New brain pathways for understanding type 2 diabetes and obesity uncovered

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

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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

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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

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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

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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

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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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