Chapter 12. Psychopathology: Biological Basis of Behavioral Disorders
Follow us on Facebook and Twitter, or subscribe to our mailing list, to receive news updates. Learn more.
By Chris Wodskou, CBC News For the past 25 years, people suffering from depression have been treated with antidepressant drugs like Zoloft, Prozac and Paxil — three of the world’s best-selling selective serotonin reuptake inhibitors, or SSRIs. But people are questioning whether these drugs are the appropriate treatment for depression, and if they could even be causing harm. The drugs are designed to address a chemical imbalance in the brain and thereby relieve the symptoms of depression. In this case, it’s a shortage of serotonin that antidepressants work to correct. In fact, there are pharmaceutical treatments targeting chemical imbalances for just about every form of mental illness, from schizophrenia to ADHD, and a raft of anxiety disorders. Hundreds of millions of prescriptions are written for antipsychotic, antidepressant and anti-anxiety medications every year in the United States alone, producing billions of dollars in revenue for pharmaceutical companies. But what if the very premise behind these drugs is flawed? What if mental illnesses like depression aren’t really caused by chemical imbalances, and that millions of the people who are prescribed those drugs derive no benefit from them? And what if those drugs could actually make their mental illness worse and more intractable over the long term? Investigative journalist Robert Whitaker argued that psychiatric drugs are a largely ineffective way of treating mental illness in his 2010 book called Anatomy of an Epidemic: Magic Bullets, Psychiatric Drugs and the Astonishing Rise of Mental Illness in America. Whitaker maintains that the foundation of modern psychiatry, the chemical imbalance model, is scientifically unproven. © CBC 2014
Link ID: 19712 - Posted: 06.09.2014
By Meeri Kim, Many of us find ourselves swimming along in the tranquil sea of life when suddenly a crisis hits — a death in the family, the loss of a job, a bad breakup. Some power through and find calm waters again, while others drown in depression. Scientists continue to search for the underlying genes and neurobiology that dictate our reactions to stress. Now, a study using mice has found a switch-like mechanism between resilience and defeat in an area of the brain that plays an important role in regulating emotions and has been linked with mood and anxiety disorders. (Bo Li/Cold Spring Harbor Laboratory) - Researchers at Cold Spring Harbor Laboratory identify the neurons in the brain that determine if a mouse will learn to cope with stress or become depressed. These neurons, located in a region of the brain known as the medial prefrontal cortex (top, green image) become hyperactive in depressed mice. The bottom panel is close-up of above image - yellow indicates activation. The team showed that this enhanced activity causes depression. After artificially enhancing the activity of neurons in that part of the brain — the medial prefrontal cortex — mice that previously fought to avoid electric shocks started to act helpless. Rather than leaping for an open escape route, they sat in a corner taking the pain — presumably out of a belief that nothing they could do would change their circumstances. “This helpless behavior is quite similar to what clinicians see in depressed individuals — an inability to take action to avoid or correct a difficult situation,” said study author and neuroscientist Bo Li of the Cold Spring Harbor Laboratory in New York. The results were published online May 27 in the Journal of Neuroscience. © 1996-2014 The Washington Post
Link ID: 19704 - Posted: 06.06.2014
by Bethany Brookshire We all respond to stress in different ways. Some of us work harder. Others drink more or eat our feelings. Sometimes we experience sleep loss, heart palpitations or sweats. When the stress dissipates, many of us go back to our daily lives, none the worse for wear. We are resilient. But some people find that stress is a first step on the way to a major depressive episode. It’s not quite clear what’s different between people who go back to normal after stress, and those who descend into depression. “One of the most important questions is, how do the brains of resilient animals (or humans) differ from those that are vulnerable to depression following stress?” asks John Morrison, a neuroscientist at the Icahn School of Medicine at Mount Sinai in New York. A new study from Minghui Wang and colleagues at Cold Spring Harbor Laboratory in New York provides a new hint. Mice with a depressive-like response to stress have stronger connections between neurons in the medial prefrontal cortex of the brain following the stress. Resilient mice show weaker connections. The mechanism could help scientists understand why some people respond to stress with depression, while others are able to shake it off. The prefrontal cortex is best known for its role in executive function — thought, memory, prediction and other tasks. But dysfunction in some areas of the cortex, particularly one called Brodmann area 25, has been linked with recurring major depressive disorder. Scientists have been electrically stimulating this area to relieve depression in patients. But researchers still don’t understand what makes this brain area important in depression, and how dysfunctions might occur. “I’ve had a long interest in the mechanism of human diseases like depression,” says study coauthor Bo Li, a cellular and behavioral neuroscientist at Cold Spring Harbor. “The idea has been to identify an area that is responsible, to link a mechanism in the brain to a behavior.” Wang, Li and their colleagues were especially interested in changes to the mouse prefrontal cortex following stress. © Society for Science & the Public 2000 - 2013.
