some 60-year-olds as sharp as 20-year-olds, but their brains still create new cells. Brain cells may not grow as fast as bone or skin cells, but grow they do, particularly in the hippocampus. "It's the area of the brain that's very important to memory and is affected by Alzheimer's disease," Parasuraman says. 

Novel experiences and new learning help new brain cells become part of the circuitry. Parasuraman points to a study of terminally ill cancer patients whose brains were still forming new neurons. "If a person who's in a terminally ill state can generate new neurons, then surely healthy people can," Parasuraman says. 

Brain games and new experiences may build up "white matter," which insulates neurons as they carry signals, Greenwood says. In older brains, this white matter insulation develops holes and signals go awry. 

Older adult gamers are winning skills to help them move through life, Parasuraman says. "We are looking at everyday problem solving," he says. "Are you better at balancing a checkbook? Are you better at making decisions in a grocery store? We're finding you get better at those tasks (after playing the video games in the study)." 

Moving large muscle groups also builds brain matter. In one study detailed in the book, older, sedentary people began walking or did stretching exercises for 45 minutes, three times a week. "Those people actually became smarter over time," Greenwood says. "You don't have to be running Ironman marathons. You can just walk briskly three or four times a week." 

Another best bet for an active mind is a nutritious diet that limits calories to the minimum amount needed to keep a body healthy. No starvation diets, though. "The strongest evidence we have is not very pleasant, which is dietary restriction, reducing calories," Parasuraman says. "That clearly improves longevity and cognition. The evidence in animals is very strong. Such dietary restriction may never be popular. But perhaps every-other-day fasting as an approximation to it is something people would tolerate: You eat normally one day, and the next day you don't." 

Popping supplements won't fill a nutritionally deficient diet, Parasuraman says. "A lot of people think, 'I can eat junk food and then take a pill.' No. You have to eat fruits and vegetables, leafy vegetables. It has to be part of the regular diet because otherwise it's not absorbed." 

Fat cells help make up cell membranes. The unsaturated fats found in fish and olive oils may boost flexibility in these membranes. The more flexible membranes are, the better they may work, scientists theorize. Saturated fats such as butter have to go because these fats vie with healthy fats for a place in the cell membrane, Greenwood explains. 

Greenwood and Parasuraman want people to know that getting old doesn't mean getting senile. "The bottom line message of the book is really a hopeful one," Greenwood says. "There are lots of things that you can do (to keep your brain healthy)." 

Source: George Mason University [April 04, 2012]

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Why the brain is more reluctant to function as we age

New findings, led by neuroscientists at the University of Bristol and published this week in the journal Neurobiology of Aging, reveal a novel mechanism through which the brain may become more reluctant to function as we grow older. 

It is not fully understood why the brain's cognitive functions such as memory and speech decline as we age. Although work published this year suggests cognitive decline can be detectable before 50 years of age. The research, led by Professor Andy Randall and Dr Jon Brown from the University's School of Physiology and Pharmacology, identified a novel cellular mechanism underpinning changes to the activity of neurones which may underlie cognitive decline during normal healthy aging. 

The brain largely uses electrical signals to encode and convey information. Modifications to this electrical activity are likely to underpin age-dependent changes to cognitive abilities. 

The researchers examined the brain's electrical activity by making recordings of electrical signals in single cells of the hippocampus, a structure with a crucial role in cognitive function. In this way they characterised what is known as "neuronal excitability" — this is a descriptor of how easy it is to produce brief, but very large, electrical signals called action potentials; these occur in practically all nerve cells and are absolutely essential for communication within all the circuits of the nervous system. 

Action potentials are triggered near the neurone's cell body and once produced travel rapidly through the massively branching structure of the nerve cell, along the way activating the synapses the nerve cell makes with the numerous other nerve cells to which it is connected. 

The Bristol group identified that in the aged brain it is more difficult to make hippocampal neurones generate action potentials. Furthermore they demonstrated that this relative reluctance to produce action potential arises from changes to the activation properties of membrane proteins called sodium channels, which mediate the rapid upstroke of the action potential by allowing a flow of sodium ions into neurones. 

Professor Randall, Professor in Applied Neurophysiology said: "Much of our work is about understanding dysfunctional electrical signalling in the diseased brain, in particular Alzheimer's disease. We began to question, however, why even the healthy brain can slow down once you reach my age. Previous investigations elsewhere have described age-related changes in processes that are triggered by action potentials, but our findings are significant because they show that generating the action potential in the first place is harder work in aged brain cells. 

