STEROID ORIGINALLY DISCOVERED IN THE DOGFISH SHARK ATTACKS PARKINSON’S-RELATED TOXIN IN ANIMAL MODEL
Newswise — WASHINGTON — A synthesized steroid mirroring one naturally made by the dogfish shark prevents the buildup of a lethal protein implicated in some neurodegenerative diseases, reports an international research team studying an animal model of Parkinson’s disease. The clustering of this protein, alpha-synuclein (α-synuclein), is the hallmark of Parkinson’s and dementia with Lewy bodies, suggesting a new potential compound for therapeutic research. The finding, published online in Proceedings of the National Academy of Sciences, also demonstrated that the synthesized steroid, called squalamine, reduced the toxicity of α-synuclein clumps that already existed. The pre-clinical study results show that squalamine prevents and eliminates α-synuclein build up inside neurons by unsticking the protein from the inner wall of nerve cells, where it clings and builds up into toxic clumps, researchers say. The animal model used for this study, C. elegans, is a nematode worm genetically engineered to produce human α-synuclein in its muscles. As these worms age, α-synuclein builds up within their muscle cells causing cell damage and paralysis. “We could literally see that squalamine, given orally to the worms, did not allow α-synuclein to cluster, and prevented muscular paralysis inside the worms,” says the study’s co-senior author, Michael Zasloff, MD, PhD, professor of surgery and pediatrics at Georgetown University School of Medicine and scientific director of the MedStar Georgetown Transplant Institute.The study’s lead author, graduate student Michele Perni, and other co-senior authors, Michele Vendruscolo, PhD and Christopher M. Dobson, DPhil, ScD, are from Cambridge University. An additional co-senior author, Adriaan Bax, PhD, is from National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK), part of the National Institutes of Health (NIH) in Bethesda, Maryland. Scientists from the Netherlands, Italy and Spain also contributed to this research. Zasloff, an expert in innate immune systems, has been studying squalamine for more than 20 years. He discovered it in dogfish sharks in 1993 and synthesized it in 1995 (in a process that does not involve use of any natural shark tissue). His research, as well as that by other scientists, has established antiviral and anticancer properties of the compound. This is the first study to show it has neurological benefits in in vivo models of Parkinson’s. In Parkinson’s disease, α-synuclein, a normal protein present within the nervous system, forms toxic clumps that damage and ultimately destroy the neurons in which they form. Considerable research has been directed at discovering compounds that prevent the formation of these masses, thereby representing potential therapeutics for Parkinson’s disease. In this study, the researchers demonstrated in a series of in vitro experiments that squalamine, a positively charged molecule with a high affinity for negatively charged membranes, could literally “kick off” α-synuclein from negatively charged membranes, where the protein binds, preventing the formation of the toxic clumps. The research team also showed that squalamine could protect healthy human neuronal cells from being damaged by exposure to pre-formed toxic masses of α-synuclein, by preventing them from adhering to the outer membrane of the neuronal cells. The researchers then extended these studies to a living system, C. elegans, a well-studied model of Parkinson’s disease. “Orally administered squalamine prevented the formation of toxic α-synuclein clumps in this complex animal, and rescued the animal from loss of mobility,” Zasloff explains. “This experiment taught us that the basic mechanism demonstrated in vitro achieved the anticipated outcome in an animal.” The study's co-senior author, Professor Christopher Dobson, DPhil, Master of St John's College, University of Cambridge says, "Squalamine gives us a first generation compound, which we believe that we can incrementally improve through further studies of the underlying mechanism by which it affects the aggregation of alpha-synuclein." Zasloff says a clinical trial with squalamine in Parkinson’s disease is being planned. “Squalamine could be especially suited to work in the gut with the goal of treating the gastrointestinal symptoms of Parkinson’s,” he adds. Zasloff is the inventor on a patent application that has been filed related to the technology described in this paper. The other authors report having no personal financial interests related to the study. Additional authors include Celine Galvagnion, Georg Meisl, Martin B. D. Müller, Pavan K. Challa, Patrick Flagmeier, Samuel I. A. Cohen, Pietro Sormanni, Gabriella T. Heller, Francesco A. Aprile, Tuomas P. J. Knowles, Michele Vendruscolo, Serene W. Chen, Ryan Limbocker and Julius Kirkegaard from the University of Cambridge, England; Alexander S. Maltsev, from NIDDK; Ellen A. Nollen, from the European Research Institute for the Biology of Aging, Groningen, The Netherlands; Roberta Cascella, Cristina Cecchi, and Fabrizio Chiti, from the University of Florence; and Nunilo Cremades, from the University of Zaragoza, Spain. The study was funded by the NIH Intramural Research Program, the Boehringer Ingelheim Fonds, the European Research Council (ERC), and the Centre for Misfolding Diseases at Cambridge. About Georgetown University Medical CenterGeorgetown University Medical Center (GUMC) is an internationally recognized academic medical center with a three-part mission of research, teaching and patient care (through MedStar Health). GUMC’s mission is carried out with a strong emphasis on public service and a dedication to the Catholic, Jesuit principle of cura personalis -- or "care of the whole person." The Medical Center includes the School of Medicine and the School of Nursing & Health Studies, both nationally ranked; Georgetown Lombardi Comprehensive Cancer Center, designated as a comprehensive cancer center by the National Cancer Institute; and the Biomedical Graduate Research Organization, which accounts for the majority of externally funded research at GUMC including a Clinical and Translational Science Award from the National Institutes of Health. Connect with GUMC on Facebook (Facebook.com/GUMCUpdate), Twitter (@gumedcenter) and Instagram (@gumedcenter).
