New brain pathways for understanding type 2 diabetes and obesity uncovered

Researchers at UT Southwestern Medical Center have identified neural pathways that increase understanding of how the brain regulates body weight, energy expenditure, and blood glucose levels — a discovery that can lead to new therapies for treating Type 2 diabetes and obesity.The study, published in Nature Neuroscience, found that melanocortin 4 receptors (MC4Rs) expressed by neurons that control the autonomic nervous system are key in regulating glucose metabolism and energy expenditure, said senior author Dr. Joel Elmquist, Director of the Division of Hypothalamic Research, and Professor of Internal Medicine, Pharmacology, and Psychiatry.”A number of previous studies have demonstrated that MC4Rs are key regulators of energy expenditure and glucose homeostasis, but the key neurons required to regulate these responses were unclear,” said Dr. Elmquist, who holds the Carl H. Westcott Distinguished Chair in Medical Research, and the Maclin Family Distinguished Professorship in Medical Science, in Honor of Dr. Roy A. Brinkley. “In the current study, we found that expression of these receptors by neurons that control the sympathetic nervous system, seem to be key regulators of metabolism. In particular, these cells regulate blood glucose levels and the ability of white fat to become ‘brown or beige’ fat.”Using mouse models, the team of researchers, including co-first authors Dr. Eric Berglund, Assistant Professor in the Advanced Imaging Research Center and Pharmacology, and Dr. Tiemin Liu, a postdoctoral research fellow in Internal Medicine, deleted MC4Rs in neurons controlling the sympathetic nervous system. …

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Ever-so-slight delay improves decision-making accuracy

Columbia University Medical Center (CUMC) researchers have found that decision-making accuracy can be improved by postponing the onset of a decision by a mere fraction of a second. The results could further our understanding of neuropsychiatric conditions characterized by abnormalities in cognitive function and lead to new training strategies to improve decision-making in high-stake environments. The study was published in the March 5 online issue of the journal PLoS One.”Decision making isn’t always easy, and sometimes we make errors on seemingly trivial tasks, especially if multiple sources of information compete for our attention,” said first author Tobias Teichert, PhD, a postdoctoral research scientist in neuroscience at CUMC at the time of the study and now an assistant professor of psychiatry at the University of Pittsburgh. “We have identified a novel mechanism that is surprisingly effective at improving response accuracy.The mechanism requires that decision-makers do nothing — just briefly. “Postponing the onset of the decision process by as little as 50 to 100 milliseconds enables the brain to focus attention on the most relevant information and block out irrelevant distractors,” said last author Jack Grinband, PhD, associate research scientist in the Taub Institute and assistant professor of clinical radiology (physics). “This way, rather than working longer or harder at making the decision, the brain simply postpones the decision onset to a more beneficial point in time.”In making decisions, the brain integrates many small pieces of potentially contradictory sensory information. “Imagine that you’re coming up to a traffic light — the target — and need to decide whether the light is red or green,” said Dr. Teichert. “There is typically little ambiguity, and you make the correct decision quickly, in a matter of tens of milliseconds.”The decision process itself, however, does not distinguish between relevant and irrelevant information. Hence, a task is made more difficult if irrelevant information — a distractor — interferes with the processing of the target. …

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Brain differences linked to insomnia identified by researchers

Johns Hopkins researchers report that people with chronic insomnia show more plasticity and activity than good sleepers in the part of the brain that controls movement.”Insomnia is not a nighttime disorder,” says study leader Rachel E. Salas, M.D., an assistant professor of neurology at the Johns Hopkins University School of Medicine. “It’s a 24-hour brain condition, like a light switch that is always on. Our research adds information about differences in the brain associated with it.”Salas and her team, reporting in the March issue of the journal Sleep, found that the motor cortex in those with chronic insomnia was more adaptable to change — more plastic — than in a group of good sleepers. They also found more “excitability” among neurons in the same region of the brain among those with chronic insomnia, adding evidence to the notion that insomniacs are in a constant state of heightened information processing that may interfere with sleep.Researchers say they hope their study opens the door to better diagnosis and treatment of the most common and often intractable sleep disorder that affects an estimated 15 percent of the United States population.To conduct the study, Salas and her colleagues from the Department of Psychiatry and Behavioral Sciences and the Department of Physical Medicine and Rehabilitation used transcranial magnetic stimulation (TMS), which painlessly and noninvasively delivers electromagnetic currents to precise locations in the brain and can temporarily and safely disrupt the function of the targeted area. TMS is approved by the U.S. Food and Drug Administration to treat some patients with depression by stimulating nerve cells in the region of the brain involved in mood control.The study included 28 adult participants — 18 who suffered from insomnia for a year or more and 10 considered good sleepers with no reports of trouble sleeping. Each participant was outfitted with electrodes on their dominant thumb as well as an accelerometer to measure the speed and direction of the thumb.The researchers then gave each subject 65 electrical pulses using TMS, stimulating areas of the motor cortex and watching for involuntary thumb movements linked to the stimulation. Subsequently, the researchers trained each participant for 30 minutes, teaching them to move their thumb in the opposite direction of the original involuntary movement. They then introduced the electrical pulses once again.The idea was to measure the extent to which participants’ brains could learn to move their thumbs involuntarily in the newly trained direction. …