"Also by identifying sodium channels as the likely culprit for this reluctance to produce action potentials, our work even points to ways in which we might be able modify age-related changes to neuronal excitability, and by inference cognitive ability." 

Source: University of Bristol [February 01, 2012]

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Why Are Older People Happier?

Older people tend to be happier. But why? Some psychologists believe that cognitive processes are responsible -- in particular, focusing on and remembering positive events and leaving behind negative ones; those processes, they think, help older people regulate their emotions, letting them view life in a sunnier light. "There is a lot of good theory about this age difference in happiness," says psychologist Derek M. Isaacowitz of Northeastern University, "but much of the research does not provide direct evidence" of the links between such phenomena and actual happiness. 

In a new article in Perspectives on Psychological Science, a journal published by the Association for Psychological Science, Isaacowitz and the late Fredda Blanchard-Fields of Georgia Institute of Technology argue for more rigorous research. 

Researchers, including the authors, have found that older people shown pictures of faces or situations tend to focus on and remember the happier ones more and the negative ones less. Other studies have discovered that as people age, they seek out situations that will lift their moods -- for instance, pruning social circles of friends or acquaintances who might bring them down. Still other work finds that older adults learn to let go of loss and disappointment over unachieved goals, and hew their goals toward greater wellbeing. 

What's missing, say the authors, are consistently demonstrated direct links between these strategies and phenomena and changes of mood for the better. One reason, Isaacowitz suggests, is that lab tests yield results that are not straightforward. "When we try to use those cognitive processes to predict change of mood, they don't always do so," he explains. "Sometimes looking at positive pictures doesn't make people feel better." A closer review of the literature also reveals contradictions. Some people -- younger ones, for instance -- may make themselves feel better by accentuating the negative in others' situations or characteristics. And whereas some psychologists find that high scores on certain cognitive tests correlate in older people with the ability to keep their spirits up, other researchers hypothesize that happiness in later life is an effect of cognitive losses -- which force older people to concentrate on simpler, happier thoughts. 

More rigorous methods probably won't overthrow the current theories, says Isaacowitz, but they will complicate the picture. "It won't be as easy to say old people are happier. But even if they are happier on average, we still want to know in what situations does this particular strategy make this particular person with these particular qualities or strengths feel good." 

Source: Association for Psychological Science [January 05, 2012]

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Study Looks at the Nature of Change in Our Aging, Changing Brains

As we get older, our cognitive abilities change, improving when we're younger and declining as we age. Scientists posit a hierarchical structure within which these abilities are organized. There's the "lowest" level -- measured by specific tests, such as story memory or word memory; the second level, which groups various skills involved in a category of cognitive ability, such as memory, perceptual speed, or reasoning; and finally, the "general," or G, factor, a sort of statistical aggregate of all the thinking abilities. 

What happens to this structure as we age? That was the question Timothy A. Salthouse, Brown-Forman professor of psychology at the University of Virginia, investigated in a new study appearing in an upcoming issue of Psychological Science, a journal published by the Association for Psychological Science. His findings advance psychologists' understanding of the complexities of the aging brain. 

"There are three hypotheses about how this works," says Salthouse. "One is that abilities become more strongly integrated with one another as we age." That theory suggests the general factor influences cognitive aging the most. The second -- based on the idea that connectivity among different brain regions lessens with age -- "is almost the opposite: that the changes in cognitive abilities become more rather than less independent with age." The third was Salthouse's hypothesis: The structure remains constant throughout the aging process. 

Using a sample of 1,490 healthy adults ages 18 to 89, Salthouse performed analyses of the scores on 16 tests of five cognitive abilities -- vocabulary, reasoning, spatial relations, memory, and perceptual speed. The primary analyses were on the changes in the test scores across an interval of about two and a half years. 

The findings confirmed Salthouse's hunch: "The effects of aging on memory, on reasoning, on spatial relations, and so on are not necessarily constant. But the structure within which these changes are occurring does not seem to change as a function of age." In normal, healthy people, "the direction and magnitude of change may be different" when we're 18 or 88, he says. "But it appears that the qualitative nature of cognitive change remains the same throughout adulthood." 

The study could inform other research investigating "what allows some people to age more gracefully than others," says Salthouse. That is, do people who stay mentally sharper maintain their ability structures better than those who become more forgetful or less agile at reasoning? And in the future, applying what we know about the structures of change could enhance "interventions that we think will improve cognitive functioning" at any age or stage of life. 