Newswise — Many infectious diseases are one and done; people get sick once and then they are protected from another bout of the same illness. For some of these infections – chickenpox, for example – a small number of microbes persist in the body long after the symptoms have gone away. Often, such microbes can reactivate when the person’s immunity has waned with age or illness, and cause disease again. Now, researchers at Washington University School of Medicine in St. Louis studying leishmaniasis, a tropical disease that kills tens of thousands of people every year, believe they have found an explanation for the seemingly paradoxical connection between long-term infection and long-term immunity. By constantly reminding the immune system what the parasite that causes leishmaniasis looks like, a persistent infection keeps the immune system on alert against new encounters, even while it carries the risk of causing disease later in life, the researchers found. Understanding how persistent infection leads to long-term immunity could help researchers design vaccines and treatments for persistent pathogens. The research is published the week of Jan. 16 in Proceedings of the National Academy of Sciences. “People had been thinking of the role of the immune system in persistent infection in terms of mowing down any pathogens that reactivate in order to protect the body from disease,” said Stephen Beverley, PhD, the Marvin A. Brennecke Professor of Molecular Microbiology and the study’s senior author. “What was often overlooked was that in the process of doing this, the immune system is constantly being stimulated, which potentially promotes protection against future illness.” In a persistent infection, a small population of microbes remains in the body long after the patient’s symptoms are gone. In addition to the parasite that causes leishmaniasis, many kinds of microbes can cause persistent infections, including bacteria responsible for tuberculosis and viruses that lead to herpes and chickenpox. “A lot of pathogens cause persistent infections, but the process was something of a black box,” said Michael Mandell, PhD, the first author on the study. Mandell, who conducted the research for the study as a graduate student, is now an assistant professor at the University of New Mexico. “Nobody really knew what was going on during persistent infection and why it was associated with immunity.” To find out, Mandell and Beverley studied Leishmania, a group of parasites that cause ulcers on the skin and can infect internal organs. An estimated 250 million people worldwide are infected with the parasite – found in tropical areas – and 12 million have active disease. The disease can be disfiguring or even fatal, but once a person is infected, he or she is protected from getting sick a second time. In other words, infection confers long-term immunity. People are thought to continue to harbor the parasite at low numbers for years after they recover from the disease, including some people treated with anti-leishmania drugs. This persistence may be to the benefit of their human hosts; studies in mice have shown that completely clearing the parasite often makes the animals susceptible to another bout of disease if they encounter the parasite again. Studying mice, the researchers used fluorescent markers to distinguish different types of mouse cells, and found that most of the parasites live in immune cells capable of killing the parasites. Yet, despite their dangerous homes, the parasites appeared normal in shape and size. Further, most of the parasites continued to multiply, yet the total number of parasites stayed the same over time. “Mike Mandell called it the ‘Jimmy Hoffa effect’ because we couldn’t locate the body,” Beverley said. “We were unable to show directly that the parasites were being killed. But some of them must have been dying because the numbers weren’t going up.” The immune cells that housed the parasites are responsible for killing pathogens and activating a more robust immune response. It is this process – the ongoing multiplication and killing of parasites – that the researchers believe underlies the long-term immunity associated with persistent infection, and thus explains why people typically can’t get sick with the same pathogen twice. “It seems that our immunologic memory needs reminding sometimes,” Mandell said. “As the persistent parasites replicate and get killed, they are continually stimulating the immune system, keeping it primed and ready for any new encounters with the parasite.” These findings suggest that there are benefits as well as dangers to persistent infection, and, for some organisms at least, developing a vaccine that elicits life-long immunity might require a live vaccine that has the ability to persist without sickening people. “Usually scientists design vaccines to get sterilizing immunity. They’re trying to just kill all the bugs,” Beverley said. “But what you really need is protection against the pathologic consequences of the disease, not necessarily sterilizing immunity. For some of these organisms, solid, long-term protection may come at the price of persistent infection.”