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Could PTSD involve immune cell response to stress? Study in mice raises question

Chronic stress that produces inflammation and anxiety in mice appears to prime their immune systems for a prolonged fight, causing the animals to have an excessive reaction to a single acute stressor weeks later, new research suggests.After the mice recovered from the effects of chronic stress, a single stressful event 24 days later quickly returned them to a chronically stressed state in biological and behavioral terms. Mice that had not experienced the chronic stress were unaffected by the single acute stressor.The study further showed that immune cells called to action as a result of chronic stress ended up on standby in the animals’ spleens and were launched from that organ to respond to the later stressor.Mice without spleens did not experience the same reactivation with the second stressor, signifying the spleen’s role as a reservoir for primed immune cells to remain until they’re activated in response to another stressor.The excessive immune response and anxiety initiated by a brief stressor mimic symptoms of post-traumatic stress disorder.The Ohio State University scientists are cautious about extending their findings to humans. But they say their decade of work with this model of stress suggests that the immune system has a significant role in affecting behavior. And they are the first to study this re-establishment of anxiety in animals with a later acute stressor.“No one else has done a study of this length to see what happens to recovered animals if we subject them again to stress,” said Jonathan Godbout, a lead author of the study and associate professor of neuroscience at Ohio State. “That retriggering is a component of post-traumatic stress. The previously stressed mice are living a normal rodent life, and then this acute stress brings everything back. Animals that have never been exposed to stress before were unaffected by that one event – it didn’t change behavioral or physiological properties.”The research is published online in the journal Biological Psychiatry.These scientists previously determined that in mice with chronic stress, cells from the immune system were recruited to the brain and promoted symptoms of anxiety. The findings identified a subset of immune cells, called monocytes, that could be targeted by drugs for treatment of mood disorders – including, potentially, the recurrent anxiety initiated by stress that is a characteristic of PTSD.The research reveals new ways of thinking about the cellular mechanisms behind the effects of stress, identifying two-way communication from the central nervous system to the periphery – the rest of the body – and back to the central nervous system that ultimately influences behavior.“We haven’t proffered that there is a cellular component to PTSD, but there very well might be. And it’s very possible that it sits in the periphery as we’ve been describing in the mouse,” said John Sheridan, senior author of the study, professor of oral biology and associate director of Ohio State’s Institute for Behavioral Medicine Research.In this model of stress, male mice living together are given time to establish a hierarchy, and then an aggressive male is added to the group for two hours at a time. The resident mice are repeatedly defeated, and this social defeat over six days leads to an inflammatory immune response and anxiety-like behavior.This kind of stress triggers the sympathetic nervous system and a commonly known fight-or-flight response. …

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Addicts and Disease

Commentary.Former National Institute on Drug Abuse (NIDA) director Alan Leshner has been vilified by many for referring to addiction as a chronic, relapsing “brain disease.” What often goes unmentioned is Leshner’s far more interesting characterization of addiction as the “quintessential biobehavioral disorder.”Multifactorial illnesses present special challenges to our way of thinking about disease. Addiction and other biopsychosocial disorders often show symptoms at odds with disease, as people generally understand it. For patients and medical professionals alike, questions about the disease aspect of addiction tie into larger fears about the medicalization of human behavior.These confusions are mostly understandable. Everybody knows what cancer is—a disease of the cells. Schizophrenia? Some kind of brain illness. But addiction? Addiction strikes many people as too much a part …

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Frequent school moves can increase the risk of psychotic symptoms in early adolescence

Researchers at Warwick Medical School have shown that frequently changing schools during childhood can increase the risk of psychotic symptoms in later years.The study, published in American Academy of Child and Adolescent Psychiatry, found that school mobility during childhood heightens the risk of developing psychotic-like symptoms in early adolescence by up to 60%.Suffering from psychotic-like symptoms at young age is strongly associated with mental health problems in adulthood, including psychotic disorders and suicide.Professor Swaran Singh, who led the study, explained, “Changing schools can be very stressful for students. Our study found that the process of moving schools may itself increase the risk of psychotic symptoms — independent of other factors. But additionally, being involved in bullying, sometimes as a consequence of repeated school moves, may exacerbate risk for the individual.”At the age of 12, participants in the study were interviewed to assess for the presence of psychotic-like symptoms including hallucinations, delusions and thought interference in the previous six months. Those that had moved school three or more times were found to be 60% more likely to display at least one definite psychotic symptom.The authors suggested that moving schools often may lead to feelings of low self-esteem and a sense of social defeat. This feeling of being excluded from the majority could also render physiological consequences leading to sensitisation of the mesolimbic dopamine system, heightening the risk of psychotic-like symptoms in vulnerable individuals.Dr Cath Winsper, Senior Research Fellow at Warwick Medical School and part of the study group said, “It’s clear that we need to keep school mobility in mind when clinically assessing young people with psychotic disorders. It should be explored as a matter of course as the impact can be both serious and potentially long lasting. Schools should develop strategies to help these students to establish themselves in their new environment.”Story Source:The above story is based on materials provided by University of Warwick. Note: Materials may be edited for content and length.