Joy Jernigan TODAY contributor Depression is a serious medical condition that affects millions of Americans — and nearly twice as many women as men. Symptoms can include persistent feelings of sadness or hopelessness and loss of interest in activities that were once pleasurable, according to the National Institute of Mental Health. Other symptoms include feelings of guilt or worthlessness, irritability, changes in appetite, increased fatigue, difficulty concentrating — even recurrent thoughts of suicide. About 12 million American women suffer from depression each year, women like Debi Lee. Although depression is treatable, most commonly with medications or counseling, many never seek help, often because they are too embarrassed or ashamed. "Depression is really a physical illness," said Dr. Andrew Leuchter, a psychiatrist at the Semel Institute for Neuroscience and Human Behavior at University of California, Los Angeles. It's a disorder that even can be seen in brain scans, with images clearly showing the difference between a normal functioning brain and the brain of someone suffering from depression. "When you show this image to a person who's struggling with depression and you show them that their brain looks different than the quote so-called healthy person, what's their reaction?" Shriver asked. "It's commonly one of relief," Leuchter said. Now, Dr. Leuchter says there's an innovative new treatment called synchronized transcranial magnetic stimulation, or sTMS, that may have the potential to provide relief. Dr. Leuchter, a consultant and stockholder in the company behind sTMS, says it syncs to each patient's brain, then stimulates it with low levels of magnetic energy, 30 minutes a day for several weeks.
Link ID: 19689 - Posted: 06.04.2014
By Lara Salahi A team of researchers at Massachusetts General Hospital have embarked on a new project to create an implantable device in the brain that would read and alter the emotions of someone with a mental illness. The team is working in collaboration with researchers at the University of California, San Francisco, on a new program funded by the Department of Defense’s Defense Advanced Research Projects Agency (DARPA). The researchers are working to create an implantable device that can sense abnormal activity in the brain using algorithms, and then deliver electrical impulses to certain parts of the brain that would suppress the abnormal signals. “Imagine if I have an addiction to alcohol and I have a craving,” Jose Carmena, a researcher at the University of California, Berkeley, who is involved in the project, told MIT Technology Review. “We could detect that feeling and then stimulate inside the brain to stop it from happening.” Mental illness and suicide rates among the US military have spiked over the past decade, the National Institute of Mental Healthreports. The current research is part of DARPA’s emerging neurotechnology therapy program which investigates new approaches to treat neuropsychological illnesses among military servicemembers and veterans. Their goal is to treat at least seven psychiatric conditions, including depression, post-traumatic stress disorder, addiction, and fibromyalgia.