Newswise — An international collaboration led by clinical researchers at the Wellcome Trust Sanger Institute has shown proof-of-concept that truly personalised therapy will be possible in the future for people with cancer. Details of how a knowledge bank could be used to find the best treatment option for people with acute myeloid leukaemia (AML) are published today in Nature Genetics. AML is an aggressive blood cancer that develops in bone marrow cells. Earlier this year, the team reported there are 11 types of AML, each with distinct genetic features. Now they report how a patient's individual genetic details can be incorporated into predicting the outcome and treatment choice for that patient. They built a knowledge bank using data from 1,540 patients with AML who participated in clinical trials in Germany and Austria, combining information on genetic features, treatment schedule and outcome for each person. From this, the team developed a tool that shows how the experience captured in the knowledge bank could be used to provide personalised information about the best treatment options for a new patient. There are two major treatment options for young patients with AML - a stem cell transplant or chemotherapy. Stem cell transplants cure more patients overall but up to one in four people die from complications of the transplant and a further one in four experience long-term side effects. Weighing up the benefits of better cure rates with transplant against the risks of worse early mortality is a harrowing decision for patients and their clinicians. The team showed that these benefits and risks could be accurately calculated for an individual patient, enabling therapeutic choices to become personalised. The team estimates that up to one in three patients would be prescribed a different treatment regimen using the tool compared with current practice. In the long term they hope the tool could spare one in ten young AML patients from a transplant while maintaining overall survival rates. Senior author Dr Peter Campbell of the Wellcome Trust Sanger Institute said: "The knowledge bank approach makes far more detailed and accurate predictions about the likely future course of a patient with AML than what we can make in the clinic at the moment. Current guides use a simple set of rules based on only a few genetic findings. For any given patient, using the new tool we can compare the likely future outcomes under a transplant route versus a standard chemotherapy route - this means that we can make a treatment choice that is personally tailored to the unique features of that particular patient." The tool is currently available for scientists to use in research but needs further testing before it can be used to prescribe treatments in AML clinics. Lead author Dr Moritz Gerstung of the European Bioinformatics Institute said: "It has long been recognised that cancer is a complex genetic disease. Our study provides an example of how detailed genetic and clinical information can be rationally incorporated into clinical decisions for individual patients. We tested this philosophy in one type of leukaemia, but the concept could theoretically be applied in other cancers with difficult clinical decisions as well. Our analysis reveals that knowledge banks of up to 10,000 patients would be needed to obtain the precision needed for routine clinical application." Using large scale genetic studies as a source to predict the best treatment option for future patients is an idea that Genomics England is trying to build alongside similar programmes around the world, such as the National Institutes of Health Precision Medicine Initiative in the US. The authors believe this paper is a step towards validation of genetic techniques as a route to personalised medicine. Co-senior author Dr Hartmut Döhner of University of Ulm said: "Building knowledge banks is not easy. To get accurate treatment predictions you need data from thousands of patients and all tumour types. Furthermore, such knowledge banks will need continuous updating as new therapies become approved and available. As genetic testing enters routine clinical practice, there is an opportunity to learn from patients undergoing care in our health systems. Our paper gives the first real evidence that the approach is worthwhile, how it could be used and what the scale needs to be." ###