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How chronic stress predisposes brain to mental disorders

University of California, Berkeley, researchers have shown that chronic stress generates long-term changes in the brain that may explain why people suffering chronic stress are prone to mental problems such as anxiety and mood disorders later in life.Their findings could lead to new therapies to reduce the risk of developing mental illness after stressful events.Doctors know that people with stress-related illnesses, such as post-traumatic stress disorder (PTSD), have abnormalities in the brain, including differences in the amount of gray matter versus white matter. Gray matter consists mostly of cells — neurons, which store and process information, and support cells called glia — while white matter is composed of axons, which create a network of fibers that interconnect neurons. White matter gets its name from the white, fatty myelin sheath that surrounds the axons and speeds the flow of electrical signals from cell to cell.How chronic stress creates these long-lasting changes in brain structure is a mystery that researchers are only now beginning to unravel.In a series of experiments, Daniela Kaufer, UC Berkeley associate professor of integrative biology, and her colleagues, including graduate students Sundari Chetty and Aaron Freidman, discovered that chronic stress generates more myelin-producing cells and fewer neurons than normal. This results in an excess of myelin — and thus, white matter — in some areas of the brain, which disrupts the delicate balance and timing of communication within the brain.”We studied only one part of the brain, the hippocampus, but our findings could provide insight into how white matter is changing in conditions such as schizophrenia, autism, depression, suicide, ADHD and PTSD,” she said.The hippocampus regulates memory and emotions, and plays a role in various emotional disorders.Kaufer and her colleagues published their findings in the Feb. 11 issue of the journal Molecular Psychiatry.Does stress affect brain connectivity?Kaufer’s findings suggest a mechanism that may explain some changes in brain connectivity in people with PTSD, for example. One can imagine, she said, that PTSD patients could develop a stronger connectivity between the hippocampus and the amygdala — the seat of the brain’s fight or flight response — and lower than normal connectivity between the hippocampus and prefrontal cortex, which moderates our responses.”You can imagine that if your amygdala and hippocampus are better connected, that could mean that your fear responses are much quicker, which is something you see in stress survivors,” she said. “On the other hand, if your connections are not so good to the prefrontal cortex, your ability to shut down responses is impaired. So, when you are in a stressful situation, the inhibitory pathways from the prefrontal cortex telling you not to get stressed don’t work as well as the amygdala shouting to the hippocampus, ‘This is terrible!’ You have a much bigger response than you should.”She is involved in a study to test this hypothesis in PTSD patients, and continues to study brain changes in rodents subjected to chronic stress or to adverse environments in early life.Stress tweaks stem cellsKaufer’s lab, which conducts research on the molecular and cellular effects of acute and chronic stress, focused in this study on neural stem cells in the hippocampus of the brains of adult rats. These stem cells were previously thought to mature only into neurons or a type of glial cell called an astrocyte. The researchers found, however, that chronic stress also made stem cells in the hippocampus mature into another type of glial cell called an oligodendrocyte, which produces the myelin that sheaths nerve cells.The finding, which they demonstrated in rats and cultured rat brain cells, suggests a key role for oligodendrocytes in long-term and perhaps permanent changes in the brain that could set the stage for later mental problems. …

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Excess weight linked to brain changes that may relate to memory, emotions, and appetite

Being overweight appears related to reduced levels of a molecule that reflects brain cell health in the hippocampus, a part of the brain involved in memory, learning, and emotions, and likely also involved in appetite control, according to a study performed by researchers at SUNY Downstate Medical Center and other institutions. The results of the study were published in Neuroimage: Clinical.Jeremy D. Coplan, MD, professor of psychiatry at SUNY Downstate, led a multicenter team that visualized the molecule, N-acetyl-aspartate (NAA), using magnetic resonance spectroscopy, a non-invasive magnetic resonance imaging (MRI) application. NAA is associated with brain cell health. Overweight study participants exhibited lower levels of NAA in the hippocampus than normal weight subjects. The effect was independent of age, sex, and psychiatric diagnoses.The importance of the hippocampus — a seahorse-shaped organ deep within the brain — to the formation and preservation of memory and to emotional control is well known, Dr. Coplan notes, but its role in appetite control is less established.”The relevance of the finding is that being overweight is associated with specific changes in a part of the brain that is crucial to memory formation and emotions, and probably to appetite,” said Dr. Coplan. The study is believed to be the first human research documenting the association of NAA with body weight.”Whether low NAA is a consequence of being overweight, causes being overweight, or a combination of both remains to be determined,” Dr. Coplan added. …

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Gender influences symptoms of genetic disorder NF1

