Medication does not reduce risk of recurrent cardiac events among patients with diabetes

Use of the drug aleglitazar, which has shown the ability to lower glucose levels and have favorable effects on cholesterol, did not reduce the risk of cardiovascular death, heart attack or stroke among patients with type 2 diabetes and recent heart attack or unstable angina, according to a JAMA study released online to coincide with presentation at the 2014 American College of Cardiology Scientific Sessions.Cardiovascular disease remains the dominant cause of death among patients with type 2 diabetes. No drug therapy specifically directed against diabetes nor strategy for tight glucose control has been shown to unequivocally reduce the rate of cardiovascular complications in this population, according to background information in the article. In phase 2 trials, aleglitazar significantly reduced glycated hemoglobin levels (measure of blood glucose over an extended period of time), triglycerides, and low-density lipoprotein cholesterol and increased high-density lipoprotein cholesterol (HDL-C).A. Michael Lincoff, M.D., of the Cleveland Clinic, and colleagues conducted a phase 3 trial in which 7,226 patients hospitalized for heart attack or unstable angina with type 2 diabetes were randomly assigned to receive aleglitazar or placebo daily. The AleCardio trial was conducted in 720 hospitals in 26 countries throughout North America, Latin America, Europe, and Asia-Pacific regions.The trial was terminated early (July 2013) after an average follow-up of 104 weeks, due to lack of efficacy and a higher rate of adverse events in the aleglitazar group.The researchers found that although aleglitazar reduced glycated hemoglobin and improved serum HDL-C and triglyceride levels, the drug did not decrease the time to cardiovascular death, nonfatal heart attack, or nonfatal stroke (primary end points). These events occurred in 344 patients (9.5 percent) in the aleglitazar group and 360 patients (10.0 percent) in the placebo group.Aleglitazar use was associated with increased risk of kidney abnormalities, bone fractures, gastrointestinal bleeding, and hypoglycemia (low blood sugars).”These findings do not support the use of aleglitazar in this setting with a goal of reducing cardiovascular risk,” the authors conclude.Story Source:The above story is based on materials provided by The JAMA Network Journals. Note: Materials may be edited for content and length.

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Analysis supports use of risk equations to guide statin therapy

In an analysis of almost 11,000 patients, an assessment of equations that help guide whether a patient should begin taking a statin (cholesterol lowering medication) found that observed and predicted 5-year atherosclerotic cardiovascular disease risks were similar, suggesting that these equations are helpful for clinical decision making, according to a JAMA study released online to coincide with presentation at the 2014 American College of Cardiology Scientific Sessions.The American College of Cardiology (ACC) and the American Heart Association (AHA) recently published the 2013 Guideline on the Assessment of Cardiovascular Risk. As part of this guideline, a group of experts developed the Pooled Cohort risk equations, which were designed to estimate 10-year risk for nonfatal myocardial infarction (MI; heart attack), coronary heart disease (CHD) death, and nonfatal or fatal stroke, according to background information in the article.Paul Muntner, Ph.D., of the University of Alabama at Birmingham, and colleagues examined the Pooled Cohort risk equations in adults (age 45 to 79 years) enrolled in the Reasons for Geographic and Racial Differences in Stroke (REGARDS) study between January 2003 and October 2007, and followed up through December 2010. The researchers studied participants for whom atherosclerotic CVD risk may trigger a discussion of statin initiation (patients without clinical atherosclerotic CVD or diabetes, low-density lipoprotein cholesterol level between 70 and 189 mg/dL, and not taking statins; n = 10,997). Additional analyses, limited to Medicare beneficiaries (n = 3,333), added atherosclerotic CVD events identified in Medicare claims data.Among the study population (n=10,997) for whom statin treatment should be considered based on atherosclerotic CVD risk there were 338 events (192 CHD events, 146 strokes). The researchers found that the observed and predicted 5-year atherosclerotic CVD incidence rates were similar.There were 234 atherosclerotic CVD events (120 CHD events, 114 strokes) among the subset of Medicare beneficiaries and the observed and predicted 5-year atherosclerotic CVD incidence rates were also similar for the various risk categories in this population.”These findings support the validity of the Pooled Cohort risk equations to inform clinical management decisions,” the authors write. “Because the Pooled Cohort risk equations were designed to estimate 10-year atherosclerotic cardiovascular disease risk, studies are needed to ensure its accurate calibration over a longer duration.”Story Source:The above story is based on materials provided by The JAMA Network Journals. Note: Materials may be edited for content and length.