Newswise — New Brunswick, N.J. - Cervical cancer is almost always caused by the high-risk types of the human papillomavirus (HPV), which nearly every sexually active person will be exposed to in their lifetime. People with healthy immune systems are able to clear the virus, but when the high risk strains “hijack” or infect specific cells of the cervix it can lead to abnormal cell growth and precancerous changes. Over time and with persistent infection, this leads to cervical cancer. HPV infection can also lead to penile, anal and throat and mouth cancers. Unfortunately, according to the Centers for Disease Control and Prevention (CDC), incidence rates of HPV-associated cancers have continued to rise, with approximately 39,000 new HPV-associated cancers diagnosed each year in the United States. People who smoke or have lowered immune systems also have increased risk of developing HPV-related cancers. How is it prevented? HPV infection and therefore cervical cancer can be prevented by vaccination. There are now two FDA vaccines approved for males and females between ages nine and 26, and according to the latest recommendations from the CDC, all children between nine and 13 should complete the vaccine series. Children younger than 15 should receive two doses of the vaccine six months apart and those over age 15 should complete a three-dose series. Rutgers Cancer Institute of New Jersey is joining with the nation’s 68 other National Cancer Institute-designated cancer centers in supporting these newly revised recommendations. Keep in mind, for a woman, vaccination does NOT mean she should refrain from receiving a routine gynecological screening known as a Pap smear since the vaccine does not 100 percent guarantee against the development of cervical cancer. How is it detected? Pap smears detect precancerous changes that occur in cells and also can now test for HPV infection. The American Congress of Obstetricians and Gynecologists recommends that women begin annual screening for cervical cancer at age 21. A woman should consult with her doctor about the frequency of screening, as it depends on age, results from prior testing, and other health factors.Symptoms are also important for detection. These can include abnormal vaginal bleeding, discharge, bleeding after intercourse, or back pain. A woman should seek care if she develops any of these warning signs as well as maintain routine and appropriate screenings with her gynecologist. How is it treated? Precancerous changes of the cervix are treated with simple procedures. Treatment can prevent precancerous changes from becoming cervical cancer. Early stage cervical cancer is curable with surgery. Remember, by quitting smoking, vaccinating against HPV, undergoing regular Pap smears and protecting yourself against sexually-transmitted diseases, you can help reduce your risk to developing cervical cancer. Ruth Stephenson, DO, is a gynecologic oncologist at Rutgers Cancer Institute of New Jersey.
Newswise — Alcohol use disorders (AUDs) develop with time and in stages. Following the initiation of drinking, some people progress to problem drinking, and then develop a “cluster” of specific problems to comprise an AUD. However, not all stages of AUD development have been studied equally. This report examines high-risk families to understand underlying influences across multiple stages of AUD development. Researchers scrutinized four transitions in AUD development using data on adolescents and young adults from high-risk families: time to first drink, first drink to first problem, first drink to first diagnosis, and first problem to first diagnosis. Potential influences included parental AUD, parental separation, peer substance use, ever use of marijuana by offspring, trauma exposures, and different psychopathologies across transitions. Results showed that significant influences across all transitions were fairly consistent, with externalizing psychopathologies and ever use of marijuana increasing the likelihood of transition at each stage. Peer and parental influences – especially maternal AUD – were linked to initiation and some later stages. Given increasingly permissive attitudes toward marijuana use in the United States, the authors suggest that more research be directed toward understanding the association of AUD development with marijuana use. SEE ORIGINAL STUDY
Newswise — For the millions of older adults who suffer from osteoarthritis in their lower extremities (hip, knee, ankle or foot), chair yoga is proving to be an effective way to reduce pain and improve quality of life while avoiding pharmacologic treatment or adverse events. A new study, conducted by researchers at Florida Atlantic University and published in the current issue of the Journal of the American Geriatrics Society, is the first randomized controlled trial to examine the effects of chair yoga on pain and physical function in older adults with osteoarthritis. For the study, researchers randomly assigned 131 older adults with osteoarthritis to either the “Sit ‘N’ Fit Chair Yoga©” program developed by Kristine Lee or a health education program. Participants attended 45-minute sessions twice a week for 8 weeks. Researchers measured pain, pain interference (how it affects one’s life), balance, gait speed, fatigue and functional ability, before, during and after the sessions. Results from the study found that participants in the chair yoga group, compared to those in the health education program, showed a greater reduction in pain and pain interference