A genetic disorder that affects about 1 in every 2,500 births can cause a bewildering array of clinical problems, including brain tumors, impaired vision, learning disabilities, behavioral problems, heart defects and bone deformities. The symptoms and their severity vary among patients affected by this condition, known as neurofibromatosis type 1 (NF1).Now, researchers at Washington University School of Medicine in St. Louis have identified a patient’s gender as a clear and simple guidepost to help health-care providers anticipate some of the effects of NF1. The scientists report that girls with NF1 are at greater risk of vision loss from brain tumors. They also identified gender-linked differences in male mice that may help explain why boys with NF1 are more vulnerable to learning disabilities.”This information will help us adjust our strategies for predicting the potential outcomes in patients with NF1 and recommending appropriate treatments,” said David H. Gutmann, MD, PhD, the Donald O. Schnuck Family Professor of Neurology, who treats NF1 patients at St. Louis Children’s Hospital.The findings appear online in the Annals of Neurology.Kelly Diggs-Andrews, PhD, a postdoctoral research associate in Gutmann’s laboratory, reviewed NF1 patient data collected at the Washington University Neurofibromatosis (NF) Center. In her initial assessment, Diggs-Andrews found that the number of boys and girls was almost equal in a group of nearly 100 NF1 patients who had developed brain tumors known as optic gliomas. But vision loss occurred three times more often in girls with these tumors.With help from David Wozniak, PhD, research professor of psychiatry, the scientists looked for an explanation in Nf1 mice (which, like NF1 patients, have a mutation in their Nf1 gene). …

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What falling in love does to your heart and brain

Getting struck by Cupid’s arrow may very well take your breath away and make your heart go pitter-patter this Valentine’s Day, reports sexual wellness specialists at Loyola University Health System.”Falling in love causes our body to release a flood of feel-good chemicals that trigger specific physical reactions,” said Pat Mumby, PhD, co-director of the Loyola Sexual Wellness Clinic and professor, Department of Psychiatry & Behavioral Neurosciences, Loyola University Chicago Stritch School of Medicine (SSOM). “This internal elixir of love is responsible for making our cheeks flush, our palms sweat and our hearts race.”Levels of these substances, which include dopamine, adrenaline and norepinephrine, increase when two people fall in love. Dopamine creates feelings of euphoria while adrenaline and norepinephrine are responsible for the pitter-patter of the heart, restlessness and overall preoccupation that go along with experiencing love.MRI scans indicate that love lights up the pleasure center of the brain. When we fall in love, blood flow increases in this area, which is the same part of the brain implicated in obsessive-compulsive behaviors.”Love lowers serotonin levels, which is common in people with obsessive-compulsive disorders,” said Mary Lynn, DO, co-director of the Loyola Sexual Wellness Clinic and assistant professor, Department of Obstetrics & Gynecology, SSOM. “This may explain why we concentrate on little other than our partner during the early stages of a relationship.”Doctors caution that these physical responses to love may work to our disadvantage.”The phrase ‘love is blind’ is a valid notion because we tend to idealize our partner and see only things that we want to see in the early stages of the relationship,” Dr. Mumby said. “Outsiders may have a much more objective and rational perspective on the partnership than the two people involved do.”There are three phases of love, which include lust, attraction and attachment. Lust is a hormone-driven phase where we experience desire. Blood flow to the pleasure center of the brain happens during the attraction phase, when we feel an overwhelming fixation with our partner. This behavior fades during the attachment phase, when the body develops a tolerance to the pleasure stimulants. …

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Gene that influences receptive joint attention in chimpanzees gives insight into autism

Following another’s gaze or looking in the direction someone is pointing, two examples of receptive joint attention, is significantly heritable according to new study results from researchers at the Yerkes National Primate Research Center, Emory University. Determining such communicative cues are significantly heritable means variation in this ability has a genetic basis, which led the researchers to the vasopressin receptor gene, known for its role in social bonding.The study results, which are published in Scientific Reports, give researchers insight into the biology of disorders in which receptive joint attention is compromised, such as autism spectrum disorders (ASD), and may ultimately lead to new diagnosis and treatment strategies.According to Yerkes researchers Larry Young, PhD, and Bill Hopkins, PhD, co-authors of the study, receptive joint attention is important for developing complex cognitive processes, including language and theory of mind, and poor joint attention abilities may be a core feature in children with or at risk of developing ASD.Young is division chief of Behavioral Neuroscience and Psychiatric Disorders at Yerkes, director of the Center for Translational Social Neuroscience (CTSN) at Emory and William P. Timmie Professor in the Emory University School of Medicine Department of Psychiatry and Behavioral Sciences. Yerkes researcher Hopkins is also a core faculty member in the Neuroscience Institute of Georgia State University and newly named science director of the Iowa Primate Learning Sanctuary.Young and Hopkins led a collaborative team of researchers from Yerkes, the CTSN, the Neuroscience Institute at Georgia State University and the University of Texas M.D. Anderson Cancer Center. They studied chimpanzees to determine the extent to which the animals follow gaze or pointing by a human.”We used chimpanzees in this behavioral study because their receptive joint attention abilities are well documented and their closeness to humans makes the study results the most likely to be generalizable to humans,” says Hopkins.Young’s previous research in which he showed the vasopressin receptor gene was necessary for remembering individuals (or social memories) and for social bonding in male rodents was key to designing the current study. According to Young, variation in the length of a stretch of repetitive DNA, known as junk DNA, in the control region of the vasopressin receptor gene predicted if a male prairie vole was likely to form monogamous bonds with a mate. Human-based studies suggest that a similar repetitive element, referred to as RS3, in the control region of the human vasopressin receptor gene predicts romantic relationship quality and generosity.The current research team discovered about two-thirds of chimpanzees are completely missing the RS3 element that seems to influence social relationships in humans, while the remaining one third has the human-like sequence.”Male chimpanzees with the human-like RS3 sequence displayed higher levels of joint attention and, therefore, needed fewer social cues to elicit an orienting response in the same direction as the experimenter than those missing the sequence,” says Hopkins. “There was no effect of this gene in female chimpanzees, consistent with the vole and human studies in which the vasopressin gene specifically affects male social behaviors,” Young adds.A previous study by Hopkins and his M.D. Anderson-based colleagues found male chimpanzees with the human-like RS3 sequence were more dominant than males lacking the RS3. …