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Regular physical activity reduces breast cancer risk irrespective of age

Practising sport for more than an hour day reduces the risk of contracting breast cancer, and this applies to women of any age and any weight, and also unaffected by geographical location, according to research presented to the 9th European Breast Cancer Conference (EBCC-9). Compared with the least active women, those with the highest level of physical activity reduced their risk of breast cancer by 12%, researchers say.Professor Mathieu Boniol, Research Director at the International Prevention Research Institute, Lyon, France, recently reported the results of a meta-analysis of 37 studies published between 1987 and 2013, representing over four million women. “These are all the studies looking at the relationship between physical exercise and breast cancer risk that have been published to date, so we are confident that the results of our analysis are robust,” he said.Although the results varied according to tumour type, the overall message was encouraging, the researchers say. However, in women taking hormone replacement therapy (HRT), the protective effect of exercise seemed to be cancelled out. But increased awareness of the side effects of HRT means that its use is decreasing in a number of countries, and this means that the beneficial effects of activity will most likely grow in the years to come. “Whether or not this will be the case is an interesting question and deserves to be followed up at a later date,” Prof Boniol said.Physical activity is known to have a protective role in other cancers, as well as in disorders such as cardiovascular disease. Although the mechanisms for its effect are unclear, the results are largely independent of body mass index (BMI), so the effect must be due to more than weight control. And the age at which sporting activity starts also appears to be immaterial; the researchers found no indication that breast cancer risk would decrease only when physical activity started at a young age.”Adding breast cancer, including its aggressive types, to the list of diseases that can be prevented by physical activity should encourage the development of cities that foster sport by becoming bike and walk-friendly, the creation of new sports facilities, and the promotion of exercise through education campaigns,” said Prof Boniol. “This is a low cost, simple strategy to reduce the risk of a disease that currently has a very high cost, both to healthcare systems and to patients and their families. It is good news both for individuals and for policy makers.”Dr Hilary Dobson, chair of EBCC-9’s national organising committee and who is Clinical Lead of the West of Scotland Breast Screening Service and the Lead Clinician of the West of Scotland Cancer Advisory Network (WoSCAN), commented: “These findings are important for all women, irrespective of their age and weight. …

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Continuous handling of receipts linked to higher urine BPA levels

Study participants who handled receipts printed on thermal paper continuously for 2 hours without gloves had an increase in urine bisphenol A (BPA) concentrations compared to when they wore gloves, according to a study in the February 26 issue of JAMA.Human exposure to bisphenol A (BPA) has been associated with adverse health outcomes, including reproductive function in adults and neurodevelopment in children exposed shortly before or after birth. “Exposure to BPA is primarily through dietary ingestion, including consumption of canned foods. A less-studied source of exposure is thermal receipt paper, handled daily by many people at supermarkets, ATM machines, gas stations, and other settings,” according to background information in the article. Thermal paper has a coating that is sensitive to heat, which is used in the process of printing on the paper, and has been shown to be transferred to skin with handling.Shelley Ehrlich, M.D., Sc.D., M.P.H., of Cincinnati Children’s Hospital Medical Center, and colleagues conducted a study to examine the effect of handling thermal receipts on urine BPA levels. The authors recruited 24 volunteers who provided urine samples before and after handling (with or without gloves) of receipts printed on thermal paper for a continuous two hours. BPA was detected in 83 percent (n = 20) of urine samples at the beginning of the study and in 100 percent of samples after handling receipts without gloves. The researchers observed an increase in urinary BPA concentrations after continuously handling receipts for 2 hours without gloves, but no significant increase when the participants used gloves.The clinical implications of the height of the peak level and of chronic exposure are unknown, but may be particularly relevant to populations with occupational exposure such as cashiers, who handle receipts 40 or more hours per week, the authors write. “A larger study is needed to confirm our findings and evaluate the clinical implications.”Story Source:The above story is based on materials provided by The JAMA Network Journals. Note: Materials may be edited for content and length.

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Fertilization destabilizes global grassland ecosystems