Jyoti Madhusoodanan Most people handle stress well, but some find it difficult to cope and as a result develop depression and other mood disorders. Researchers have previously been able to identify the part of the brain that controls this response, but not exactly how it does so. Now, a study in mice identifies a small group of neurons that could be responsible. The research might also help elucidate the mechanism of deep brain stimulation, a therapy that uses electrical impulses to treat depression and other neurological disorders. How an animal deals with stress is controlled by a part of the brain known as the prefrontal cortex, and the neurons in this part of the brain are known to change in structure and function in response to stressful situations1. To look at the cellular basis of the responses, neuroscientist Bo Li of Cold Spring Harbor Laboratory in New York and his colleagues subjected mice to small electric shocks at random intervals to produce stress. Most of the mice tried to avoid the shocks, but just over one-fifth did not. They also started to avoid other animals or failed to choose tasty foods over plain ones — typical signs of depressive behaviour. The researchers then looked at the animals' brains and found that a specific set of neurons in the prefrontal cortex were easily excitable in depressed mice, but much harder to excite in those resilient to the stress. Furthermore, artificially increasing the activity of these neurons caused mice that were once resilient to become susceptible to depressive behaviours. “We were surprised that we were able to see a difference between depressed and resilient animals at the level of synaptic transmission,” says Li. © 2014 Nature Publishing Group,
By NICHOLAS BAKALAR The hormone estrogen is the recommended treatment for menopausal night sweats and hot flashes, but some women are unable or unwilling to use it. Now a clinical trial suggests that the antidepressant venlafaxine, often used as an alternative, is equally effective. In an eight-week placebo-controlled double-blind study, researchers randomly assigned 339 perimenopausal and postmenopausal women to one of three treatments: 0.5 milligrams a day of estrogen (in the form of estradiol), 75 milligrams a day of the antidepressant venlafaxine (a generic form of Effexor), or a placebo. Before the start of the study, all the women had had symptoms at least 14 times a week. Compared to the rate before the study — an average of 8.1 episodes a day — the frequency of hot flashes and night sweats declined by 52.9 percent in the estradiol group, 47.6 percent in the Effexor group, and 28.6 percent among those who took a placebo. Both Effexor and estradiol were effective treatments, but the study, published online in JAMA Internal Medicine, was not large enough to show that one was significantly better than the other. “Women have important choices of different medications to discuss with their doctors,” said the lead author, Dr. Hadine Joffe, an associate professor of psychiatry at Harvard. “They should know, as they think about these options, that both are effective.” © 2014 The New York Times Company
Keyword: Hormones & Behavior
Link ID: 19673 - Posted: 05.31.2014
By JENEEN INTERLANDI Bessel van der Kolk sat cross-legged on an oversize pillow in the center of a smallish room overlooking the Pacific Ocean in Big Sur. He wore khaki pants, a blue fleece zip-up and square wire-rimmed glasses. His feet were bare. It was the third day of his workshop, “Trauma Memory and Recovery of the Self,” and 30 or so workshop participants — all of them trauma victims or trauma therapists — lined the room’s perimeter. They, too, sat barefoot on cushy pillows, eyeing van der Kolk, notebooks in hand. For two days, they had listened to his lectures on the social history, neurobiology and clinical realities of post-traumatic stress disorder and its lesser-known sibling, complex trauma. Now, finally, he was about to demonstrate an actual therapeutic technique, and his gaze was fixed on the subject of his experiment: a 36-year-old Iraq war veteran named Eugene, who sat directly across from van der Kolk, looking mournful and expectant. Van der Kolk began as he often does, with a personal anecdote. “My mother was very unnurturing and unloving,” he said. “But I have a full memory and a complete sense of what it is like to be loved and nurtured by her.” That’s because, he explained, he had done the very exercise that we were about to try on Eugene. Here’s how it would work: Eugene would recreate the trauma that haunted him most by calling on people in the room to play certain roles. He would confront those people — with his anger, sorrow, remorse and confusion — and they would respond in character, apologizing, forgiving or validating his feelings as needed. By projecting his “inner world” into three-dimensional space, Eugene would be able to rewrite his troubled history more thoroughly than other forms of role-play therapy might allow. If the experiment succeeded, the bad memories would be supplemented with an alternative narrative — one that provided feelings of acceptance or forgiveness or love. The exercise, which van der Kolk calls a “structure” but which is also known as psychomotor therapy, was developed by Albert Pesso, a dancer who studied with Martha Graham. He taught it to van der Kolk about two decades ago. Though it has never been tested in a controlled study, van der Kolk says he has had some success with it in workshops like this one. He likes to try it whenever he has a small group and a willing volunteer. © 2014 The New York Times Company
