RI Hospital: Cognitive behavioral therapy benefits patients with body dysmorphic disorder

Patients reported considerable improvements in symptoms and disability PROVIDENCE, R.I. – In a recent study, researchers at Rhode Island Hospital found significant benefits of cognitive behavioral therapy as a treatment modality for patients with Body Dysmorphic Disorder (BDD). BDD is a common, often severe, and under-recognized body image disorder that affects an estimated 1.7 percent to 2.4 percent of the population. This study demonstrated significant improvement in patients' BDD symptoms and level of disability, as well as high levels of patient satisfaction with the treatment. The study is published online in advance of print in the journal Behavior Therapy. Researchers first developed the manualized treatment and then studied 36 adults with BDD who were randomly selected to either receive 22 cognitive behavioral therapy (CBT) sessions over 24 weeks, or placed on a 12-week wait list. Assessments were conducted pre-treatment, monthly, post-treatment and at three- and six-month follow-up appointments. Post-treatment, patients reported high satisfaction with the treatment, and BDD symptoms such as depression; insight regarding inaccurate beliefs about appearance; and disability in work, social life/leisure, and family life/home responsibilities significantly improved. "BDD is a common and often debilitating disorder, and there are very few proven effective treatments," said Katharine Phillips, M.D., director of the Body Dysmorphic Disorder program at Rhode Island Hospital, "This study suggests that using cognitive behavioral therapy that specifically targets BDD symptoms can result in significant improvements in symptoms and ability to function in daily life. We are currently conducting a study, funded by the National Institute of Mental Health, to more definitively test this treatment and compare it to the most commonly received type of therapy for BDD." CBT uses standard core elements relevant to all BDD patients, such as psychoeducation, cognitive interventions, exposure to avoided situations (which are usually social situations), and prevention of excessive repetitive behaviors (such as mirror checking or compulsive grooming). Treatment ends with relapse prevention strategies and booster sessions focused on helping patients maintain the gains they have made during treatment. Optional treatment modules focus on symptoms and behaviors that some, but not all, patients with this disorder engage in (such as compulsive skin picking or surgery seeking), which enables clinicians to tailor the treatment to individual patient needs. BDD typically starts during early adolescence. The disorder consists of intrusive, time-consuming preoccupations about perceived defects in one's physical appearance (for example, acne, hair loss, or nose size) whereas the perceived flaws are actually minimal or even nonexistent in the eyes of others. Individuals with BDD may engage in obsessive grooming, skin picking or plastic surgery (which appears to usually be ineffective). BDD also often leads to social impairments, missed work or school and difficulty forming and maintaining meaningful relationships. It is associated with high lifetime rates of psychiatric hospitalization and suicide. "Cognitive behavioral therapy is an often-helpful approach to treating BDD," Phillips said. "It can be tailored to meet the needs of a wide range of patients and includes unique strategies to address symptoms that distinguish BDD from other disorders." Phillips continued, "While more research is needed, we conclude from this study that CBT is an appropriate, feasible, and very promising alternative treatment for those suffering from this often misunderstood and severe mental illness." ### The study was funded in part by the National Institute of Mental Health (R34 MH070490). Phillips' principal affiliation is Rhode Island Hospital, a member hospital of the Lifespan health system in Rhode Island. She is also a member of the Department of Psychiatry and Human Behavior at The Warren Alpert Medical School of Brown University. Other researchers involved in the study were Elizabeth Didie of Rhode Island Hospital and the Alpert Medical School; and Sabine Wilhelm, Jeanne M. Fama, Jennifer L. Greenberg and Aparna Keshavia of Massachusetts General Hospital; Ulrike Buhlmann of the Institute of Psychology, Humboldt-Universität zu in Berlin, Germany; and Gail Steketee of Boston University. About Rhode Island Hospital Founded in 1863, Rhode Island Hospital in Providence, R.I., is a private, not-for-profit hospital and is the principal teaching hospital of The Warren Alpert Medical School of Brown University. A major trauma center for southeastern New England, the hospital is dedicated to being on the cutting edge of medicine and research. Last year, Rhode Island Hospital received more than $55 million in external research funding. It is also home to Hasbro Children's Hospital, the state's only facility dedicated to pediatric care. For more information on Rhode Island Hospital, visit http://www.rhodeislandhospital.org, follow us on Twitter @RIHospital or like us on Facebook http://www.facebook.com/rhodeislandhospitalpage. For more information on this and other mental health related topic, please visit MHC Continuing Education

Anxiety linked to higher long-term risk of stroke

American Heart Association Rapid Access Journal Report The greater your anxiety level, the higher your risk of having a stroke, according to new research published in the American Heart Association journal Stroke. The study is the first in which researchers linked anxiety and stroke independent of other factors such as depression. Anxiety disorders are one of the most prevalent mental health problems. Symptoms include feeling unusually worried, stressed, nervous or tense. Over a 22 year period, researchers studied a nationally representative group of 6,019 people 25-74 years old in the first National Health and Nutrition Examination Survey (NHANES I). Participants underwent an interview and took blood tests, medical examinations and completed psychological questionnaires to gauge anxiety and depression levels. Researchers tracked strokes through hospital or nursing home reports and death certificates. After accounting for other factors, they found that even modest increases in anxiety were associated with greater stroke risk. People in the highest third of anxiety symptoms had a 33 percent higher stroke risk than those with the lowest levels. "Everyone has some anxiety now and then. But when it's elevated and/or chronic, it may have an effect on your vasculature years down the road," said Maya Lambiase, Ph.D., study author and cardiovascular behavioral medicine researcher in the Department of Psychiatry at the University of Pittsburgh School of Medicine, in Pittsburgh, Penn. People with high anxiety levels are more likely to smoke and be physically inactive, possibly explaining part of the anxiety-stroke link. Higher stress hormone levels, heart rate or blood pressure could also be factors, Lambiase said. In earlier work, researchers found that depression was linked to greater risk of stroke. In contrast to anxiety, depression is a persistent feeling of hopelessness, dejection, and lack of energy, among other symptoms. Stroke is the No. 4 killer and a leading cause of disability in the United States Continuing Education for MFTs ### Co-authors are Laura Kubzansky, Ph.D. and Rebecca Thurston, Ph.D. Author disclosures are on the manuscript. The National Heart, Lung, and Blood Institute and the National Institute of Mental Health funded the study. For the latest heart and stroke news, follow us on Twitter: @HeartNews. For stroke science, follow the Stroke journal at @StrokeAHA_ASA. Statements and conclusions of study authors published in American Heart Association scientific journals are solely those of the study authors and do not necessarily reflect the association's policy or position. The association makes no representation or guarantee as to their accuracy or reliability. The association receives funding primarily from individuals; foundations and corporations (including pharmaceutical, device manufacturers and other companies) also make donations and fund specific association programs and events. The association has strict policies to prevent these relationships from influencing the science content. Revenues from pharmaceutical and device corporations are available at http://www.heart.org/corporatefunding.