A new study led by University of Minnesota researchers demonstrates that fertilization of natural grasslands — either intentionally or unintentionally as a side effect of global farming and industry — is having a destabilizing effect on global grassland ecosystems. Using a network of natural grassland research sites around the world called the Nutrient Network, the study represents the first time such a large experiment has been conducted using naturally occurring sites.Led by Yann Hautier, a Marie Curie Fellow associated with both the Department of Ecology, Evolution, and Behavior at the University of Minnesota and the Institute of Evolutionary Biology and Environmental Studies at the University of Zurich, the research team included U of M associate professors Eric Seabloom and Elizabeth Borer, and research scientist Eric Lind, along with scientists from institutions around the world including Andy Hector at Oxford University’s Department of Plant Sciences. The findings were published on February 16 in the journal Nature.The researchers found that plant diversity in natural ecosystems creates more stable ecosystems over time because of less synchronized growth of plants. “This is sometimes called the portfolio effect,” says Seabloom. “If you have money in two investments and they’re both stocks, they’re going to track each other, but if one is a stock and one is a bond, they’re going to respond differently to the overall economy and are more likely to balance each other.”The researchers collected plants from each of the sites, then sorted, dried, and weighed them to monitor the number of species of plants and total amount of plants, or “biomass,” grown over time. They used this information to quantify species diversity and ecosystem stability. Says Hautier: “It was really striking to see the relationship between diversity and stability” and the similarities to data collected from artificial grasslands as part of a research effort called BioDepth, indicating that the results from natural grasslands of the Nutrient Network could be predicted from the results of artificial grasslands.”The results of our study emphasize that we need to consider not just how productive ecosystems are but also how stable they are in the long-term, and how biodiversity is related to both aspects of ecosystem functioning,” says Andy Hector.The researchers also found that grassland diversity and stability are reduced when fertilizer is added. Fertilizers are intentionally used in grassland to increase livestock fodder. Fertilizer addition is also occurring unintentionally in many places around the world because nitrogen, a common fertilizer, is released into the atmosphere from farming, industry, and burning fossil fuels. Rainfall brings nitrogen out of the atmosphere and on to grasslands, changing the growth and types of plant species. …

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Optimizing donor kidney distribution in the United States

Northwestern University’s Sanjay Mehrotra has developed an innovative model that could help ease kidney distribution inequities among regions in the U.S. and ultimately help save hundreds of lives. His mathematical model, which takes into account a number of different factors, simulates and optimizes donor kidney distribution.Mehrotra will discuss his research in a presentation titled “Addressing Allocation Inefficiencies and Geographic Disparities” at the American Association for the Advancement of Science (AAAS) annual meeting in Chicago. His presentation is part of a symposium titled “Transplant Organ Shortage: Informing National Policies Using Management Sciences” to be held from 10 to 11:30 a.m. CST Friday, Feb. 14, in Columbus IJ of the Hyatt Regency Chicago.Mehrotra also will participate in a press briefing to be held at 1 p.m. CST the same day in Vevey Room 3 of the Swisstel Chicago.In addition to Mehrotra, two other Northwestern professors will discuss issues related to organ shortage during both the symposium and press briefing.Michael Abecassis, M.D., chief of the division of organ transplantation and founding director of the Comprehensive Transplant Center at Northwestern University Feinberg School of Medicine, will offer a brief overview of the current issues facing organ allocation.John Friedewald, M.D., associate professor in medicine and surgery at Feinberg and director of clinical research at Northwestern University Feinberg School of Medicine Comprehensive Transplant Center and transplant nephrologist at Northwestern Memorial Hospital, will speak about policy changes in kidney allocation that were developed during his recent term as chair of the United Network for Organ Sharing Kidney Transplantation Committee.Nearly 100,000 people in the United States are waiting for kidney transplants, but only 17,000 kidneys are available annually from both living and deceased donors. There are major regional inequalities in access to organs because of supply and demand disparities among different areas of the country. A person in one state might get a kidney within a year, while someone in another state might wait up to four years. As a consequence, nearly 5,000 people die each year waiting for a kidney transplant.Logistically, organ allocation is a difficult problem. …

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Brain may flush out toxins during sleep; Sleep clears brain of molecules associated with neurodegeneration: Study

Oct. 17, 2013 — A good night’s rest may literally clear the mind. Using mice, researchers showed for the first time that the space between brain cells may increase during sleep, allowing the brain to flush out toxins that build up during waking hours. These results suggest a new role for sleep in health and disease. The study was funded by the National Institute of Neurological Disorders and Stroke (NINDS), part of the NIH.”Sleep changes the cellular structure of the brain. It appears to be a completely different state,” said Maiken Nedergaard, M.D., D.M.Sc., co-director of the Center for Translational Neuromedicine at the University of Rochester Medical Center in New York, and a leader of the study.For centuries, scientists and philosophers have wondered why people sleep and how it affects the brain. Only recently have scientists shown that sleep is important for storing memories. In this study, Dr. Nedergaard and her colleagues unexpectedly found that sleep may be also be the period when the brain cleanses itself of toxic molecules.Their results, published in Science, show that during sleep a plumbing system called the glymphatic system may open, letting fluid flow rapidly through the brain. Dr. …

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Participation in cardiac rehab program improves recovery in stroke patients