during their sessions, and that reduction in pain interference lasted for about three months after the 8-week chair yoga program was completed. The 8-week chair yoga program also was associated with reductions in fatigue and improvement in gait speed during the study session, but not post session. “With osteoarthritis-associated pain, there is interference in everyday living, limiting functional and social activities as well as diminishing life enjoyment,” said Juyoung Park, Ph.D., co-author and co-principal investigator of the study, Hartford Geriatric Social Work Faculty Scholar and an associate professor in FAU’s College for Design and Social Inquiry. “The effect of pain on everyday living is most directly captured by pain interference, and our findings demonstrate that chair yoga reduced pain interference in everyday activities.” Regular exercise has proven to help relieve osteoarthritis pain, however, the ability to participate in exercise declines with age, and many dropout before they can even receive benefits. Although the Arthritis Foundation recommends yoga to reduce joint pain, improve flexibility and balance, and reduce stress and tension, many older adults cannot participate in standing exercises because of lack of muscle strength, pain and balance as well as the fear of falling due to impaired balance. Chair yoga is practiced sitting in a chair or standing while holding the chair for support, and is well suited to older adults who cannot participate in standing yoga or exercise. “Currently, the only treatment for osteoarthritis, which has no cure, includes lifestyle changes and pharmacologic treatments that are not without adverse events,” said Ruth McCaffrey, D.N.P., A.R.N.P., co-author and emeritus professor in FAU’s College of Nursing. “The long-term goal of this research is to address the non-pharmacologic management of lower extremity osteoarthritis pain and physical function in older adults, and our study provides evidence that chair yoga may be an effective approach for achieving this goal.” The overall goal of this interdisciplinary program is to decrease pain, and improve physical and psychosocial functions of elderly individuals with osteoarthritis who are unable to participate in other exercise and yoga programs. Park and McCaffrey conducted the study with Patricia Liehr, Ph.D., R.N., co-principal investigator, co-author and a professor in FAU’s College of Nursing; David Newman, Ph.D., co-author and an assistant professor in FAU’s College of Nursing; and Joseph G. Ouslander, M.D., co-author, senior associate dean of geriatric programs and chair and professor of the Department of Integrated Medical Science in FAU’s Charles E. Schmidt College of Medicine. “The potential impact of this study on public health is high, as this program provides an approach for keeping community-dwelling elders active even when they cannot participate in traditional exercise that challenges their balance,” said Liehr. Osteoarthritis is the most common form of arthritis in older adults. Consequences associated with osteoarthritis include pain, joint stiffness and functional limitation of activities of daily living. Osteoarthritis is the leading cause of long-term disability among older adults and affects more than 33 percent of people over the age of 65 in the U.S. Annually, osteoarthritis accounts for more than 11 million physician and outpatient visits, 662,000 hospitalizations and an estimated $81 billion in costs for medical and surgical treatments. The World Health Organization estimates that osteoarthritis affects about 10 percent of men and 18 percent of women worldwide. This project is supported by the National Institutes of Health (NIH)/National Center for Complementary and Integrative Health (NCCIH) through grant number 1R15AT007352-01A1.
CAN A WEIGHT LOSS PROGRAM RESULT IN PHYSICAL ACTIVITY IMPROVEMENTS AMONG OLDER ADULTS WITH TYPE 2 DIABETES?
Newswise — Individuals with obesity and type 2 diabetes have lower physical activity (PA) levels than the general population. Given the known health benefits of PA, it is important that lifestyle treatment programs for this population produce significant long-term improvements in PA. This study used a waist-worn tracking device to assess PA levels among 2400 older adults with type 2 diabetes over four years. Participants who were randomly assigned to the lifestyle treatment group were over two times as likely to achieve the study PA goal of at least 175 minutes/week. In addition, they were 1.5 times more likely to maintain this level of PA after four years, compared to those assigned to a basic diabetes education group. Yet, not all participants met the PA goal and some performed very little PA after four years. So, lifestyle programs may need to better address barriers to maintaining PA so that this behavior becomes a life-long habit. For more information about this research, view the abstract or contact the investigators.