Source: Association for Psychological Science [November 22, 2011]

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People with Parkinson's disease more likely to have leg restlessness than restless leg syndrome

People with Parkinson's disease may be more likely to have a movement disorder called leg motor restlessness, but not true restless legs syndrome as previous studies have suggested, according to a study published in the Nov. 9, 2011, online issue of Neurology®, the medical journal of the American Academy of Neurology. 

Restless legs syndrome is a sleep and movement disorder. People with the disorder have the urge to move their legs to stop uncomfortable sensations. The urge occurs when the person is at rest, in the evening, and is temporarily relieved by movement. In leg motor restlessness, people also have the urge to move their legs, but it is either not worse when they are at rest or during the evening or it does not go away when they move their legs. 

Because restless legs syndrome and Parkinson's disease both respond to the drug dopamine, researchers have looked for connections between the two disorders. Some studies have shown that people with Parkinson's disease are more likely also to have restless legs syndrome than people who don't have Parkinson's disease. But those studies have looked at people with advanced cases of Parkinson's who have taken dopamine drugs for many years. 

The current study is the first to look at the issue in people who were recently diagnosed with Parkinson's disease and have not yet taken any dopamine drugs. The Norwegian study compared 200 people with early Parkinson's disease to 173 people of similar ages who did not have Parkinson's disease. 

The study found that restless legs syndrome was not significantly more common in people with Parkinson's disease than it was in those without the disease. But people with Parkinson's were nearly three times more likely to have leg motor restlessness than those without Parkinson's. A total of 26 people with Parkinson's disease and 10 people without the disease had leg motor restlessness. 

"This finding could possibly be because people who have not yet taken dopamine for their Parkinson's disease have a dopamine deficiency in their brains, which is similar to when people develop motor restlessness after taking antipsychotic drugs that block dopamine in the brain," said study author Michaela D. Gjerstad, PhD, of Stavanger University Hospital in Norway and a Fellow of the American Academy of Neurology. 

John Morgan, MD, PhD, of Georgia Health Sciences University in Augusta, who wrote an editorial regarding the study, said, "Time will tell whether the majority of these people with leg motor restlessness will go on to develop restless legs syndrome, or whether the restlessness improves after they start taking dopamine drugs. Further study of this group of people will be quite interesting." 

Source: American Academy of Neurology [November 09, 2011]

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Researchers identify diabetes link to cognitive impairment in older adults

Many complications of diabetes, including kidney disease, foot problems and vision problems are generally well recognized. But the disease's impact on the brain is often overlooked. 

For the past five years, a team led by Beth Israel Deaconess Medical Center (BIDMC) neurophysiologist Vera Novak, MD, PhD, has been studying the effects of diabetes on cognitive health in older individuals and has determined that memory loss, depression and other types of cognitive impairment are a serious consequence of this widespread disease. 

Now, Novak's team has identified a key mechanism behind this course of events. In a study published in the November 2011 issue of the journal Diabetes Care, they report that in older patients with diabetes, two adhesion molecules – sVCAM and sICAM – cause inflammation in the brain, triggering a series of events that affect blood vessels and, eventually, cause brain tissue to atrophy. Importantly, they found that the gray matter in the brain's frontal and temporal regions -- responsible for such critical functions as decision-making, language, verbal memory and complex tasks – is the area most affected by these events. 

"In our previous work, we had found that patients with diabetes had significantly more brain atrophy than did a control group," explains Novak, Director of the Syncope and Falls in the Elderly (SAFE) Program in the Division of Gerontology at BIDMC and Associate Professor of Medicine at Harvard Medical School. "In fact, at the age of 65, the average person's brain shrinks about one percent a year, but in a diabetic patient, brain volume can be lowered by as much as 15 percent." 

Diabetes develops when glucose builds up in the blood instead of entering the body's cells to be used as energy. Known as hyperglycemia, this condition often goes hand-in-hand with inflammation. Novak wanted to determine if chronic inflammation of the blood vessels was causing altered blood flow to the brain in patients with diabetes. 

To test this hypothesis, Novak's team recruited 147 study subjects, averaging 65 years of age. Seventy one of the subjects had type 2 diabetes and had been taking medication to manage their conditions for at least five years. The other 76 were age and sex-matched non-diabetic controls. 