Oct. 16, 2013 — Stroke patients who participate in a cardiac rehabilitation program for six months make rapid gains in how far and fast they can walk, the use of weakened limbs and their ability to sit and stand, according to a study presented today at the Canadian Stroke Congress.On average, participants saw a 21-per-cent improvement in the strength and range of motion of weakened limbs; a 19-per-cent improvement in walking speed; and a 16-per-cent improvement in the distance they could walk.”There should be a seamless referral of patients with mild to moderate effects of stroke to the network of established outpatient cardiac rehab programs in Canada,” says lead researcher Dr. Susan Marzolini of Toronto Rehabilitation Institute/University Health Network. “Early referral is also important. In our study, those who started the cardiac rehab program earlier had the strongest results.”Cardiac rehabilitation incorporates exercise training (aerobic and resistance/strength training), nutrition counseling, risk factor counseling and management (lipids, blood pressure, diabetes, weight management, smoking cessation and psychosocial management,) delivered by an interprofessional health care team.All of the 120 patients who participated in the study saw improved recovery.The largest gains in walking function were among those who were referred to the program the earliest. Participants were, on average, two years post-stroke but the study included people who had experienced a stroke from three months to five years previously.In most cases, rehabilitation ends at three months post-stroke, when it has been assumed that spontaneous recovery is over and people reach a plateau, Dr. Marzolini says.For those who entered the six-month cardiac rehab program after standard care, “we didn’t see a plateau, we saw a huge improvement in the group. We’re finding even more benefits from exercise alone than we ever thought.””We have manufactured these three-month plateaus with our biases about how the brain works,” says Dr. Dale Corbett, Scientific Director of the Canadian Partnership for Stroke Recovery (CPSR), a joint initiative of the Heart and Stroke Foundation and Canada’s leading stroke research centres, which funded the study. “Recovery continues for months and years after stroke.”A 2011 audit of stroke services in Canada found that only 37 per cent of stroke patients with moderate to severe impairments receive standard rehabilitation in the weeks after stroke, despite overwhelming evidence of its benefits.”The results of this study are exciting because this exercise program is a very cost-effective intervention for improving the quality of life for those living with the effects of stroke,” says Canadian Stroke Congress Co-Chair Dr. …

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Plant community plays key role in controlling greenhouse gas emissions from carbon rich moorlands

Sep. 18, 2013 — Different moorland plants, particularly heather and cotton grass, can strongly influence climate warming effects on greenhouse gas emissions, researchers from Lancaster University, The University of Manchester and the Centre for Ecology & Hydrology have discovered.The findings, published this week in the journal Ecology Letters, show valuable carbon stores, which lie deep below peaty moorlands, are at risk from changes in climate and from land management techniques that alter plant diversity.But the study found that the make-up of the plant community could also play a key role in controlling greenhouse gas emissions from these carbon rich ecosystems, as not all vegetation types respond in the same way to warming.The research, supported by a Natural Environment Research Council (NERC) grant, took place at Moor House National Nature Reserve, high up in the North Pennines, a long-term, ecological monitoring site for the UK Environmental Change Network.The newly set up experimental site manipulated both temperature and the composition and diversity of vegetation at the same time, allowing the team to study the combined effects of these global change phenomena for the first time.Temperatures were increased by around 1°C using open-topped, passive warming chambers, specially built on site, which mimicked the predicted effects of global warming.The researchers found that when heather was present, warming increased the amount of CO2 taken up from the atmosphere, making the ecosystem a greater sink for this greenhouse gas. However, when cotton grass was present, the CO2 sink strength of system decreased with warming, and the amount of methane released increased.Professor Richard Bardgett, who led the research team, and has recently moved to The University of Manchester, said: “What surprised us was that changes in vegetation, which can result from land management or climate change itself, also had such a strong impact on greenhouse gas emissions and even changed the way that warming affected them.”In other words, the diversity and make-up of the vegetation, which can be altered by the way the land is farmed, can completely change the sink strength of the ecosystem for carbon dioxide. This means that the way we manage peat land vegetation will strongly influence the way that peat land carbon sink strength responds to future climate change.”Dr Sue Ward, the Senior Research Associate for the project at Lancaster Environment Centre, said: “Setting up this experiment allowed us to test how greenhouse gas emissions are affected by a combination of changes in climate and changes in plant communities.”By taking gas samples every month of the year, we were able to show that the types of plants growing in these ecosystems can modify the effects of increase in temperature.”Dr Ward said the study would be of interest and relevance to ecological and climate change scientists and policy makers.”Changes in vegetation as well as physical changes in climate should be taken into account when looking at how global change affects carbon cycling,” she added. “Otherwise a vital part is missing — the biology is a key ingredient.”Professor Nick Ostle, from the Centre for Ecology & Hydrology, a joint partner in the research, said: “This ‘real-world’ study of the response of peat lands to climate change is unique, making these findings even more important.”It seems that the identity of the plants present in these landscapes will exert a strong influence on the effect of climate warming on soil CO2 emissions back to the atmosphere. If this is true then we can expect similar responses in other carbon rich systems in the Arctic and Boreal regions.”