Johns Hopkins research may improve early detection of dementia

Using scores obtained from cognitive tests, Johns Hopkins researchers think they have developed a model that could help determine whether memory loss in older adults is benign or a stop on the way to Alzheimer's disease. The risk of developing dementia increases markedly when a person is diagnosed with mild cognitive impairment, a noticeable and measurable decline in intellectual abilities that does not seriously interfere with daily life. But physicians have no reliable way to predict which people with mild cognitive impairment are likely to be in the 5 to 10 percent a year who progress to dementia. In a proof-of-concept study, the Johns Hopkins investigators analyzed records of 528 people age 60 and over, who were referred to the Johns Hopkins Medical Psychology Clinic for cognitive testing as part of a dementia work-up between 1996 and 2004. The results were compared to those of 135 healthy older adults who participated in a study of normal aging. Both groups completed tests of memory, language, attention, processing speed and drawing abilities from which 13 scores were recorded Nursing CEUs Since each person is naturally more skillful in some areas than in others, the scores of healthy adults showed a symmetrical, bell-shaped range: Most of their scores were high, a few were a bit lower, and a few were even lower. By grouping the patients into cohorts based on the severity of their dementia, the researchers found a trend in the test scores that is likely to mimic the deterioration of an individual's scores over time. At the outset, he says, Alzheimer's disease subtly disrupts some mental abilities, while leaving others intact. Thus, well before a person develops clear cognitive impairment, his or her performance declines slightly on a few measures. When shown on a graph, these changes cause the healthy symmetric, bell-shaped curve to shift and become asymmetrical. Regardless of how low a person's test scores were, the researchers determined that lopsidedness in their score distribution correlated with dementia. They predicted that people with low scores that were evenly distributed were not likely to develop dementia. But those with clearly lopsided test score distributions on the 13 measures administered were already experiencing varying levels of dementia. "Departures from the normal bell-shaped pattern of variability on cognitive tests might determine which people with low scores develop dementia," says David J. Schretlen, Ph.D., a professor of psychiatry and behavioral sciences at the Johns Hopkins University School of Medicine and leader of a study published online Nov. 12 in the journal Neuropsychology. Since these declines can be subtle, the researchers also increased the precision of cognitive testing by accounting for the effects of age, sex, race and education on test performance. The challenge for doctors, Schretlen explains, is that most normal, healthy people will produce a few low scores on cognitive testing. That makes it nearly impossible to know at the outset whether a patient who reports forgetfulness and produces one or two low scores has a benign form of mild cognitive impairment, or is in the earliest stage of dementia. As a result, doctors often tell such patients to return for follow-up testing in a year or two. But if future research confirms it, this new statistical model could help doctors get the prognosis right earlier in the disease, at the first visit, and start treating patients accordingly. Mostly, Schretlen says, doctors could use the new model to reassure patients who are not at risk of dementia, while fast-tracking interventions for those who are. Because there currently are no effective treatments for Alzheimer's disease, those likely headed that way could be counseled to take the good time they have to organize their affairs, and do things they have always wanted to do. They also could be fast-tracked into clinical trials of medications to slow the progression of dementia. "If we are going to have any hope of helping patients with Alzheimer's disease, we need to do it as early as possible," Schretlen says. "Once the brain deteriorates, there's no coming back." Recent failures of drugs in late-stage clinical trials for Alzheimer's disease have been a real blow, he adds, but new treatments are being developed. The new way of reading existing test scores follows a 2008 study by the same researchers showing that one of every six healthy adults scored poorly on two or more of 10 tests in a brief cognitive battery — even though there was nothing wrong with them. The main reason it is difficult to tell whether older people have benign mild cognitive impairment or not is because they are not routinely screened for cognitive impairment, he says. A visit to a specialist comes only after someone has noticed symptoms, and then cognitive testing is interpreted without the benefit of a baseline assessment. What would solve this problem, he says, would be for everyone over the age of 55 to get routine neurocognitive testing every five years. ### The study was supported by the Therapeutic Cognitive Neuroscience Fund; the Benjamin and Adith Miller Family Endowment on Aging, Alzheimer's and Autism; the William and Mary Ann Wockenfuss Research Fund Endowment; and the National Institutes of Health's National Institute of Mental Health (MH60504). Under an agreement with Psychological Assessment Resources, Inc., Schretlen is entitled to a share of royalties on sales of a test and software used in the study. The terms of this arrangement are being managed by The Johns Hopkins University in accordance with its conflict-of-interest policies. Other Johns Hopkins researchers involved in the study include Gila Z. Reckess, Ph.D.; Mark Varvaris, B.A.; and Barry Gordon, M.D., Ph.D. For more information about Schretlen, click here. Johns Hopkins Medicine (JHM), headquartered in Baltimore, Maryland, is a $6.7 billion integrated global health enterprise and one of the leading health care systems in the United States. JHM unites physicians and scientists of the Johns Hopkins University School of Medicine with the organizations, health professionals and facilities of The Johns Hopkins Hospital and Health System. JHM's vision, "Together, we will deliver the promise of medicine," is supported by its mission to improve the health of the community and the world by setting the standard of excellence in medical education, research and clinical care. Diverse and inclusive, JHM educates medical students, scientists, health care professionals and the public; conducts biomedical research; and provides patient-centered medicine to prevent, diagnose and treat human illness. JHM operates six academic and community hospitals, four suburban health care and surgery centers, and more than 30 primary health care outpatient sites. The Johns Hopkins Hospital, opened in 1889, was ranked number one in the nation for 21 years in a row by U.S. News & World Report. For more information about Johns Hopkins Medicine, its research, education and clinical programs, and for the latest health, science and research news, visit http://www.hopkinsmedicine.org Aging and Long Term Care CE Course Johns Hopkins Medicine Media Relations and Public Affairs