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Theatre offers promise for youth with autism

Oct. 22, 2013 — A novel autism intervention program using theatre to teach reciprocal communication skills is improving social deficits in adolescents with the disorder that now affects an estimated one in 88 children, Vanderbilt University researchers released today in the journal Autism Research.The newly released study assessed the effectiveness of a two-week theatre camp on children with autism spectrum disorder and found significant improvements were made in social perception, social cognition and home living skills by the end of the camp. There were also positive changes in the participants’ physiological stress and reductions in self-reported parental stress.Called SENSE Theatre, the Social Emotional Neuroscience & Endocrinology (SENSE) program evaluates the social functioning of children with autism and related neurodevelopmental disorders.Camp participants ages 8 to 17 years join with typically developing peers who are specially trained to serve as models for social interaction and communication, skills that are difficult for children with autism. The camp uses techniques such as role-play and improvisation and culminates in public performances of a play.”The findings show that treatment can be delivered in an unconventional setting, and children with autism can learn from unconventional ‘interventionists’ — their typically developing peer,” said lead author Blythe Corbett, Ph.D., associate professor of Psychiatry and Vanderbilt Kennedy Center investigator.Social perception and interaction skills were measured before and after the camp using neuropsychological measures, play with peers and parental reporting. Significant differences were found in face processing, social awareness and social cognition, and duration of interaction with familiar peers increased significantly over the course of the camp.Additionally, the stress hormone cortisol was measured through saliva samples taken both at home and throughout the camp to compare the stress level of participants at home, at the beginning of the camp and at the end of the camp. Cortisol levels rose on the first day of camp when compared to home values but declined by the end of treatment and during post-treatment play with peers.”Our findings show that the SENSE Theatre program contributes to improvement in core social deficits when engaging with peers both on and off the stage,” Corbett said. “This research also shows it’s never too late to make a significant difference in the lives of children and youth with autism spectrum disorder, as [this program] targets children who are much older than kids who are participating in early intervention, yet we are still seeing significant gains in the core deficits of autism, and in a rather brief intervention.”This research was supported by the Martin McCoy-Jesperson Discovery Grant in Positive Psychology and a grant from the National Institute of Mental Health (Grant No. R01 MH085717).Corbett will continue using theatre techniques to study areas of social functioning among children with autism through a newly awarded grant from the National Institute of Mental Health (Grant No. R34 MH097793). This forthcoming study will explore treatment length and peer familiarity as factors in optimizing and generalizing gains and will enroll more than 30 youth with autism ages 8 to 16 in a 10-week program model beginning January 2014.

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How Schizophrenia affects the brain

Sep. 11, 2013 — It’s hard to fully understand a mental disease like schizophrenia without peering into the human brain. Now, a study by University of Iowa psychiatry professor Nancy Andreasen uses brain scans to document how schizophrenia impacts brain tissue as well as the effects of anti-psychotic drugs on those who have relapses.Andreasen’s study, published in the American Journal of Psychiatry, documented brain changes seen in MRI scans from more than 200 patients beginning with their first episode and continuing with scans at regular intervals for up to 15 years. The study is considered the largest longitudinal, brain-scan data set ever compiled, Andreasen says. Schizophrenia affects roughly 3.5 million people, or about one percent of the U.S. population, according to the National Institutes of Health. Globally, some 24 million are affected, according to the World Health Organization.The scans showed that people at their first episode had less brain tissue than healthy individuals. The findings suggest that those who have schizophrenia are being affected by something before they show outward signs of the disease.”There are several studies, mine included, that show people with schizophrenia have smaller-than-average cranial size,” explains Andreasen, whose appointment is in the Carver College of Medicine. “Since cranial development is completed within the first few years of life, there may be some aspect of earliest development — perhaps things such as pregnancy complications or exposure to viruses — that on average, affected people with schizophrenia.”Andreasen’s team learned from the brain scans that those affected with schizophrenia suffered the most brain tissue loss in the two years after the first episode, but then the damage curiously plateaued — to the group’s surprise. The finding may help doctors identify the most effective time periods to prevent tissue loss and other negative effects of the illness, Andreasen says.The researchers also analyzed the effect of medication on the brain tissue. …

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Brain imaging study reveals the wandering mind behind insomnia