Newswise — CHICAGO - Northwestern Medicine scientists have discovered the genetic driver of a rare and lethal childhood leukemia and identified a targeted molecular therapy that halts the proliferation of leukemic cells. The finding also has implications for treating other types of cancer. Mixed lineage leukemia (MLL) primarily strikes newborns and infants. Less than 10 to 20 percent of those children (300 cases are seen in the United States per year) live no more than five years after being diagnosed. “We’ve spent the last 20 years in my laboratory trying to molecularly understand how MLL translocations cause this rare and devastating form of leukemia in children so that we can use this information to develop an effective therapy for this cancer,” said lead investigator Ali Shilatifard. “Now we’ve made a fundamentally important breakthrough.” The paper was published Jan. 5 in the journal Cell. Shilatifard, the chair and professor of biochemistry and molecular genetics and professor of pediatrics, his graduate student Kevin Liang and their colleagues at Northwestern University Feinberg School of Medicine are extremely hopeful about this breakthrough and are in the process of pushing their findings into clinic for the treatment of childhood leukemia. Shilatifard also is a member of the Robert H. Lurie Comprehensive Cancer Center of Northwestern University. “Mixed lineage leukemia is caused when an errant chromosome 11 on the MLL gene breaks and attaches to other chromosomes such as chromosome 19, where it doesn’t belong,” said Liang, the paper’s first author. “The mutation produces a protein that drives the pathogenesis of leukemia.” Most research related to this cancer has focused on the errant version of chromosome 11. But there are two copies of chromosome 11, and the Shilatifard group wanted to investigate the wild-type version. Shilatifard’s laboratory discovered that individual cells with the pediatric leukemia had extremely low levels of a protein produced by the wild-type MLL gene. Shilatifard and Liang reasoned if they could beef up the levels of the wild-type MLL protein, it would displace the mutated version that drives cancer, and it could cure leukemia. Through their detailed molecular and biochemical screens, Shilatifard’s lab identified a compound that stabilized the wild-type MLL and interfered with the mutant protein driving leukemia. To test its effectiveness, in collaboration with John Crispino’s lab of Northwestern University and his fellow Andrew Volk, they grew mixed lineage leukemia cells in a culture and transplanted them into mice. They then injected the therapeutic compound into the mice. The result: the wild-type MLL bounced back to healthy levels, and the leukemic cells were not able to grow as rapidly. Northwestern scientists are now synthesizing better compounds and hope to eventually launch a Phase I trial to test these compounds in Chicago. Other Northwestern authors in the manuscript include Stacy A. Marshall, Ashley R. Woodfin, Elizabeth T. Bartom and Edwin R. Smith. The study was also done in collaboration with colleagues at Stowers Institute, where Shilatifard’s laboratory used to be prior to his joining Northwestern Medicine in 2014. Shilatifard’s laboratory is supported by the Outstanding Investigator Award from the National Cancer Institute grant R35CA197569 of the National Institutes of Health.
Newswise — Montreal, – New research findings show that bilingual people are great at saving brain power, that is. To do a task, the brain recruits different networks, or the highways on which different types of information flow, depending on the task to be done. The team of Ana Inés Ansaldo, PhD, a researcher at the Centre de recherche de l’Institut universitaire de gériatrie de Montréal and a professor at Université de Montréal, compared what are known as functional brain connections between seniors who are monolingual and seniors who are bilingual. Her team established that years of bilingualism change how the brain carries out tasks that require concentrating on one piece of information without becoming distracted by other information. This makes the brain more efficient and economical with its resources. To arrive at this finding, Dr. Ansaldo’s team asked two groups of seniors (one of monolinguals and one of bilinguals) to perform a task that involved focusing on visual information while ignoring spatial information. The researchers compared the networks between different brain areas as people did the task. They found that monolinguals recruited a larger circuit with multiple connections, whereas bilinguals recruited a smaller circuit that was more appropriate for the required information. These findings were published in the Journal of Neurolinguistics. Two different ways of doing the same taskThe participants did a task that required them to focus on visual information (the colour of an object) while ignoring spatial information (the position of the object). The research team observed that the monolingual brain allocates a number of regions linked to visual and motor function and interference control, which are located in the frontal lobes. This means that the monolingual brain needs to recruit multiple brain regions to do the task. “After years of daily practice managing interference between two languages, bilinguals become experts at selecting relevant information and ignoring information that can distract from a task. In this case, bilinguals showed higher connectivity between visual processing areas located at the back of the brain. This area is specialized in detecting the visual characteristics of objects and therefore is specialized in the task used in this study. These data indicate that the bilingual brain is more efficient and economical, as it recruits