Nurturing may protect kids from brain changes linked to poverty

Growing up in poverty can have long-lasting, negative consequences for a child. But for poor children raised by parents who lack nurturing skills, the effects may be particularly worrisome, according to a new study at Washington University School of Medicine in St. Louis. Among children living in poverty, the researchers identified changes in the brain that can lead to lifelong problems like depression, learning difficulties and limitations in the ability to cope with stress. The study showed that the extent of those changes was influenced strongly by whether parents were nurturing. The good news, according to the researchers, is that a nurturing home life may offset some of the negative changes in brain anatomy among poor children. And the findings suggest that teaching nurturing skills to parents — particularly those living in poverty — may provide a lifetime benefit for their children. The study is published online Oct. 28 and will appear in the November issue of JAMA Pediatrics. Using magnetic resonance imaging (MRI), the researchers found that poor children with parents who were not very nurturing were likely to have less gray and white matter in the brain. Gray matter is closely linked to intelligence, while white matter often is linked to the brain's ability to transmit signals between various cells and structures. The MRI scans also revealed that two key brain structures were smaller in children who were living in poverty: the amygdala, a key structure in emotional health, and the hippocampus, an area of the brain that is critical to learning and memory. "We've known for many years from behavioral studies that exposure to poverty is one of the most powerful predictors of poor developmental outcomes for children," said principal investigator Joan L. Luby, MD, a Washington University child psychiatrist at St. Louis Children's Hospital. "A growing number of neuroscience and brain-imaging studies recently have shown that poverty also has a negative effect on brain development. "What's new is that our research shows the effects of poverty on the developing brain, particularly in the hippocampus, are strongly influenced by parenting and life stresses that the children experience." Luby, a professor of psychiatry and director of the university's Early Emotional Development Program, is in the midst of a long-term study of childhood depression. As part of the Preschool Depression Study, she has been following 305 healthy and depressed kids since they were in preschool. As the children have grown, they also have received MRI scans that track brain development. "We actually stumbled upon this finding," she said. "Initially, we thought we would have to control for the effects of poverty, but as we attempted to control for it, we realized that poverty was really driving some of the outcomes of interest, and that caused us to change our focus to poverty, which was not the initial aim of this study." In the new study, Luby's team looked at scans from 145 children enrolled in the depression study. Some were depressed, others healthy, and others had been diagnosed with different psychiatric disorders such as ADHD (attention-deficit hyperactivity disorder). As she studied these children, Luby said it became clear that poverty and stressful life events, which often go hand in hand, were affecting brain development. The researchers measured poverty using what's called an income-to-needs ratio, which takes a family's size and annual income into account. The current federal poverty level is $23,550 for a family of four. Although the investigators found that poverty had a powerful impact on gray matter, white matter, hippocampal and amygdala volumes, they found that the main driver of changes among poor children in the volume of the hippocampus was not lack of money but the extent to which poor parents nurture their children. The hippocampus is a key brain region of interest in studying the risk for impairments. Luby's team rated nurturing using observations made by the researchers — who were unaware of characteristics such as income level or whether a child had a psychiatric diagnosis — when the children came to the clinic for an appointment. And on one of the clinic visits, the researchers rated parental nurturing using a test of the child's impatience and of a parent's patience with that child. AUDIO: Poverty can interfere with healthy development in children and can have long-lasting, negative consequences. Now researchers at Washington University School of Medicine in St. Louis have found that if poor... Click here for more information. While waiting to see a health professional, a child was given a gift-wrapped package, and that child's parent or caregiver was given paperwork to fill out. The child, meanwhile, was told that s/he could not open the package until the caregiver completed the paperwork, a task that researchers estimated would take about 10 minutes. Luby's team found that parents living in poverty appeared more stressed and less able to nurture their children during that exercise. In cases where poor parents were rated as good nurturers, the children were less likely to exhibit the same anatomical changes in the brain as poor children with less nurturing parents. "Parents can be less emotionally responsive for a whole host of reasons," Luby said. "They may work two jobs or regularly find themselves trying to scrounge together money for food. Perhaps they live in an unsafe environment. They may be facing many stresses, and some don't have the capacity to invest in supportive parenting as much as parents who don't have to live in the midst of those adverse circumstances." The researchers also found that poorer children were more likely to experience stressful life events, which can influence brain development. Anything from moving to a new house to changing schools to having parents who fight regularly to the death of a loved one is considered a stressful life event. Luby believes this study could provide policymakers with at least a partial answer to the question of what it is about poverty that can be so detrimental to a child's long-term developmental outcome. Because it appears that a nurturing parent or caregiver may prevent some of the changes in brain anatomy that this study identified, Luby said it is vital that society invest in public health prevention programs that target parental nurturing skills. She suggested that a key next step would be to determine if there are sensitive developmental periods when interventions with parents might have the most powerful impact. "Children who experience positive caregiver support don't necessarily experience the developmental, cognitive and emotional problems that can affect children who don't receive as much nurturing, and that is tremendously important," Luby said. "This study gives us a feasible, tangible target with the suggestion that early interventions that focus on parenting may provide a tremendous payoff." Aspira Continuing Education Online Courses ### Funding for this research comes from the National Institute of Mental Health (NIMH) of the National Institutes of Health (NIH). NIH grant numbers 2R01 MH064769-06A1, PA-07-070 NIMH R01 and 5K01 MH090515-04. Luby J, Belden A, Botteron K, Marrus N, Harms MP, Babb C, Nishino T, Barch D. The effects of poverty on childhood brain development: The mediating effect of caregiving and stressful life events. JAMA Pediatrics vol. 167 (11), November 2013, published online Oct. 28, 2013. http://archpedi.jamanetwork.com/journal.aspx Washington University School of Medicine's 2,100 employed and volunteer faculty physicians also are the medical staff of Barnes-Jewish and St. Louis Children's hospitals. The School of Medicine is one of the leading medical research, teaching and patient care institutions in the nation, currently ranked sixth in the nation by U.S. News & World Report. Through its affiliations with Barnes-Jewish and St. Louis Children's hospitals, the School of Medicine is linked to BJC HealthCare.