Aug. 30, 2013 — new brain imaging study may help explain why people with insomnia often complain that they struggle to concentrate during the day even when objective evidence of a cognitive problem is lacking.”We found that insomnia subjects did not properly turn on brain regions critical to a working memory task and did not turn off ‘mind-wandering’ brain regions irrelevant to the task,” said lead author Sean P.A. Drummond, PhD, associate professor in the department of psychiatry at the University of California, San Diego, and the VA San Diego Healthcare System, and Secretary/Treasurer of the Sleep Research Society. “Based on these results, it is not surprising that someone with insomnia would feel like they are working harder to do the same job as a healthy sleeper.”The research team led by Drummond and co-principal investigator Matthew Walker, PhD, studied 25 people with primary insomnia and 25 good sleepers. Participants had an average age of 32 years. The study subjects underwent a functional magnetic resonance imaging scan while performing a working memory task.Results published in the September issue of the journal Sleep show that participants with insomnia did not differ from good sleepers in objective cognitive performance on the working memory task. However, the MRI scans revealed that people with insomnia could not modulate activity in brain regions typically used to perform the task.As the task got harder, good sleepers used more resources within the working memory network of the brain, especially the dorsolateral prefrontal cortex. Insomnia subjects, however, were unable to recruit more resources in these brain regions. Furthermore, as the task got harder, participants with insomnia did not dial down the “default mode” regions of the brain that are normally only active when our minds are wandering.”The data help us understand that people with insomnia not only have trouble sleeping at night, but their brains are not functioning as efficiently during the day,” said Drummond. “Some aspects of insomnia are as much of a daytime problem as a nighttime problem. …

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A cautionary note on oxytocin as a treatment for psychiatric disorders

Aug. 12, 2013 — The hormone oxytocin is known for its widespread effects on social and reproductive processes, and recent data from intranasal administration in humans has produced hope for its use as a therapeutic in autism, schizophrenia, and other disorders.However, this leap to human use is happening without previous animal studies of long-term oxytocin administration, and without knowledge of the neurobiological mechanisms involved in the behavioral findings.A new study now published in Biological Psychiatry indicates that the promising short-term effects often observed after a single dose of oxytocin may not translate to positive effects after long-term administration.This research was led by Dr. Karen Bales, Professor and Vice Chair of Psychology at the University of California. She and her colleagues examined the long-term effects of oxytocin treatment using the prairie vole, a small rodent that forms strong life-long pair bonds and is thus often used in studies of social behavior.Both male and female voles were treated with one of three dosages of intranasal oxytocin, administered daily from weaning through sexual maturity. During this time, the researchers observed and recorded the voles’ social interactions. They also conducted tests of social and anxiety-related behaviors in the adult voles, after the oxytocin treatment had finished, allowing them to measure any long-term effects.As expected, oxytocin treatment increased social behavior in male voles, similar to the effects repeatedly observed in humans. However, the long-term effects were concerning, with male voles showing deficits in their typical behaviors.”In this study, we showed that long-term exposure to oxytocin in adolescent male prairie voles led to disruption of social bond formation in these males as adults,” explained Bales. “Male prairie voles which received a dose similar to that being tested in humans, or even a lower dose, did not form pair-bonds normally with their pair-mate. Instead these males chose to associate with a strange female.”This important finding should suggest caution in the long-term use of intranasal oxytocin in developing humans.”The fact that long term treatment with oxytocin had the opposite impact of initial doses with the same substance suggests that special strategies will be needed if oxytocin is ever to become a long-term treatment for autism or schizophrenia,” said Dr. John Krystal, Editor of Biological Psychiatry.Bales agrees, and added, “In our continuing research program, we also have preliminary data suggesting that these treatments caused long-term changes in the oxytocin system. …

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Human cells respond in healthy, unhealthy ways to different kinds of happiness

July 29, 2013 — Human bodies recognize at the molecular level that not all happiness is created equal, responding in ways that can help or hinder physical health, according to new research led by Barbara L. Fredrickson, Kenan Distinguished Professor of psychology in the College of Arts and Sciences at the University of North Carolina at Chapel Hill.The sense of well-being derived from “a noble purpose” may provide cellular health benefits, whereas “simple self-gratification” may have negative effects, despite an overall perceived sense of happiness, researchers found. “A functional genomic perspective on human well-being” was published July 29 in Proceedings of the National Academy of Sciences.”Philosophers have long distinguished two basic forms of well-being: a ‘hedonic’ [hee-DON-ic] form representing an individual’s pleasurable experiences, and a deeper ‘eudaimonic,’ [u-DY-moh-nick] form that results from striving toward meaning and a noble purpose beyond simple self-gratification,” wrote Fredrickson and her colleagues.It’s the difference, for example, between enjoying a good meal and feeling connected to a larger community through a service project, she said. Both give us a sense of happiness, but each is experienced very differently in the body’s cells.”We know from many studies that both forms of well-being are associated with improved physical and mental health, beyond the effects of reduced stress and depression,” Fredrickson said. “But we have had less information on the biological bases for these relationships.”Collaborating with a team from the University of California at Los Angeles led by Steven W. Cole, professor of medicine, psychiatry and behavioral sciences, Fredrickson and her colleagues looked at the biological influence of hedonic and eudaimonic well-being through the human genome. They were interested in the pattern of gene expression within people’s immune cells.Past work by Cole and colleagues had discovered a systematic shift in gene expression associated with chronic stress, a shift “characterized by increased expression of genes involved in inflammation” that are implicated in a wide variety of human ills, including arthritis and heart disease, and “decreased expression of genes involved in … antiviral responses,” the study noted. Cole and colleagues coined the phrase “conserved transcriptional response to adversity” or CTRA to describe this shift. In short, the functional genomic fingerprint of chronic stress sets us up for illness, Fredrickson said.But if all happiness is created equal, and equally opposite to ill-being, then patterns of gene expression should be the same regardless of hedonic or eudaimonic well-being. Not so, found the researchers.Eudaimonic well-being was, indeed, associated with a significant decrease in the stress-related CTRA gene expression profile. …