Study subjects underwent a series of cognitive tests, balance tests and standard blood-pressure and blood-glucose tests. Serum samples were also collected to measure adhesion molecules and several other markers of systemic inflammation. To determine perfusion (blood flow) measures in the brain, patients also underwent functional MRI testing, in which a specialized imaging technique known as arterial spin labeling (developed by BIDMC MR physicist David Alsop, PhD) was used in conjunction with a standard MRI to measure vascular reactivity in several brain regions and to show changes in blood flow. 

As predicted, the scans showed that the diabetic patients not only had greater blood vessel constriction than the control subjects, but they also had more atrophied brain tissue, particularly gray matter. The results also showed that, in the patients with diabetes, the frontal, temporal and parietal regions of the brain were most affected. Similarly, the team's measurements of serum markers confirmed that high glucose levels were strongly correlated with higher levels of inflammatory cytokines. 

"It appears that chronic hyperglycemia and insulin resistance – the hallmarks of diabetes – trigger the release of adhesion molecules [sVCAM and sICAM] and set off a cascade of events leading to the development of chronic inflammation," says Novak. "Once chronic inflammation sets in, blood vessels constrict, blood flow is reduced, and brain tissue is damaged. " 

This discovery now provides two biomarkers of altered vascular reactivity in the brain. "If these markers can be identified before the brain is damaged, we can take steps to try and intervene," says Novak, explaining that some data indicates that medications may improve vascoreactivity. 

But more important, she says, the new findings provide still more reason for doctors and patients to focus greater attention on the management – and prevention – of diabetes. 

"Cognitive decline affects a person's ability to successfully complete even the simplest of everyday tasks, such as walking, talking or writing," says Novak. "There are currently 25.8 million cases of type 2 diabetes in the United States alone, which is more than eight percent of our total population. The effects of diabetes on the brain have been grossly neglected, and, as our findings confirm, are issues that need to be addressed." 

Source: Beth Israel Deaconess Medical Center [November 08, 2011]

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The new old age – today's pensioners are very different to yesterday's

Old people today have more sex, are more likely to be divorced, are cleverer and feel better, reveals a long-term research project comparing what it is like to be old today with 30 years ago. "It's time to start talking about the 'new old age'," says researcher Ingmar Skoog. 

The number of elderly is rising worldwide, and it is estimated that average life expectancy in Europe will reach 100 by the end of the century. 

At the same time, old age and what we expect from it are changing. An extensive research project at the University of Gothenburg's Sahlgrenska Academy has spent a number of years comparing the elderly of the 1970s with those of today. The project, known as the H70 study, reveals that old age has changed drastically in a number of ways. 

For example, the proportion of elderly with schooling beyond secondary level has risen from 14% to almost 40% for both genders. This is reflected in a better performance in intelligence tests by today's 70-year-olds than their counterparts back in the 1970s. 

The proportion of married people has increased, as has the proportion of divorcees. The elderly are also now more sexually active, and the number with sexual problems such as impotence has fallen. 

The results of the long-term study can also be contradictory, not least when it comes to social networking: 

"The H70 study shows that the elderly are more outgoing today than they were in the 1970s – they talk more to their neighbours, for example – yet the percentage of elderly who feel lonely has increased significantly," says professor Ingmar Skoog from the University of Gothenburg's Sahlgrenska Academy, who leads the study. 

Old people's mental health does not seem to have changed, however. Dementia disorders are no more prevalent today than they were 30 years ago, and while more old people consider themselves to be mildly depressed, more severe forms of depression have not become more common. Meanwhile the elderly are coping better with everyday life: the number needing help with cleaning has fallen from 25% to 12%, and only 4% need help taking a bath, down from 14% in the 1970s. 

"Our conclusion is that pensioners are generally healthier and perkier today than they were 30 years ago," says Skoog. "This may be of interest both in the debate about where to set the retirement age and in terms of the baby boomers now hitting retirement age." 

The H70 study in Gothenburg began back in 1971. More than 1,000 70-year-old men and women born in 1901-02 were examined by doctors and interviewed about their lives to obtain a picture of diseases in elderly populations, risk factors and their functional capacity and social networks. The participants were examined again at the age of 75 and then at regular intervals until the final participant died at the age of 105. The year 2000 brought the start of a new study of 70-year-olds born in 1930, who were examined using the same methods, making it possible to follow a specific generation through life and compare different generations.  

Source: University of Gothenburg [October 31, 2011]

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