Past weight loss an overlooked factor in disordered eating

PHILADELPHIA (September 24, 2013)— Dieters and weight loss researchers are familiar with the principle: The more weight you've lost, the harder it is to keep it off. A complex and vicious cycle of biological and behavioral factors make it so. But eating disorder research has largely overlooked this influence, and Dr. Michael Lowe, a professor of psychology at Drexel University, has published a flurry of research studies showing that needs to change. "The focus of eating disorder research has very much been on the state of patients' thoughts, beliefs, emotions and personalities," Lowe said. "And while these mental influences are undoubtedly part of the problem, historically there has been very little focus on how their current and past body weights contribute to their eating disorder." Lowe and colleagues' studies – about a dozen on bulimia nervosa have been published in the past several years – show that having an elevated past body weight, and being at a body weight well below highest past weight, may help cause and perpetuate disordered eating. The latest of Lowe's studies was just published in The Journal of Abnormal Psychology, the top journal for eating disorder research, and is the team's first to address this principle in anorexia nervosa. The findings, Lowe says, show that researchers and clinicians need to start taking into account how a person's historical and current body weight contribute to disordered eating. "This fundamentally changes the assumption that the problem is primarily psychological or emotional," Lowe said. The new study, led by doctoral student Laura A. Berner, was based on data collected at the Renfrew Center for eating disorders in Philadelphia, where Lowe is also a consultant. The researchers found that the level of eating disorder symptoms, as well as degree of improvement during treatment, depends on how much weight patients with anorexia nervosa had lost from their previous highest weight (a measure called "weight suppression"), how much they currently weigh and the interaction between the two LSW Continuing Education After controlling for patients' body mass index (BMI, which is a known indicator of disease severity), they found that patients with greater weight suppression had more severe symptoms of anorexia than patients whose low weight was closer to their historical highest weight. Standard measures of disordered eating such as shape concerns, eating concerns, binge eating, depression and menstrual abnormalities were correlated with weight suppression, current BMI, or both. Lowe said that researchers and clinicians who already use weight or BMI as an absolute measure of eating disorder severity should also consider weight suppression as a relative measure. These findings also may have important implications for treatment. "The standards for treating anorexia nervosa are all about 'how much weight do they need to gain to meet a minimally healthy body weight for their height,'" Lowe said. "What we've rarely asked, is 'what is this patient's weight history?'" Lowe said his ongoing research suggests that the answer is that many patients weighed more than their peers before developing anorexia nervosa. "If the patient's body somehow 'remembers' that past higher weight, then even at the minimally healthy body weight she is still going to be struggling mightily to maintain her weight," Lowe said. "That perspective is new. It suggests that future treatments might work toward finding a healthier 'balance point' between what patients once weighed and what they currently weigh." "It is really helpful to have more than one way to look at weight in the eating disorders; we now have evidence that absolute weight and relative weight are both important in predicting difficulties in our work towards full recovery," said Dr. Susan Ice, vice president and chief medical officer of The Renfrew Center. "And it is immensely satisfying to find that science has discovered that there is physical memory or a kind of 'wisdom' in the body." ### Lowe and his research team were recently funded by the National Institute of Mental Health to further investigate the role of these weight-related variables on bulimia nervosa. Individuals with symptoms of bulimia who are interested in participating in this federally funded study may call 215-762-1313 or email TEDS@drexel.edu for additional information. Another research laboratory at Drexel, the Laboratory for Innovations in Health-Related Behavior Change, is recruiting participants who have experienced binge eating problems but do not engage in compensatory behaviors such as self-induced vomiting or laxative use. One project is investigating a new smartphone app for binge eating and the other is evaluating an in-person treatment. Individuals who are interested in participating in these research studies may call 215-762-4900. Paper in the Journal of Abnormal Psychology: http://dx.doi.org/10.1037/a0033930

Ability to delay gratification may be linked to social trust, new CU-Boulder study finds

A person's ability to delay gratification—forgoing a smaller reward now for a larger reward in the future—may depend on how trustworthy the person perceives the reward-giver to be, according to a new study by researchers at the University of Colorado Boulder. A body of research that stretches back more than a half-century has shown that the ability to delay gratification is linked to a number of better life outcomes. On average, people who were able to delay gratification as children go on to have higher SAT scores, for example. They also tend to be more socially conscious as adolescents, less obese as adults, and less likely to abuse drugs or alcohol. But despite the long history of studying delayed gratification, little research has focused on the role of social trust in a person's ability to wait for a larger payoff in the future. "Most of the time, when people talk about delaying gratification, they talk about basic processes of evaluation and self-control," said Laura Michaelson, a CU-Boulder doctoral student in the Department of Psychology and Neuroscience and co-lead author of the new study appearing in the online journal Frontiers in Psychology. In general, people who choose not to delay gratification have often been characterized as irrational and as having poor impulse control. But if the role of social trust is considered, it introduces the possibility that the person who is choosing not to delay gratification may be acting rationally after all, the researchers said. "If you don't trust someone, it's rational not to wait for them to give you $20 in a month instead of $15 now," said study co-lead author Alejandro de la Vega, also a doctoral student in CU-Boulder's Department of Psychology and Neuroscience. To determine the role of social trust, the research team—which also included Christopher Chatham, a former CU-Boulder doctoral student now at Brown University, and psychology and neuroscience Professor Yuko Munakata—recruited participants using Amazon's Mechanical Turk, an online tool that can be used by scientists to quickly connect with a large number of people from a broad range of backgrounds. The researchers paid participants up to $1 to participate in an experiment in which they were asked to read the profiles of three fictional characters and then rate them on their trustworthiness. Participants were then asked whether they would opt to take a smaller amount of money offered immediately from each character or a larger amount of money that they would have to wait to collect. The results showed that the participants were less likely to delay gratification when they distrusted the person who was offering the reward. A second experiment—which relied on a larger group but asked each participant to read the profile of only one character—had similar results. The second study also paired one of three sketches of a face with each character. "This offers an alternative explanation for why certain populations might be notoriously bad at delaying gratification or notoriously impulsive, like criminals and addicts," Michaelson said. "It had been chalked up to a lack of self-control. But it may be the case that they are poor at delaying gratification because they have low social trust." The findings could have implications for determining the best intervention strategies to use with children who find it difficult to delay gratification. Creating environments in which children can develop social trust, for example, could be more effective than having those children work solely on self-control, Michaelson said. The findings also may be important for adults, especially in terms of economic decision-making, de la Vega said. Economists are interested in delayed gratification as it relates to making investments or building up savings instead of spending money immediately. The new CU-Boulder study suggests that how much a person trusts an investment banker or an economic adviser could affect the person's decisions about saving and spending Social Worker Continuing Education "These economic decisions are not being made in a complete vacuum," de la Vega said. "They might really be affected by how you perceive the person you're interacting with." The research team plans to follow up this study with research that involves participants interacting in person with the people who are offering the rewards. "There is a very real possibility the this relationship between social trust and delaying gratification might be even more strong and even more salient when you're in a real situation," Michaelson said. ### Read the full study online at http://www.frontiersin.org/Cognition/10.3389/fpsyg.2013.00355/abstract.