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Isolated psychiatric episodes rare, but possible, in common form of autoimmune encephalitis

July 26, 2013 — A small percentage of people diagnosed with a mysterious neurological condition may only experience psychiatric changes — such as delusional thinking, hallucinations, and aggressive behavior — according to a new study by researchers in the Perelman School of Medicine at the University of Pennsylvania. In addition, people who had previously been diagnosed with this disease, called anti-NMDA receptor (anti-NMDAR) encephalitis, had relapses that only involved psychiatric behavior.In an article published Online First in JAMA Neurology, researchers suggest that, while isolated psychiatric episodes are rare in anti-NMDAR encephalitis cases, abnormal test findings or subtle neurological symptoms should prompt screening for the condition, as it is treatable with immunotherapies.Within a large group of 571 patients with confirmed Anti-NMDAR Encephalitis, only 23 patients (4 percent) had isolated psychiatric episodes. Of the 23, 5 patients experienced the onset of behavior changes as their only symptoms, without neurological changes, while 18 patients had psychiatric symptoms emerge at the outset of a relapse of Anti-NMDAR Encephalitis in which no neurological changes were identified. After being treated for the condition, 83 percent of these patients recovered substantially or completely.”While many patients with Anti-NMDAR Encephalitis present with isolated psychiatric symptoms, most of these patients subsequently develop, in a matter of days, additional neurological symptoms which help to make the diagnosis of the disease. In the current study, we find out that a small percentage of patients do not develop neurological symptoms, or sometimes these are very subtle and transitory. Studies using brain MRI and analysis of the cerebrospinal fluid may help to demonstrate signs of inflammation,” said Josep Dalmau, MD, PhD, adjunct professor of Neurology. “For patients who have been previously diagnosed with Anti-NMDAR Encephalitis and are in remission, any behavior change may present a relapse and should be tested quickly and treated aggressively.”Anti-NMDAR Encephalitis is one of the most common forms of autoimmune encephalitis, and symptoms can include psychiatric symptoms, memory issues, speech disorders, seizures, involuntary movements, and loss of consciousness. In an earlier Penn Medicine study, 38 percent of all patients (and 46 percent of females with the condition) were found to have a tumor, most commonly it was an ovarian tumor. When correctly diagnosed and treated early, Anti-NMDAR Encephalitis can be effectively treated.”For patients with new psychotic symptoms that are evaluated in centers where an MRI, EEG or spinal fluid test may not have been administered, there is a chance that Anti-NMDAR Encephalitis may be missed,” said lead author Matthew Kayser, MD, PhD, postdoctoral fellow and attending physician in Psychiatry at Penn. “However, the likelihood of pure or isolated new-onset psychosis to be anti-NMDAR encephalitis gradually decreases if no other symptoms emerge during the first 4 weeks of psychosis.”Anti-NMDAR Encephalitis was first characterized by Penn’s Josep Dalmau, MD, PhD, adjunct professor of Neurology, and David R. …

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Bipolar disorder takes different path in patients who binge eat, study suggests