Link ID: 19647 - Posted: 05.23.2014
|By Ann Graybiel and Kyle Smith For children and adults who have conditions such as obsessive-compulsive disorder (OCD), Tourette syndrome or autism, repetitive thoughts and actions can occur even if the individuals do not want them to. In OCD a thought that repeats again and again—“my hands are dirty, my hands are dirty”—can recur in a habitual way. Such conditions occur in people from different countries and cultures, suggesting that they represent a core dysfunction related to an imbalance between behaviors. These problems appear to reflect disturbances in brain circuits that are different from, but allied with, the normal habit circuits. Researchers in our group and that of Susanne Ahmari at the University of Pittsburgh have tested whether these OCD circuits can be controlled. Our lab group stimulated the neocortex and striatum in mice that were genetically engineered to have OCD-like traits. These mice groom themselves excessively, especially around the face. In the lab we mimicked a problem that people with OCD often have because they react excessively and repetitively to some trigger stimulus in the environment. We conditioned the mice to learn that after a tone sounded a drop of water would fall on their noses about a second later. We also performed the same routine with normal (“control”) mice. The OCD-like mice started by just grooming when the water drop came, but then began to start grooming in response to the tone alone, and kept grooming all the way through when the drop fell. The control mice learned to suppress this early grooming, which after all was a wasted effort because the water drop came later. The OCD-like mice groomed compulsively every time the external cue sounded. Using optogenetics—a technique that controls the activity of brain cells by shining light on them—we then excited a pathway that connects a small region in the cortex with the striatum. The pathway has been implicated in suppressing behaviors. This treatment immediately blocked the compulsive early grooming in the mutant mice! Yet when the water drop came, they could groom normally. And the optogenetic stimulation did not affect other normal behaviors such as eating; it selectively blocked the compulsive aspect of behavior. © 2014 Scientific American
Kevin Loria Music was among the least of Mr. B's concerns. As a 59-year-old Dutch man living with extremely severe obsessive compulsive disorder for 46 years, he had other things on his mind. His OCD was so severe it led to moderate anxiety and mild depression. Not only was his condition extreme, but it was also resistant to traditional treatment. It got so bad that he opted to receive an implant to stimulate his brain constantly with electricity — a treatment, called deep brain stimulation (DBS), that has been shown to successfully treat OCD in the past. It worked, but had a very peculiar side effect. As researchers write in a study published in the journal Frontiers in Behavioral Neuroscience, it turned Mr. B. into a Johnny Cash fanatic, though he'd never really listened to The Man in Black before. Mr. B. had listened to the same music for decades, but was never a devout music lover. He was a Rolling Stones and Beatles fan (with a preference for the Stones), and listened to Dutch music as well. But just months after flying to Minneapolis and having two sets of electrodes tunneled into his brain for the shock therapy, he had a mind-blowing run-in with the song "Ring of Fire" playing on the radio. Something about Cash's deep bass-baritone voice resonated with him at that moment. His life had already changed. After the surgical implants and therapy, his OCD had gone from extremely severe to mild, and his depression and anxiety were at a level lower than mild. But when he heard Cash croon, another change began. Mr. B. bought all the Johnny Cash music he could find and stopped listening to anything else — no more Beatles, no more Stones, no more Nederpop. Instead, he played Cash all the time, and especially loved the songs from the '70s and '80s. "Folsom Prison Blues," "Ring Of Fire," and "Sunday Morning Come-Down" are his favorites. They make him feel like a hero, he told doctors. © 2014 Business Insider, Inc.
André Aleman & Damiaan Denys According to the World Health Organization, almost 1 million people kill themselves every year. That is more than the number that die in homicides and war combined. A further 10 million to 20 million people attempt it. Suicide is one of the three leading causes of death in the economically most productive age group — those aged 15–44 years — and rates have risen since the economic crisis triggered by the banking crash in 2008 (see 'Suicide rates in Europe'). For example, the number of suicides per year in the Netherlands rose by 30% between 2008 and 2012, from 1,353 to 1,753. In the United States, the average suicide costs society US$1.06 million according to the US Centers for Disease Control and Prevention. Despite its enormous societal impact, little progress has been made in the scientific understanding or treatment of suicidal behaviour. We do know that up to 90% of suicides occur in people with a clinically diagnosable psychiatric disorder1. Large epidemiological studies have shown mental disorders, particularly depression and alcohol addiction, to be major risk factors2. And there is compelling evidence that adequate prevention and treatment of such disorders can reduce suicide rates2. But psychiatry has long neglected the topic. Other than as symptoms of borderline personality disorder and mood disorders, suicide, suicide attempts and suicidal thoughts were not listed in the fourth edition of the Diagnostic and Statistical Manual of Mental Disorders (DSM-IV). The DSM-5 (published last year) does not code suicidal behaviour — the most prominent emergency in psychiatry in primary care. Suicidality is perceived as a medical complication rather than as a disorder in its own right. © 2014 Nature Publishing Group