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NASA’s Voyager 1 spacecraft embarks on historic journey into interstellar space

Sep. 12, 2013 — NASA’s Voyager 1 spacecraft officially is the first human-made object to venture into interstellar space. The 36-year-old probe is about 12 billion miles (19 billion kilometers) from our sun.New and unexpected data indicate Voyager 1 has been traveling for about one year through plasma, or ionized gas, present in the space between stars. Voyager is in a transitional region immediately outside the solar bubble, where some effects from our sun are still evident. A report on the analysis of this new data, an effort led by Don Gurnett and the plasma wave science team at the University of Iowa, Iowa City, is published in Thursday’s edition of the journal Science.”Now that we have new, key data, we believe this is mankind’s historic leap into interstellar space,” said Ed Stone, Voyager project scientist based at the California Institute of Technology, Pasadena. “The Voyager team needed time to analyze those observations and make sense of them. But we can now answer the question we’ve all been asking — ‘Are we there yet?’ Yes, we are.”Voyager 1 first detected the increased pressure of interstellar space on the heliosphere, the bubble of charged particles surrounding the sun that reaches far beyond the outer planets, in 2004. Scientists then ramped up their search for evidence of the spacecraft’s interstellar arrival, knowing the data analysis and interpretation could take months or years.Voyager 1 does not have a working plasma sensor, so scientists needed a different way to measure the spacecraft’s plasma environment to make a definitive determination of its location. A coronal mass ejection, or a massive burst of solar wind and magnetic fields, that erupted from the sun in March 2012 provided scientists the data they needed. When this unexpected gift from the sun eventually arrived at Voyager 1’s location 13 months later, in April 2013, the plasma around the spacecraft began to vibrate like a violin string. …

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How chromosome ends influence cellular aging

Sep. 11, 2013 — By studying processes that occur at the ends of chromosomes, a team of Heidelberg researchers has unravelled an important mechanism towards a better understanding of cellular aging. The scientists focused on the length of the chromosome ends, the so-called telomeres, which can be experimentally manipulated. Their research, which was conducted at the Center for Molecular Biology of Heidelberg University (ZMBH), allows for new approaches in the development of therapies for tissue loss and organ failure associated with senescence (cellular aging). The research results may also be significant for cancer treatment. They were recently published in the journal Nature Structural & Molecular Biology.Share This:Each cell contains a set of chromosomes in which the vast majority of our genetic information is stored in the form of DNA. This information must be protected to ensure the proper functioning of the cell. To achieve this, the very ends of the chromosomes, the telomeres, play an important role in protecting the chromosomal DNA from being degraded. “We can imagine that telomeres are analogous to the plastic caps at the ends of our shoelaces. Without them, the ends of the laces get frayed and eventually the entire shoelace does not function properly,” explains Dr. …

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Early-onset Parkinson’s disease linked to genetic deletion

Sep. 9, 2013 — Scientists at the Centre for Addiction and Mental Health (CAMH) and University Health Network (UHN) have found a new link between early-onset Parkinson’s disease and a piece of DNA missing from chromosome 22. The findings help shed new light on the molecular changes that lead to Parkinson’s disease.The study appears online today in JAMA Neurology.Among people aged 35 to 64 who were missing DNA from a specific part of chromosome 22, the research team found a marked increase in the number of cases of Parkinson’s disease, compared to expected rates of Parkinson’s disease in the general population from the same age group.The deletion, which occurs when a person is born with about 50 genes missing on one chromosome 22, is associated with 22q11.2 deletion syndrome. People with this condition may have heart or other birth defects, learning or speech difficulties, and some develop schizophrenia. It occurs in an estimated 1 in 2,000 to 4,000 births, but is believed to be under-diagnosed.”22q11.2 deletion syndrome has been fairly well studied in childhood and adolescence, but less is known about its effects as people age,” said Dr. Anne Bassett, Director of CAMH’s Clinical Genetics Research Program and Director of the Dalglish Family Hearts and Minds Clinic at UHN, the world’s first clinic dedicated to adults with 22q11.2 deletion syndrome. A few cases of patients with the syndrome who had Parkinson’s disease symptoms had been previously reported, which suggested that the two conditions might be linked.Parkinson’s disease is one of the most common neurodegenerative disorders worldwide, typically affecting people over the age of 65. Earlier onset of Parkinson’s disease, before age 50, is rare and has been associated with several other genetic changes that are not on chromosome 22.The researchers studied 159 adults with 22q11.2 deletion syndrome to discover how many had been clinically diagnosed with Parkinson’s disease. For three individuals with the deletion and Parkinson’s disease who were deceased, brain tissue was also examined.”Through a post-mortem examination, we were able to show that all three patients had a loss of neurons that was typical of that seen in Parkinson’s disease. The examination also helped to show that the symptoms of Parkinson’s disease were not related to side effects of the medications commonly used to treat schizophrenia,” added Dr.Rasmus Kiehl, neuropathologist in UHN’s Laboratory Medicine Program, who co-authored the report with CAMH graduate student Nancy Butcher. …