Research uncovers new details about brain anatomy and language in young children

PROVIDENCE, R.I. [Brown University] — Researchers from Brown University and King's College London have gained surprising new insights into how brain anatomy influences language acquisition in young children. Their study, published in the Journal of Neuroscience, found that the explosion of language acquisition that typically occurs in children between 2 and 4 years old is not reflected in substantial changes in brain asymmetry. Structures that support language ability tend to be localized on the left side of the brain. For that reason, the researchers expected to see more myelin — the fatty material that insulates nerve fibers and helps electrical signals zip around the brain — developing on the left side in children entering the critical period of language acquisition. But that is not what the research showed. "What we actually saw was that the asymmetry of myelin was there right from the beginning, even in the youngest children in the study, around the age of 1," said the study's lead author, Jonathan O'Muircheartaigh, the Sir Henry Wellcome Postdoctoral Fellow at King's College London. "Rather than increasing, those asymmetries remained pretty constant over time." That finding, the researchers say, underscores the importance of environment during this critical period for language. O'Muircheartaigh is currently working in Brown University's Advanced Baby Imaging Lab. The lab uses a specialized MRI technique to look at the formation of myelin in babies and toddlers. Babies are born with little myelin, but its growth accelerates rapidly in the first few years of life. The researchers imaged the brains of 108 children between ages 1 and 6, looking for myelin growth in and around areas of the brain known to support language. While asymmetry in myelin remained constant over time, the relationship between specific asymmetries and language ability did change, the study found. To investigate that relationship, the researchers compared the brain scans to a battery of language tests given to each child in the study. The comparison showed that asymmetries in different parts of the brain appear to predict language ability at different ages. "Regions of the brain that weren't important to successful language in toddlers became more important in older children, about the time they start school," O'Muircheartaigh said. "As language becomes more complex and children become more proficient, it seems as if they use different regions of the brain to support it." Interestingly, the association between asymmetry and language was generally weakest during the critical language period. "We found that between the ages of 2 and 4, myelin asymmetry doesn't predict language very well," O'Muircheartaigh said. "So if it's not a child's brain anatomy predicting their language skills, it suggests their environment might be more influential." The researchers hope this study will provide a helpful baseline for future research aimed at pinpointing brain structures that might predict developmental disorders. "Disorders like autism, dyslexia, and ADHD all have specific deficits in language ability," O'Muircheartaigh said. "Before we do studies looking at abnormalities we need to know how typical children develop. That's what this study is about." "This work is important, as it is the first to investigate the relationship between brain structure and language across early childhood and demonstrate how this relationship changes with age," said Sean Deoni, assistant professor of engineering, who oversees the Advanced Baby Imaging Lab. "The study highlights the advantage of collaborative work, combining expertise in pediatric imaging at Brown and neuropsychology from the King's College London Institute of Psychiatry, making this work possible." ### Other authors on the paper include Douglas Dean, Holly Dirks, Nicole Waskiewicz, and Katie Lehman from Brown's Baby Imaging Lab, and Beth Jerskey from Brown's Alpert Medical School. The work was funded by the National Institutes of Mental Health and the Wellcome Trust. Editors: Brown University has a fiber link television studio available for domestic and international live and taped interviews, and maintains an ISDN line for radio interviews. For more information, call (401) 863-2476 ASW Continuing Education -------------------------------------------------------------------------------- [ Back to EurekAlert! ] [ Print | E-mail Share Share ] [ Close Window ] AAAS and EurekAlert! are not responsible for the accuracy of news releases posted to EurekAlert! by contributing institutions or for the use of any information through the EurekAlert! system. HOME DISCLAIMER PRIVACY POLICY TERMS & CONDITIONS CONTACT US TOP Copyright ©2013 by AAAS, the science society.

NIMH Grantee Receives 2013 Nobel Prize

Congratulations to current NIMH grantee Thomas C. Südhof, M.D., at Stanford University School of Medicine, for winning the Nobel Prize in Physiology or Medicine for his work on how the brain sends and receives chemical messages. Thomas C. Südhof, M.D. Thomas C. Südhof, M.D. Stanford University School of Medicine “We are extremely proud of Dr. Südhof,” said National Institute of Mental Health (NIMH) Director Thomas Insel, M.D. “NIMH has supported Dr. Südhof's ground-breaking research for more than two decades as part of our commitment to understanding the fundamental mechanisms of brain function." The human brain houses about 100 billion neurons—about half the number of stars in the Milky Way. Each of these neurons “converses” with, on average, thousands of other neurons, sending molecular messages in a matter of milliseconds, about the same timeframe as a camera flash. How these messages are sent in such a rapid and precise manner has long been a mystery to neuroscientists. When these messages go awry, mental disorders such as schizophrenia, autism, and depression may arise. Specifically, Dr. Südhof parsed the proteins that are used in a synapse—the gap between neurons where one neuron reaches out to talk to another via chemical messengers known as neurotransmitters. These specialized spaces are comprised of three components: the messenger or presynaptic neuron, the recipient or postsynaptic neuron, and the cleft or space between these two neurons. Dr. Südhof’s work identified key molecules involved in the rapid release of neurotransmitters from the terminals of presynaptic neurons and revealed how electrical signals in the form of calcium ions instruct a protein called synaptotagmin. Once calcium binds to synaptotagmin, the protein serves as a switch for neurotransmitter-carrying cellular shuttles called vesicles to fuse with the outer surface of the presynaptic neuron and release these chemical messengers into the synaptic cleft. Upon release, the neurotransmitters cross the synaptic cleft and bind to docking sites or receptors on the postsynaptic neuron, triggering an electrical signal to pulse through it. Südhof’s work revealed that synaptotagmins also act as universal calcium sensors in non-neuronal cells, functioning, for example, in the release of hormones such as insulin from pancreatic beta cells. Dr. Südhof shares the world’s most prestigious science award with James E. Rothman, Ph.D., at Yale University, and Randy W. Schekman, Ph.D., at the University of California, Berkeley. Dr. Rothman unraveled protein machinery that allows vesicles to fuse with their targets to permit transfer of cargo. Dr. Schekman discovered a set of genes that were required for vesicle traffic. The researchers will share a prize that totals roughly $1.2 million USD. Previously, Dr. Südhof and Richard H. Scheller, Ph.D., at Genentech, collected the 2013 Albert Lasker Basic Medical Research Award for their work. Known as “America’s Nobels,” the Lasker Awards often predict future Nobel Prize recipients. The National Institutes of Health (NIH) has supported Dr. Südhof’s research over the past 22 years. In turn, Dr. Südhof has served on several study sections at the NIH Center for Scientific Review, in addition to the Molecular, Cellular, and Developmental Neuroscience study section at NIMH. Over the years, Dr. Südhof’s work on the neurotransmitter release machinery has been supported with research program grants as well as center grants from NIMH. He is also the recipient of an NIMH MERIT (Method to Extend Research in Time) award, which along with an additional NIMH grant and funding from the Howard Hughes Medical Institute helped support his Nobel work. MERIT awards provide up to 10 years of stable research support for highly productive outstanding investigators working on projects well aligned with the mission of NIMH Social Worker Continuing Education Dr. Südof also holds an NIH TR01 award for work to facilitate the creation of neurons from non-neuronal cells (skin fibroblasts of human patients). This work is anticipated to provide a novel way for scientists to study the biological effects of gene mutations associated with neuropsychiatric diseases