Link ID: 19642 - Posted: 05.21.2014
Dr Lucy Maddox There has been much heated debate in recent weeks about whether cognitive behavioural therapy for psychosis has been totally over-egged. One stance is that Nice (the National Institute for Clinical Excellence) has recommended a treatment with little or no evidence base. Another is that CBT is a helpful intervention for many people experiencing psychotic-like phenomena. But what is CBT for psychosis? What does it look like? And how can knowing this help us to understand the issues being argued about? Psychosis is an umbrella term for a collection of symptoms. These symptoms get classed as "positive" or "negative", which is not to infer that some are good and some are bad, but rather to capture the fact that some of the symptoms add something new and others take something away. Positive symptoms are those that add an unusual experience of some kind, eg seeing things that others can't (hallucinations) or strongly believing things that don't make sense to others (delusions). Negative symptoms involve something being taken away from the person, eg a lack of enjoyment (anhedonia), motivation (avolition), or a lack of emotion. Whilst a recent meta-analysis has shown only limited evidence for the effectiveness of CBT for psychosis and suggested that previous results are inflated, we should be cautious about using this one meta-analysis to chuck out CBT for psychosis. Among other potential holes that could be poked in its conclusions is the fact that the analysis uses psychotic symptoms as the only outcome measure for effectiveness, which might not be the best or only thing we should be looking at. Many other reviews and individual studies do report reductions in psychotic symptoms from CBT for psychosis, including delusions and hallucinations and some of the brain processing correlates of these positive symptoms (eg Kumari et al 2011). Perhaps more interestingly though, they also report benefits from CBT in domains other than the psychotic symptoms themselves. (eg Wykes et al, 2009). © 2014 Guardian News and Media Limited
Link ID: 19639 - Posted: 05.20.2014
by Laura Sanders An injectable form of a newer, more expensive schizophrenia drug works no better than an older drug, scientists report May 21 in the Journal of the American Medical Association. In a randomized clinical trial of 311 people with schizophrenia, injections of paliperidone palmitate failed to alleviate schizophrenia symptoms just as often as did injections of haloperidol decanoate, a drug that’s been around for decades. A single injection of paliperidone palmitate, a second-generation antipsychotic, costs about $1000 in the United States. An injection of haloperidol costs only about $35. The two drugs caused different side effects: In some patients, haloperidol led to muscle tremors and restlessness and paliperidone palmitate caused weight gain. Knowledge of these different side effects — and not differences in effectiveness — might be useful in deciding which drug a person ought to take. © Society for Science & the Public 2000 - 2013.
Link ID: 19638 - Posted: 05.20.2014
By ABIGAIL ZUGER, M.D. Sweet revenge comes in many delectable forms, among them the receipt of accolades for work long scorned. And then to get to tell the whole story at length and without a single interruption — small wonder that the Nobel laureate Dr. Stanley B. Prusiner, a renowned neurologist at the University of California, San Francisco, writes with a cheerful bounce. Once disparaged, his scientific work is now hailed as visionary, and his memoir takes the reader on a leisurely and immensely readable victory lap from then to now. In the process, two stories unfold. The first is the progress of Dr. Prusiner’s thinking on the transmissible proteins he named prions (PREE-ons) in 1982, starting with his first experiments on an obscure disease of sheep and ending with the most recent work linking prions to an array of human neurological catastrophes, including Alzheimer’s disease. The science is convoluted, like the proteins, and for the uninitiated the best way to achieve a rudimentary grasp of the subject is to hear it the way Dr. Prusiner tells it, from the very beginning. But a parallel narrative turns out to be equally fascinating: perhaps not since James D. Watson’s 1968 memoir “The Double Helix“ has the down and dirty business of world-class science been given such an airing. Dr. Watson raised eyebrows with his gossipy account of the serious task of unraveling the genetic code — and he was working in genteel postwar Britain at the time, with experimental science still at least in theory a gentleman’s game. That illusion is long gone: The stakes are considerably higher now, the competition fierce, the pace frantic, and Dr. Prusiner, 71, revisits quite a few of the battles that punctuated his long research career. He was an underachiever in high school and then an achiever in college and medical school, captivated by the laboratory early on. He finished his medical training on the neurology wards in San Francisco, where he met the patient who would set the course of his career: a slim, tanned 60-year-old woman from Marin County who was having trouble unzipping her golf bag. Months later she was dead of Creutzfeldt-Jakob disease, one of several related and invariably fatal neurological diseases (mad cow among them) that leave the brain of the affected human or animal riddled with holes, a useless sponge. © 2014 The New York Times Company