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Newly discovered ‘switch’ plays dual role in memory formation

Aug. 13, 2013 — Researchers at Johns Hopkins have uncovered a protein switch that can either increase or decrease memory-building activity in brain cells, depending on the signals it detects. Its dual role means the protein is key to understanding the complex network of signals that shapes our brain’s circuitry, the researchers say. A description of their discovery appears in the July 31 issue of the Journal of Neuroscience.Share This:”What’s interesting about this protein, AGAP3, is that it is effectively double-sided: One side beefs up synapses in response to brain activity, while the other side helps bring synapse-building back down to the brain’s resting state,” says Rick Huganir, Ph.D., a professor and director of the Solomon H. Snyder Department of Neuroscience at the Johns Hopkins University School of Medicine and co-director of the Brain Science Institute at Johns Hopkins. “The fact that it links these two opposing activities indicates AGAP3 may turn out to be central to controlling the strength of synapses.”Huganir has long studied how connections between brain cells, known as synapses, are strengthened and weakened to form or erase memories. The new discovery came about when he and postdoctoral fellow Yuko Oku, Ph.D., investigated the chain reaction of signals involved in one type of synaptic strengthening.In a study of the proteins that interact with one of the known proteins from that chain reaction, the previously unknown AGAP3 turned up. It contained not only a site designed to bind another protein involved in the chain reaction that leads from brain stimulation to learning, but also a second site involved in bringing synapse-building activity down to normal levels after a burst of activity. Although it might seem the two different functions are behaving at cross-purposes, Oku says, it also could be that nature’s bundling of these functions together in a single protein is an elegant way of enabling learning and memory while preventing dangerous overstimulation. More research is needed, Oku says, to figure out whether AGAP3’s two sites coordinate by affecting each other’s activity, or are effectively free agents.Share this story on Facebook, Twitter, and Google:Other social bookmarking and sharing tools:|Story Source: The above story is based on materials provided by Johns Hopkins Medicine, via EurekAlert!, a service of AAAS. …

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Brain’s flexible hub network helps humans adapt