DSM-5 and RDoC: Shared Interests

Thomas R. Insel, M.D., Director, NIMH Jeffrey A. Lieberman, M.D., President-elect, APA NIMH and APA have a shared interest in ensuring that patients and health providers have the best available tools and information today to identify and treat mental health issues, while we continue to invest in improving and advancing mental disorder diagnostics for the future. Today, the American Psychiatric Association's (APA) Diagnostic and Statistical Manual of Mental Disorders (DSM), along with the International Classification of Diseases (ICD) represents the best information currently available for clinical diagnosis of mental disorders. Patients, families, and insurers can be confident that effective treatments are available and that the DSM is the key resource for delivering the best available care. The National Institute of Mental Health (NIMH) has not changed its position on DSM-5. As NIMH's Research Domain Criteria (RDoC) project website states, "The diagnostic categories represented in the DSM-IV and the International Classification of Diseases-10 (ICD-10, containing virtually identical disorder codes) remain the contemporary consensus standard for how mental disorders are diagnosed and treated." Yet, what may be realistically feasible today for practitioners is no longer sufficient for researchers. Looking forward, laying the groundwork for a future diagnostic system that more directly reflects modern brain science will require openness to rethinking traditional categories. It is increasingly evident that mental illness will be best understood as disorders of brain structure and function that implicate specific domains of cognition, emotion, and behavior. This is the focus of the NIMH’s Research Domain Criteria (RDoC) project. RDoC is an attempt to create a new kind of taxonomy for mental disorders by bringing the power of modern research approaches in genetics, neuroscience, and behavioral science to the problem of mental illness ceus for social workers The evolution of diagnosis does not mean that mental disorders are any less real and serious than other illnesses. Indeed, the science of diagnosis has been evolving throughout medicine. For example, subtypes of cancers once defined by where they occurred in the body are now classified on the basis of their underlying genetic and molecular causes. All medical disciplines advance through research progress in characterizing diseases and disorders. DSM-5 and RDoC represent complementary, not competing, frameworks for this goal. DSM-5, which will be released May 18, reflects the scientific progress seen since the manual's last edition was published in 1994. RDoC is a new, comprehensive effort to redefine the research agenda for mental illness. As research findings begin to emerge from the RDoC effort, these findings may be incorporated into future DSM revisions and clinical practice guidelines. But this is a long-term undertaking. It will take years to fulfill the promise that this research effort represents for transforming the diagnosis and treatment of mental disorders. By continuing to work together, our two organizations are committed to improving outcomes for people with some of the most disabling disorders in all of medicine.

Autism Risk Unrelated to Total Vaccine Exposure in Early Childhood

A child’s risk for developing an autism spectrum disorder (ASD) is not increased by receiving “too many vaccines too soon,” according to a new study published in The Journal of Pediatrics. Although previous scientific evidence has shown that vaccines do not cause autism, more than 1 in 10 parents refuse or delay vaccinations for their young children. A main safety concern of these parents is the number of vaccines administered, both on a single day and over the course of a child’s first 2 years of life. In the first study of its kind, researchers from the CDC and Abt Associates, Inc. compared vaccine records for over 1000 children born from 1994–1999, some of whom were later diagnosed with ASD. The researchers calculated the total number of vaccine antigens each child received between birth and age 2, as well as the maximum number of antigens each child received on a single day. The study found that the total number of vaccine antigens received was the same between children with ASD and those without ASD. Additionally, antigen number was also found to be unrelated to the development of two sub-categories of ASD—autistic disorder and ASD with regression LCSW Continuing Education The researchers concluded, “The possibility that immunological stimulation from vaccines during the first 1 or 2 years of life could be related to the development of ASD is not well-supported by what is known about the neurobiology of ASDs.”

Studying sex differences in autism focus of $15 million NIH award to Yale center

The reasons why autism spectrum disorders are almost five times more common among boys than among girls may soon be revealed, thanks to a five-year, $15 million National Institutes of Health (NIH) grant awarded to Yale School of Medicine for the Autism Centers of Excellence (ACE) research program. Led by principal investigator Kevin Pelphrey of Yale Child Study Center, the Yale ACE award is part of a $100 million National Institutes of Health grant to nine institutions investigating sex differences in autism spectrum disorders, or ASD, as well as studying ASD and limited speech. Pelphrey and a collaborative team of researchers from Yale, UCLA, Harvard, and the University of Washington, will investigate the poorly understood nature of autism in females. The team will study an unprecedented number of girls with autism and will focus on genes, brain function, and behavior throughout childhood and adolescence. The objectives are to identify causes of autism and develop novel treatments.