fewer regions and only specialized regions,” explained Dr. Ansaldo. Bilinguals have a double advantage as they ageBilinguals therefore have two cognitive benefits. First, having more centralized and specialized functional connections saves resources compared to the multiple and more diverse brain areas allocated by monolinguals to accomplish the same task. Second, bilinguals achieve the same result by not using the brain’s frontal regions, which are vulnerable to aging. This may explain why the brains of bilinguals are better equipped at staving off the signs of cognitive aging or dementia. “We have observed that bilingualism has a concrete impact on brain function and that this may have a positive impact on cognitive aging. We now need to study how this function translates to daily life, for example, when concentrating on one source of information instead of another, which is something we have to do every day. And we have yet to discover all the benefits of bilingualism,” concluded Dr. Ansaldo. ReferenceBerroir P., Ghazi-Saidi L., Dash T., Adrover-Roig D., Benali H., Ansaldo AI. “Interference control at the response level: Functional networks reveal higher efficiency in the bilingual brain”, Journal of Neurolinguistics (2016), http://dx.doi.org/10.1016/j.jneuroling.2016.09.007. Status: In Press. About the author Ana Inés Ansaldo, PhD, is a researcher at the Research Centre of the Institut universitaire de gériatrie de Montréal (IUGM) and a professor at the School of Speech Therapy and Audiology at Université de Montréal. About the Institut universitaire de gériatrie de Montréal (IUGM)The IUGM has 446 short-term and long-term beds and an ambulatory centre. It has what is considered to be the largest francophone research centre in the field of aging. A member of Université de Montréal's larger excellence in health network, the IUGM opens its doors every year to hundreds of students, trainees and researchers. Since April 1, 2015, the IUGM has been part of the CIUSSS du Centre-Sud-de-l’Île-de-Montréal. SEE ORIGINAL STUDY
Newswise — Patients who take medication for depression report more side effects if they also suffer from panic disorder, according to a new study led by researchers from the University of Illinois at Chicago published in the Journal of Clinical Psychiatry. The researchers looked at data from 808 patients with chronic depression who were given antidepressants as part of the Research Evaluating the Value of Augmenting Medication with Psychotherapy (REVAMP) trial. Of those patients, 85 also had diagnoses of panic disorder. Among all participants, 88 percent reported at least one side effect during the 12 week trial, which ran from 2002 through 2006. Every two weeks, antidepressant side effects were assessed, and categorized as gastrointestinal, cardiovascular, dermatological, neurological, genitourinary, sleep, or sexual functioning. The researchers found that patients with depression and panic disorder were more likely than those with only depression to self-report gastrointestinal (47 percent vs. 32 percent), cardiovascular (26 percent vs. 14 percent), neurological (59 percent vs. 33 percent), and genital/urinary side effects (24 percent vs. 8 percent). Co-occurring panic disorder was not associated with eye or ear issues or dermatological, sleep or sexual functioning side effects compared to participants without panic disorder. “People with panic disorder are especially sensitive to changes in their bodies,” said Stewart Shankman, professor of psychology and psychiatry at UIC and corresponding author on the paper. “It’s called ‘interoceptive awareness.’“Because these patients experience panic attacks — which are sudden, out-of-nowhere symptoms that include heart racing, shortness of breath, and feeling like you’re going to die — they are acutely attuned to changes in their bodies that may signal another panic attack coming on. So it does make sense that these tuned-in patients report more physiological side effects with antidepressant treatment.” Response to antidepressants varies greatly, and side effects are common. Many patients who experience side effects switch medication or change dosage. Some discontinue therapy altogether. Participants with co-occurring panic disorder were also more likely to report a worsening of their depressive symptoms over the 12 weeks if they reported multiple side effects. “In patients with panic disorder, the more side effects they reported, the more depressed they got,” said Shankman. “Whether the side effects are real or not doesn’t matter, but what was real was that their depression worsened as a function of their side effects.” Shankman cautions that physicians and therapists should be aware that their patients with panic disorder may report more side effects, and they should “do a thorough assessment of these side effects to try to tease out what might be the result of hypersensitivity, or what might be a side effect worth switching doses or medications for.” Co-authors on the paper are Stephanie Gorka, and Andrea Katz of UIC; Daniel Klein of Stony Brook University; Dr. John Markowitz of Columbia University College of Physicians and Surgeons; Bruce Arnow, Rachel Manber and Alan Schatzberg of the Stanford University School of Medicine; Barbara Rothbaum of Emory University School of Medicine; Dr. Michael Thase of the University of Pennsylvania School of Medicine; Dr. Martin Keller of Brown University School of Medicine; Dr. Madhukar Trivedi of University of Texas Southwestern Medical Center; and Dr. James Kocsis of Weill-Cornell Medical College. This research was supported by grants U01 MH62475, U01 MH61587, U01 MH62546, U01 MH61562, U01 MH63481, U01 MH62465, U01 MH61590, U01 MH61504 and U01 MH62491 from the National Institute of Mental Health.