Link ID: 19632 - Posted: 05.19.2014
|By Beth Skwarecki The protein family notorious for causing neurogenerative diseases such as Parkinson's—not to mention mad cow—appears to play an important role in healthy cells. “Do you think God created prions just to kill?” muses Eric R. Kandel of Columbia University. “These things have evolved initially to have a physiological function.” Kandel's work on memory helped to reveal that animals make and use prions in their nervous systems as part of an essential function: stabilizing the synapses involved with forming long-term memories. These natural prions are not infectious, but on a molecular level they chain up exactly the same way as their disease-causing brethren. (Some researchers call them “prionlike” to avoid confusion.) Now neuroscientist Kausik Si of the Stowers Institute for Medical Research in Kansas City, Mo., one of Kandel's former students, has shown that the prion's action is tightly controlled by the cell and can be turned on when a new long-term memory needs to be formed. Once the prion's chain reaction gets started, it is self-perpetuating, and thus the synapse—where neurons connect—can be maintained after the initial trigger is gone, perhaps for a lifetime. But that still does not explain how the first prion is triggered or why it happens at only certain of the synapses, which play a crucial role in forming memories. Si's work, published February 11 in PLOS Biology, traces the biochemistry of this protein-preservation process in fruit flies, showing how the cell turns on the machinery responsible for the persistence of memory—and how the memory can be stabilized at just the right time and in the right place. © 2014 Scientific American
Eleven years on, I still remember the evening I decided to kill my baby daughter. It's not something you're supposed to feel as a new parent with a warm, tiny bundle in your arms. But this is how postnatal depression can twist your logic. At the time it made perfect sense. Catherine was screaming, in pain. She had colic, there was nothing I could do about it. If an animal were in this much pain you'd put it out of its misery, so why not a human? Postnatal depression can have this kind of effect even on the most reasonable woman, yet you won't find much about it in baby books. We're expected to love our kids the moment they pop out, even while the memory of the labour pains is still raw. I knew a baby would be hard work, of course, but I expected motherhood to be fulfilling. As it happened I had a wonderful pregnancy, followed by a quick and easy birth. But the problems started soon after. Catherine wouldn’t feed, her blood sugar levels tumbled and I ended up bottle-feeding her, in tears, in a hospital room filled with posters promoting the breast. I was a Bad Mother within 48 hours. Things were no better after the first month. This was meant to be a joyous time, but all I seemed to feel was rage and resentment. In pregnancy all the attention had been on me, and suddenly I was a sideshow to this wailing thing in a crib. I was tired, tetchy and resentful. My daughter had rapidly become a ball and chain. My freedom was over. I kept hoping this was just the “baby blues” and that it would soon pass, but things only got worse. When colic set in, for around five hours each evening Catherine would scream, her face a mix of red and purple rage. No amount of pacing, tummy-rubbing or soothing words could stop this tiny demanding creature. So one night, alone with her in her room, I decided it would be best to put her out of her misery. © 2014 Guardian News and Media Limited
By RONI CARYN RABIN For decades, scientists have embarked on the long journey toward a medical breakthrough by first experimenting on laboratory animals. Mice or rats, pigs or dogs, they were usually male: Researchers avoided using female animals for fear that their reproductive cycles and hormone fluctuations would confound the results of delicately calibrated experiments. That laboratory tradition has had enormous consequences for women. Name a new drug or treatment, and odds are researchers know far more about its effect on men than on women. From sleeping pills to statins, women have been blindsided by side effects and dosage miscalculations that were not discovered until after the product hit the market. Now the National Institutes of Health says that this routine gender bias in basic research must end. In a commentary published on Wednesday in the journal Nature, Dr. Francis Collins, director of the N.I.H., and Dr. Janine A. Clayton, director of the institutes’ Office of Research on Women’s Health, warned scientists that they must begin testing their theories in female lab animals and in female tissues and cells. The N.I.H. has already taken researchers to task for their failure to include adequate numbers of women in clinical trials. The new announcement is an acknowledgment that this gender disparity begins much earlier in the research process. “Most scientists want to do the most powerful experiment to get the most durable, powerful answers,” Dr. Collins said in an interview. “For most, this has not been on the radar screen as an important issue. What we’re trying to do here is raise consciousness.” Women now make up more than half the participants in clinical research funded by the institutes, but it has taken years to get to this point, and women still are often underrepresented in clinical trials carried out by drug companies and medical device manufacturers. © 2014 The New York Times Company