ASDs are complex developmental disorders that affect how a person behaves, interacts with others, communicates, and learns. According to the Centers for Disease Control and Prevention, ASD affects approximately 1 in 88 children in the United States. "This award represents an innovative collaboration among three laboratories at Yale led by Drs. Matthew State, James McPartland, and myself," said Pelphrey, the Harris Associate Professor in the Child Study Center, and associate professor of psychology, and director of the Child Neuroscience Laboratory. "It is my hope that this award will invigorate research in autism at Yale and allow us to maintain our outstanding history of cutting edge work in this field." Alcoholism and Drug Abuse Counselors Continuing Education ### NIH created the ACE Program in 2007 to launch an intense and coordinated research program into the causes of ASD and to find new treatments. The program supports large collaborative efforts to advance the broad research goals. The program expanded this year to examine such issues as children and adults who have limited or no speech, possible links between ASD and other genetic syndromes, potential treatments, and the possible reasons why ASDs are more common among boys than girls, according to Alice Kay of the Intellectual and Developmental Disabilities Branch at the Eunice Kennedy Shriver National Institute of Child Health and Human Development (NICHD), one of five institutes funding the ACE program. In addition to the NICHD, the NIH institutes that support the ACE program are the National Institute on Deafness and Other Communication Disorders, the National Institute of Environmental Health Sciences, the National Institute of Mental Health and the National Institute of Neurological Disorders and Stroke. The eight other researchers to receive ACE funding hail from the following institutions: University of California, Emory University, Boston University, University of North Carolina at Chapel Hill, Mount Sinai School of Medicine, and Harvard Medical School. *Research reported here was supported by the National Institute Of Mental Health (NIMH) of the National Institutes of Health under Award Number R01MH100028.

Researchers pursue red flag for schizophrenia relapse

AUGUSTA, Ga. – Blood levels of a protein that helps regulate inflammation may also serve as a red flag for relapse in some schizophrenia patients, researchers said. "There are no good, objective measures of treatment efficacy or indicators for relapse," said Dr. Brian Miller, a psychiatrist specializing in schizophrenia at the Medical College of Georgia at Georgia Health Sciences University. Researchers hope monitoring levels of interleukin-6 can fill that gap for a population in which more than half of patients don't take their medications as prescribed, often because of side effects. The relapse rate is about 80 percent within two years in patients who don't take their medication properly and about half that in those who do, according to the National Institute of Mental Health LSW Continuing Education "We hope the upshot of our studies will lead to new treatment approaches and strategies for care," Miller said, including the kind of personalized, multi-drug therapies that are becoming the standard for controlling other chronic conditions such as diabetes and hypertension. "We want to attack the disease from as many directions as possible." To get a better handle on how IL-6 levels correspond to disease status, they are looking at levels in blood samples taken multiple times over several years in 305 patients enrolled in a study comparing injectable to oral medication. They also are taking one-time measurements in 80 healthy controls and comparing those to levels in 240 patients who are acutely ill, stable outpatients or stable outpatients who smoke marijuana, a drug commonly abused by patients. While many previous studies have excluded drug abusers, marijuana may increase inflammation, so they want to explore the relationship between IL-6 levels and its use, Miller said. Miller received a five-year, $920,000 National Institute of Mental Health Mentored Patient-Oriented Research Career Development Award to measure IL-6 levels as a potential indicator of how well treatment is working to control disease in these vulnerable patients and whether they are headed to relapse. Amazingly the contributions of "immune disturbances" to schizophrenia have been debated for about 100 years yet anti-inflammatory drugs aren't routinely given to patients in addition to their antipsychotic medication, Miller said. Part of the problem is physicians still have no idea what percentage of patients with this very heterogeneous disease have evidence of increased inflammation. In fact, no two patients have the exact constellation of symptoms considered disease hallmarks, such as hallucinations, delusions, disorganized speech and thinking, he said. But mounting evidence suggests inflammation's impact in schizophrenia. A British study of 50 patients experiencing their first episode of schizophrenic behavior found a handful had indicators of an immune response to their brains, called autoantibodies, and no other conditions, such as a brain infection, to explain them. What amounts to a chronic low-grade flu has been found in some patients and rare immune system disorders such as Sjögren's syndrome, which attacks moisture-producing glands resulting in dry eyes and mouth, also tend to be more common in schizophrenics. Additionally, a handful of clinical trials has shown – not surprisingly – that patients with the highest levels of pro-inflammatory factors had the best response to anti-inflammatory drugs. "It's likely we are talking about a subset of people with this illness who would be most likely to respond to anti-inflammatory therapy – in addition to standard anti-psychotics – so part of our work is to begin to piece out who those people are (and whether) they have a particular clinical picture," Miller said. "Even being able to predict relapse or improve therapy in 25 percent of patients would be a tremendous advance," he said, noting that the vast majority of schizophrenia drugs work essentially by the same mechanism. Once patients can be identified, ideally with a blood test of their IL-6 levels, the next questions are which drugs to use and for how long. Miller's primary mentor for the studies is Dr. Andrew Mellor, a molecular geneticist and immunologist who leads the Cancer Immunology, Inflammation Tolerance Program at the GHSU Cancer Center. Mellor also is Bradley-Turner & Georgia Research Alliance Eminent Scholar in Molecular Immunogenetics. Co-secondary mentors are schizophrenia experts Dr. Peter F. Buckley, Dean of the Medical College of Georgia at GHSU, and Dr. Mark Rapaport, Chair of the Department of Psychiatry and Behavioral Sciences at Emory University School of Medicine. Schizophrenia affects about 1 percent of the population, or some 2.4 million American adults. Hallucinations are a disease hallmark: patients hear voices and can even see, touch and taste things that are not real. They can become depressed, reclusive and suicidal and have an increased risk of cardiovascular and other health conditions. Patients die on average15-20 years younger than the general population. Miller, a recipient of the 2011 National Alliance on Mental Illness Exemplary Psychiatrist Award, said he felt a calling to psychiatry and specifically schizophrenia as a medical student at The Ohio State University. "The patients are wonderful and their stories are fascinating," he said, noting that the field is "wide open" to improve their care. ###