July 25, 2013 — Bipolar disorder evolves differently in patients who also binge eat, a study by Mayo Clinic, the Lindner Center of HOPE and the University of Minnesota found. Binge eating and obesity often are present among bipolar patients, but the mood disorder appears to take a different path in those who binge eat than it does in obese bipolar patients who do not, the researchers discovered.The findings are published online in the Journal of Affective Disorders.Up to 4 percent of Americans have some form of bipolar illness, and of those, just under 10 percent also have binge eating disorder — a higher rate of binge eating than seen in the general population, says co-author Mark Frye, M.D., a psychiatrist and chair of the Department of Psychiatry/Psychology at Mayo Clinic in Rochester. The Diagnostic and Statistical Manual of Mental Disorders (DSM-5) update released this spring recognizes binge eating disorder as a distinct condition, he noted.Bipolar patients who binge eat are more likely to have other mental health issues such as suicidal thoughts, psychosis, anxiety disorders and substance abuse, the study found. People with bipolar disorder who are obese but do not binge eat are more likely to have serious physical problems such as arthritis, diabetes, high blood pressure and heart disease.It was more common for women than men with bipolar disorder to binge eat or to be obese, the study showed.”The illness is more complicated, and then by definition how you would conceptualize how best to individualize treatment is more complicated,” Dr. Frye says. “It really underscores the importance of trying to stabilize mood, because we know when people are symptomatic of their bipolar illness their binge frequency is likely to increase. We want to work with treatments that can be helpful but not have weight gain as a significant side effect.”The researchers used the Mayo Clinic Bipolar Biobank, a collaborative effort by Mayo Clinic, the Lindner Center of HOPE, University of Minnesota and Mayo Clinic Health System. More research is planned to see whether there is a genetic link to binge eating disorder in bipolar disease.”Patients with bipolar disorder and binge eating disorder appear to represent a more severely ill population of bipolar patients. Identification of this subgroup of patients will help determine the underlying causes of bipolar disorder and lead to more effective and personalized treatments,” says co-author Susan McElroy, M.D., chief research officer at the Lindner Center of HOPE.The study was funded by the Marriott family. Co-authors also include Scott Crow, M.D., University of Minnesota Medical School; Nicole Mori of the Lindner Center of HOPE; and Joanna Biernacka, Ph.D., Stacey Winham, Ph.D., Jennifer Geske, Alfredo Cuellar Barboza, M.D., Mikel Prieto, M.D., Mohit Chauhan, M.D., and Lisa Seymour of Mayo Clinic.

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Note to teens: Just breathe

July 9, 2013 — In May, the Los Angeles school board voted to ban suspensions of students for “willful defiance” and directed school officials to use alternative disciplinary practices. The decision was controversial, and the question remains: How do you discipline rowdy students and keep them in the classroom while still being fair to other kids who want to learn?A team led by Dara Ghahremani, an assistant researcher in the department of psychiatry at UCLA’s Semel Institute for Neuroscience and Human Behavior conducted a study on the Youth Empowerment Seminar, or YES!, a workshop for adolescents that teaches them to manage stress, regulate their emotions, resolve conflicts and control impulsive behavior. Impulsive behavior, in particular — including acting out in class, engaging in drug or alcohol abuse, and risky sexual behaviors — is something that gets adolescents in trouble.The YES! program, run by the nonprofit International Association for Human Values, includes yoga-based breathing practices, among other techniques, and the research findings show that a little bit of breathing can go a long way. The scientists report that students who went through the four-week YES! for Schools program felt less impulsive, while students in a control group that didn’t participate in the program showed no change.The study appears in the July issue of the Journal of Adolescent Health.”The program helps teens to gain greater control over their actions by giving them tools to respond to challenging situations in constructive and mindful ways, rather than impulsively,” said Ghahremani, who conducted the study at the UCLA Center for Addictive Behaviors and UCLA’s Laboratory for Molecular Neuroimaging. “The program uses a variety of techniques, ranging from a powerful yoga-based breathing program called Sudarshan Kriya to decision-making and leadership skills that are taught via interactive group games. We found it to be a simple yet powerful approach that could potentially reduce impulsive behavior.”Ghahremani noted that teens are often just as stressed as adults.”There are home and family issues, academic pressures and, of course, social pressures,” he said. “With the immediacy and wide reach of communication technology, like Facebook, peer pressure and bullying has risen to a whole new level. Without the tools to handle such pressures, teens can often resort to impulsive acts that include violence towards others or themselves.”Impulsive behavior, or a lack of self-control, in adolescence is a key predictor of risky behavior, Ghahremani said.”Substance abuse and various mental health problems that begin in adolescence are often very difficult to shake in adulthood — there is a need for interventions that bring impulsive behavior under control in this group,” he said. …

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Brain differences seen in depressed preschoolers

July 1, 2013 — A key brain structure that regulates emotions works differently in preschoolers with depression compared with their healthy peers, according to new research at Washington University School of Medicine in St. Louis.The differences, measured using functional magnetic resonance imaging (fMRI), provide the earliest evidence yet of changes in brain function in young children with depression. The researchers say the findings could lead to ways to identify and treat depressed children earlier in the course of the illness, potentially preventing problems later in life.”The findings really hammer home that these kids are suffering from a very real disorder that requires treatment,” said lead author Michael S. Gaffrey, PhD. “We believe this study demonstrates that there are differences in the brains of these very young children and that they may mark the beginnings of a lifelong problem.”The study is published in the July issue of the Journal of the American Academy of Child & Adolescent Psychiatry.Depressed preschoolers had elevated activity in the brain’s amygdala, an almond-shaped set of neurons important in processing emotions. Earlier imaging studies identified similar changes in the amygdala region in adults, adolescents and older children with depression, but none had looked at preschoolers with depression.For the new study, scientists from Washington University’s Early Emotional Development Program studied 54 children ages 4 to 6. Before the study began, 23 of those kids had been diagnosed with depression. The other 31 had not. None of the children in the study had taken antidepressant medication.Although studies using fMRI to measure brain activity by monitoring blood flow have been used for years, this is the first time that such scans have been attempted in children this young with depression. Movements as small as a few millimeters can ruin fMRI data, so Gaffrey and his colleagues had the children participate in mock scans first. …

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