by Nathan Collins There's a new twist in mental health. People with depression seem three times as likely as those without it to have two brain lobes curled around each other. The brains of people with depression can be physically different from other brains – they are often smaller, for example – but exactly why that is so remains unclear. In humans, some studies point to changes in the size of the hippocampi, structures near the back of the brain thought to support memory formation. "There are so many studies that show a smaller hippocampus in almost every psychiatric disorder," says Jerome Maller, a neuroscientist at the Monash Alfred Psychiatry Research Centre in Melbourne, Australia, who led the latest work looking at brain lobes. "But very few can actually show or hypothesize why that is." Maller thinks he has stumbled on an explanation. He had been using a brain stimulation technique known as transcranial magnetic stimulation as a therapy for antidepressant-resistant depression. This involved using fMRI scans to create detailed maps of the brain to determine which parts to stimulate. While pouring over hundreds of those maps, Maller noticed that many of them showed signs of occipital bending. This is where occipital lobes – which are important for vision – at the back of the brain's left and right hemispheres twist around each other. So he and his colleagues scanned 51 people with and 48 without major depressive disorder. They found that about 35 per cent of those with depression and 12.5 per cent of the others showed signs of occipital bending. The difference was even greater in women: 46 per cent of women with depression had occipital bending compared with just 6 per cent of those without depression. © Copyright Reed Business Information Ltd.
By Pippa Stephens Health reporter, BBC News An anti-depressant drug could be used to slow the onset of Alzheimer's disease, say scientists in the US. Research into 23 people, and transgenic mice, found citalopram hampered a protein which helps to build destructive plaques in the brains of Alzheimer's patients. Scientists said they hoped the study could help prevent the disease. Experts said the study was "interesting" and that using an approved drug could be beneficial. Alzheimer's disease is the most common cause of dementia, affecting around 496,000 people in the UK. It affects the brain through protein plaques and tangles which lead to the death of brain cells, and a shortage of chemicals important for transmitting messages. Symptoms include loss of memory, mood changes, and problems with communication and reasoning. Researchers at the University of Pennsylvania and Washington University School of Medicine carried out the study between 2012 and 2014. They bred mice with Alzheimer's disease and looked at the levels of the peptide - or protein component - amyloid beta (AB), in the brain. AB clusters in plaques which, alongside the tau protein, are thought to trigger Alzheimer's. After giving the mice citalopram, the level of AB fell by 25%, compared to the control group, with no anti-depressant. And after two months of anti-depressants, the growth of new plaques was reduced, and existing plaques did not grow any further, the study said. But it noted the drug could not cause existing plaques to shrink, or decrease in number. BBC © 2014
By ANNE SAKER CINCINNATI — The psychologist Lynda Crane found that of the many injuries inflicted by schizophrenia, the greatest could be the pain of being forgotten. Just naming the illness somehow erased the person, something she learned when her 18-year-old son’s doctors said he had schizophrenia. Six years later, he committed suicide. “It took me a long time to come to terms with it,” Dr. Crane says. “Even I had a hard time understanding it, how this bright man, with a brilliant future, could suffer like this. One thing I learned was that as soon as you mentioned the word, people stopped seeing the person. They just saw the diagnosis and a collection of symptoms. Doug, my son, was forgotten.” For years Dr. Crane, a professor at the College of Mount St. Joseph in the western hills of Cincinnati, sought a way to enlighten her students and others about the ordinary people who live with schizophrenia despite its extraordinary burdens – the confused thinking, the delusions, the hallucinations, the anxiety and fear. Then she discovered a tool more commonly used among sociologists and anthropologists: oral history. Employing the device to examine schizophrenia has shifted her own perspective about a disease she thought she knew well. “People with schizophrenia do not lose their individuality, even when the illness is very severe,” Dr. Crane says. “What I discovered through oral history is that it’s not about schizophrenia. It’s about a complexity of life that is very hard to get at any other way.” For the past three years, on their own time and with no outside money, Dr. Crane and a fellow Mount St. Joseph psychologist, Tracy McDonough, have built the Schizophrenia Oral History Project. Other oral history collections have focused on diseases like AIDS or leprosy, but this is the first to focus on schizophrenia, they say. © 2014 The New York Times Company
Link ID: 19593 - Posted: 05.10.2014