Aug. 12, 2013 — One thing that sets humans apart from other animals is our ability to intelligently and rapidly adapt to a wide variety of new challenges — using skills learned in much different contexts to inform and guide the handling of any new task at hand.Now, research from Washington University in St. Louis offers new and compelling evidence that a well-connected core brain network based in the lateral prefrontal cortex and the posterior parietal cortex — parts of the brain most changed evolutionarily since our common ancestor with chimpanzees — contains “flexible hubs” that coordinate the brain’s responses to novel cognitive challenges.Acting as a central switching station for cognitive processing, this fronto-parietal brain network funnels incoming task instructions to those brain regions most adept at handling the cognitive task at hand, coordinating the transfer of information among processing brain regions to facilitate the rapid learning of new skills, the study finds.”Flexible hubs are brain regions that coordinate activity throughout the brain to implement tasks — like a large Internet traffic router,” suggests Michael Cole, PhD., a postdoctoral research associate in psychology at Washington University and lead author of the study published July 29 in the journal Nature Neuroscience.”Like an Internet router, flexible hubs shift which networks they communicate with based on instructions for the task at hand and can do so even for tasks never performed before,” he adds.Decades of brain research has built a consensus understanding of the brain as an interconnected network of as many as 300 distinct regional brain structures, each with its own specialized cognitive functions.Binding these processing areas together is a web of about a dozen major networks, each serving as the brain’s means for implementing distinct task functions — i.e. auditory, visual, tactile, memory, attention and motor processes.It was already known that fronto-parietal brain regions form a network that is most active during novel or non-routine tasks, but it was unknown how this network’s activity might help implement tasks.This study proposes and provides strong evidence for a “flexible hub” theory of brain function in which the fronto-parietal network is composed of flexible hubs that help to organize and coordinate processing among the other specialized networks.This study provide strong support for the flexible hub theory in two key areas.First, the study yielded new evidence that when novel tasks are processed flexible hubs within the fronto-parietal network make multiple, rapidly shifting connections with specialized processing areas scattered throughout the brain.Second, by closely analyzing activity patterns as the flexible hubs connect with various brain regions during the processing of specific tasks, researchers determined that these connection patterns include telltale characteristics that can be decoded and used to identify which specific task is being implemented by the brain.These unique patterns of connection — like the distinct strand patterns of a spider web — appear to be the brain’s mechanism for the coding and transfer of specific processing skills, the study suggests.By tracking where and when these unique connection patterns occur in the brain, researchers were able to document flexible hubs’ role in shifting previously learned and practiced problem-solving skills and protocols to novel task performance. Known as compositional coding, the process allows skills learned in one context to be re-packaged and re-used in other applications, thus shortening the learning curve for novel tasks.What’s more, by tracking the testing performance of individual study participants, the team demonstrated that the transfer of these processing skills helped participants speed their mastery of novel tasks, essentially using previously practiced processing tricks to get up to speed much more quickly for similar challenges in a novel setting.”The flexible hub theory suggests this is possible because flexible hubs build up a repertoire of task component connectivity patterns that are highly practiced and can be reused in novel combinations in situations requiring high adaptivity,” Cole explains.”It’s as if a conductor practiced short sound sequences with each section of an orchestra separately, then on the day of the performance began gesturing to some sections to play back what they learned, creating a new song that has never been played or heard before.”By improving our understanding of cognitive processes behind the brain’s handling of novel situations, the flexible hub theory may one day help us improve the way we respond to the challenges of everyday life, such as when learning to use new technology, Cole suggests.”Additionally, there is evidence building that flexible hubs in the fronto-parietal network are compromised for individuals suffering from a variety of mental disorders, reducing the ability to effectively self-regulate and therefore exacerbating symptoms,” he says.Future research may provide the means to enhance flexible hubs in ways that would allow people to increase self-regulation and reduce symptoms in a variety of mental disorders, such as depression, schizophrenia and obsessive-compulsive disorder.

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New clue on the origin of Huntington’s disease

Aug. 12, 2013 — The synapses in the brain act as key communication points between approximately one hundred billion neurons. They form a complex network connecting various centres in the brain through electrical impulses. New research from Lund University suggests that it is precisely here, in the synapses, that Huntington’s disease might begin.Share This:The researchers at Lund University looked into the brains of mice with real-time imaging methods, following some of the very first stages of the disease through advanced microscopes. What they discovered was an unprecedented degradation of synaptic activity. Long before the well documented nerve cell death, synapses that are important for communication between brain centres that control memory and learning begin to wither. This process has never been mapped before and could be an important step towards understanding the serious non-motor symptoms that affect Huntington patients long before the movement disorders start to show.”With the naked eye, we have now been able to follow the step by step events when these synapses start to break down. If we are to halt or reverse this process in the future, it is necessary to understand exactly what happens in the initial phase of the disease. Now we know more,” says Professor Jia-Yi Li, the research group leader.Huntington’s disease has long been characterized by the involuntary writhing movements faced by patients. But in fact, Huntington’s has a very broad and highly individual symptomatology. …

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New study redefines how plaques grow in heart disease

Aug. 11, 2013 — The growth of deadly plaque inside the walls of arteries may not happen as scientists believed, research from the University of Toronto and Massachusetts General Hospital has found.The research also suggests a new potential target in the treatment of atherosclerosis, a leading cause of cardiovascular disease and death globally.The research team found that macrophages, white blood cells that drive atherosclerosis, replicate inside plaques. Moreover, this growth is not reliant on cells outside the plaques called monocytes, as scientists had assumed.”Until now, the thinking was that inflammatory macrophages arise mainly from the recruitment of their precursors — monocytes — from the bloodstream,” said Clint Robbins, lead author on the study and an Assistant Professor in U of T’s Departments of Laboratory Medicine and Pathobiology, and Immunology. “Our study shows that the accumulation of macrophages also depends on their proliferation locally within the developing plaque.”The journal Nature Medicine published the study results today.The impact of the research on clinical treatments could be large. Many pharmaceutical companies are pouring resources into potential therapies that can block the recruitment of white blood cells into plaques. But if macrophages self-sustain through local cell division, blocking recruitment may not be the best strategy.”I think this work will force some major re-evaluations,” said Filip Swirski, the study’s principal investigator who is a scientist in the Center for Systems Biology at Massachusetts General Hospital and an Assistant Professor at Harvard Medical School. “People have been thinking of targeting monocyte influx to treat atherosclerosis, but they need to consider macrophage proliferation as an additional or alternative approach, especially in established disease.”That approach might be better than targeting circulating monocytes, since interrupting disease-causing processes within plaques could spare other beneficial immune responses that monocytes control, said Swirski.As well, it could help improve the current standard of care in treating atherosclerosis: statin therapy. Statins, in addition to lowering blood lipids that contribute to plaque, have anti-inflammatory properties. The researchers are now looking at whether statins might limit the spread of macrophages within plaques.”Additional targeting of macrophage proliferation may further decrease inflammation in atherosclerosis and prove clinically advantageous,” said Robbins, who is also a scientist in the Toronto General Research Institute at University Health Network.The researchers conducted their study in mice, and they caution that much more research is needed to see how the work will translate to humans. But encouragingly, they found evidence of macrophage growth in plaques from human carotid arteries.Next, the team will compare macrophage proliferation to monocyte recruitment during different stages of atherosclerosis, and look at whether all macrophages, or only subsets, replicate.