UCLA study uncovers new tools for targeting genes linked to autism

Findings could lead to future therapeutic targets UCLA researchers have combined two tools – gene expression and the use of peripheral blood -- to expand scientists' arsenal of methods for pinpointing genes that play a role in autism. Published in the June 21 online edition of the American Journal of Human Genetics, the findings could help scientists zero in on genes that offer future therapeutic targets for the disorder. "Technological advances now allow us to rapidly sequence the genome and uncover dozens of rare mutations," explained principal investigator Dr. Daniel Geschwind, the Gordon and Virginia MacDonald Distinguished Professor of Human Genetics and a professor of neurology at the David Geffen School of Medicine at UCLA. "But just because a particular genetic mutation is rare doesn't mean it's actually causing disease. We used a new approach to tease out potential precursors of autism from the occasional genetic glitch." Geschwind and his colleagues studied DNA contained in blood samples from 244 families with one healthy child and one child on the autism spectrum. The team used a hybrid method that blended tests that read the order of DNA bases with those that analyze gene expression, the process by which genes make cellular proteins. "Monitoring gene expression provides us with another line of data to inform our understanding of how autism develops," said Geschwind, who is also director of the Center for Autism Research and Treatment at the Semel Institute for Neuroscience and Behavior at UCLA. "Integrating this method with the sequencing of DNA bases expands our ability to find mutations leading to the disease." Gene expression offers a molecular signpost pointing scientists in the right direction by narrowing the field and highlighting specific areas of the genome. For example, if a gene is expressed at substantially higher or lower levels in a patient, researchers will review the patient's DNA to check if that gene has changed. "We found that we can use gene expression to help understand whether a rare mutation is causing disease or playing a role in disease development," said Geschwind. "A true mutation will alter a gene's sequence, modifying the protein or RNA it produces -- or preventing the gene from producing them entirely. "A gene mutation accompanied by a change in expression clues us to a hot spot on the genome and directs us where to look next," he added. "Not all mutations will influence gene expression, but this approach improves our ability to pinpoint those that do." The researchers used the combined method to prioritize gene targets that merit closer investigation, potentially explaining why one person develops autism and their sibling does not. Their search turned up new regions in the genome where genetic variations showed strong links to autism and altered expression patterns. Genes in these regions were more likely to be mutated in the autistic children than in their unaffected siblings. "When we looked at genes associated with nervous-system function we found significantly more genes were expressed at higher or lower levels in the children diagnosed with autism than we did in their siblings unaffected by the disorder," said Geschwind. Finally, the research team discovered that the DNA contained in peripheral blood can help shed light on diseases of the central nervous system. Brain cells and genes related to synaptic function are expressed in the blood, offering a window into gene expression. "Brain tissue from people with autism is not readily available for study, and some people are reluctant to use non-neural tissue in psychiatric disease," explained Geschwind. "But our study demonstrates that even peripheral blood can expand our knowledge of neurological disease." The team's next step will be to replicate their findings in a larger population. ### Autism is a complex brain disorder that strikes in early childhood. The condition disrupts a child's ability to communicate and develop social relationships and is often accompanied by acute behavioral challenges. Autism spectrum disorders are diagnosed in one in 110 children in the United States, affecting four times as many boys as girls. Diagnoses have expanded tenfold in the last decade. The research was supported by grants from the Simons Foundation, the National Institute of Mental Health (5R01 MH081754-04), the Wellcome Trust and Autism Speaks. Geschwind's coauthors included first author Rui Luo, Irina Voineagu, Lambertus Klei, Chaochao Cai, Jing Ou, Jennifer Lowe and Matthew State of UCLA; Stephan Sanders of Yale University; Ni Huang and Matthew Hurles of the Wellcome Trust Sanger Institute; and Su Chu and Bernie Devlin of Carnegie Mellon University. The UCLA Center for Autism Research and Treatment provides diagnosis, family counseling, clinical trials and treatment for patients with autism. UCLA is one of eight centers in the National Institutes of Health–funded Studies to Advance Autism Research and Treatment network and one of 10 original Collaborative Programs for Excellence in Autism social worker ceus

Pattern Recognition Technology May Help Predict Future Mental Illness in Teens

Pattern Recognition Technology May Help Predict Future Mental Illness in Teens


Source: NIMH

A technique combining computer-based pattern recognition and brain imaging data accurately distinguished teens at risk for mental disorders from those with low risk and may someday be useful in predicting risk in individuals, according to an NIMH-funded study published February 15, 2012, in the journal PLoS One.

Background

Research on risk for mental disorders generally describes risk factors that apply to groups. To date, no biological measures can accurately predict an individual’s risk of future mental disorders.

Mary Phillips, M.D., of the University of Pittsburgh School of Medicine, and colleagues evaluated the use of computer-based techniques that automatically find patterns in data—these techniques are collectively called machine learning—with functional magnetic resonance imaging (fMRI) data. The researchers obtained fMRI data from 32 teens, half of whom had at least one biological parent diagnosed with bipolar disorder and were therefore at genetic risk for future psychiatric disorders. The other half of teens had no history of mental disorders either personally or in their immediate families.

The teens’ brain activity was assessed as they identified the gender of actors depicting various emotional facial expressions (happy, fearful, or neutral) in a series of photographs. Previous research has linked various mental disorders, especially depression and bipolar disorder, with abnormal patterns of brain activity during this task. Based on this fMRI data, the researchers used machine learning to calculate each participant’s odds for future mental illness social worker ceus

The participants were also assessed clinically and with fMRI at the start of the study, and clinically assessed again about two years later, on average. Long-term follow up is ongoing, with successive face-to-face assessments occurring every other year.

Results

Machine learning combined with fMRI accurately identified most of the healthy teens at genetic risk of future mental disorders vs. healthy teens with low genetic risk. Four of the 16 at-risk teens were misidentified as having low risk.

At the two-year follow up, none of the at-risk teens had developed bipolar disorder, but six were diagnosed with major depression or an anxiety disorder. Among all the at-risk teens identified through machine learning, these six had received the highest odds for belonging to the at-risk group.

Three of the four at-risk teens misidentified as belonging to the low risk group at the start of the study remained healthy at the second assessment. Clinical information for the fourth teen was not available at the time of follow-up.

Significance

Though still a very preliminary study, according to the researchers, machine learning combined with fMRI shows promise for predicting individual risk of developing future mental disorders, especially in at-risk populations.

The ongoing follow-up may also yield further insights into the relationship between depression, anxiety disorders, and bipolar disorder. Many studies have shown that bipolar disorder is often preceded by depression or anxiety disorders, and that these disorders may affect the course of subsequent bipolar disorder.

What’s Next

Larger studies using machine learning and fMRI will help to better define the extent to which pattern recognition techniques can accurately identify people at risk for future mental disorders. Research in this area may also inform early treatment or prevention efforts.

Reference

Mourão-Miranda J, Oliveira L, Ladouceur CD, Marquand A, Brammer M, Birmaher B, Axelson D, Phillips ML. Pattern recognition and functional neuroimaging help to discriminate healthy adolescents at risk for mood disorders from low risk adolescents. PLoS One. 2012;7(2):e29482. Epub 2012 Feb 15. PubMed PMID: 22355302; PubMed Central PMCID: PMC3280237.

Related Funding: K01 MH083001-04; R01 MH060952-11