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Stray prenatal gene network suspected in schizophrenia

Aug. 1, 2013 — Researchers have reverse-engineered the outlines of a disrupted prenatal gene network in schizophrenia, by tracing spontaneous mutations to where and when they likely cause damage in the brain. Some people with the brain disorder may suffer from impaired birth of new neurons, or neurogenesis, in the front of their brain during prenatal development, suggests the study, which was funded by the National Institutes of Health.”Processes critical for the brain’s development can be revealed by the mutations that disrupt them,” explained Mary-Claire King, Ph.D., University of Washington (UW), Seattle, a grantee of the NIH’s National Institute of Mental Health (NIMH). “Mutations can lead to loss of integrity of a whole pathway, not just of a single gene. Our results implicate networked genes underlying a pathway responsible for orchestrating neurogenesis in the prefrontal cortex in schizophrenia.”King, and collaborators at UW and seven other research centers participating in the NIMH genetics repository, report on their discovery August 1, 2013 in the journal Cell.”By linking genomic findings to functional measures, this approach gives us additional insight into how early development differs in the brain of someone who will eventually manifest the symptoms of psychosis,” said NIMH Director Thomas R. Insel, M.D.Earlier studies had linked spontaneous mutations to non-familial schizophrenia and traced them broadly to genes involved in brain development, but little was known about convergent effects on pathways. King and colleagues set out to explore causes of schizophrenia by integrating genomic data with newly available online transcriptome resources that show where in the brain and when in development genes turn on. They compared spontaneous mutations in 105 people with schizophrenia with those in 84 unaffected siblings, in families without previous histories of the illness.Unlike most other genes, expression levels of many of the 50 mutation-containing genes that form the suspected network were highest early in fetal development, tapered off by childhood, but conspicuously increased again in early adulthood — just when schizophrenia symptoms typically first develop. This adds to evidence supporting the prevailing neurodevelopmental model of schizophrenia. The implicated genes play important roles in migration of cells in the developing brain, communication between brain cells, regulation of gene expression, and related intracellular workings.Having an older father increased the likelihood of spontaneous mutations for both affected and unaffected siblings. …

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Glucose intolerance, diabetes or insulin resistance not linked with pathological features of Alzheimer’s disease

July 29, 2013 — Glucose intolerance or insulin resistance do not appear to be associated with pathological features of Alzheimer disease (AD) or detection of the accumulation of the brain protein β-amyloid (Αβ), according to a report published by JAMA Neurology, a JAMA Network publication.Glucose intolerance and diabetes mellitus have been proposed as risk factors for the development of AD, but evidence of this has not been consistent, the study background notes.Madhav Thambisetty, M.D., Ph.D., of the National Institute on Aging, Baltimore, and colleagues investigated the association between glucose intolerance and insulin resistance and brain Αβ burden with autopsies and imaging with carbon 11-labeled Pittsburgh Compound B positron emission tomography.”The relationship among diabetes mellitus, insulin and AD is an important area of investigation. However, whether cognitive impairment seen in those with diabetes is mediated by excess pathological features of AD or other related abnormalities, such as vascular disease, remains unclear,” the authors comment.Two groups of participants were involved in the study. One group consisted of 197 participants enrolled in the Baltimore Longitudinal Study of Aging who had two or more oral glucose tolerance tests (OGTT) while they were alive and then underwent a brain autopsy when they died. The second group included 53 living study participants who had two or more OGTTs and underwent imaging.”In this prospective cohort with multiple assessments of glucose intolerance and insulin resistance, measures of glucose and insulin homeostasis are not associated with AD pathology and likely play little role in AD pathogenesis,” the study concludes. “Long-term therapeutic trials are important to elucidate this issue.”

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