Chapter 12. Psychopathology: Biological Basis of Behavioral Disorders
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By NICHOLAS BAKALAR Five antidepressant drugs are approved by the Food and Drug Administration for treating obsessive-compulsive disorder. But they are sometimes ineffective, and guidelines suggest adding an antipsychotic drug to the regimen. Now scientists have found that adding cognitive behavioral therapy, or C.B.T., may be more effective than an antipsychotic. Researchers studied 100 people with O.C.D. who were taking antidepressants without sufficient improvement. They randomized 40 to the antipsychotic risperidone (brand name Risperdal), 20 to a placebo pill, and 40 to exposure and ritual prevention, a special form of C.B.T. delivered twice a week over eight weeks. All continued their antidepressants as well. The study was published online in JAMA Psychiatry, and several of the authors have financial relationships with pharmaceutical companies. Using well-validated scales and questionnaires, the researchers found that 80 percent of the C.B.T. patients responded with reduced symptoms and improved functioning and quality of life. About 23 percent got better on risperidone, and 15 percent on the placebo. “It’s important to discontinue antipsychotics if there isn’t continued benefit after four weeks,” said the lead author, Dr. Helen Blair Simpson, a professor of psychiatry at Columbia. “O.C.D. patients who still have symptoms should first be offered the addition of C.B.T., and some will achieve minimal symptoms. “There’s a hopeful message here,” she added. “There are good treatments.” Copyright 2013 The New York Times Company
Keyword: OCD - Obsessive Compulsive Disorder
Link ID: 18674 - Posted: 09.19.2013
By JEREMY W. PETERS and MICHAEL LUO WASHINGTON — Despite deep divisions that have kept Congress from passing new gun safety laws for almost two decades, there is one aspect of gun control on which many Democrats, Republicans and even the National Rifle Association agree: the need to give mental health providers better resources to treat dangerous people and prevent them from buying weapons. Yet efforts to improve the country’s fraying mental health system to help prevent mass shootings have stalled on Capitol Hill, tied up in the broader fight over expanded background checks and limits on weapons sales. Now the shooting at the Washington Navy Yard by a man who authorities say showed telltale signs of psychosis is spurring a push to move ahead with bipartisan mental health policy changes. The new debate over gun control is beginning to turn not on weapons or ammunition, but on the question of whether to spend more money on treating and preventing mental illness. Proponents again face a steep uphill push, but they see an opening even if it remains unclear whether any changes under consideration could have headed off the latest attack, in which the authorities say Aaron Alexis, a former Navy reservist, bought the shotgun he used in Virginia. “Given the clear connection between recent mass shootings and mental illness, the Senate should not delay bipartisan legislation that would help address this issue,” Senators Kelly Ayotte, Republican of New Hampshire, and Mark Begich, Democrat of Alaska, wrote Wednesday in a joint statement to the Senate leadership. The legislation they are pushing, which was held up when a more sweeping gun measure was defeated earlier this year, would establish programs to train teachers to recognize the signs of mental illness and how to defuse potentially violent situations. © 2013 The New York Times Company
By JIM DWYER Here are law students on a Tuesday morning in 2013, hearing that researchers hope over the next decade or so to map the wiring of the human brain, seeing how individual cells link to bigger circuits. A decade is a sprint, less time than since 9/11, to use one benchmark. The scientists want to lift the hood and get a look at the human mind. The students, in a seminar at Fordham University School of Law taught by Prof. Deborah W. Denno, wonder what that will mean for the law. Over and over, they put questions to a guest speaker, Joshua R. Sanes, director of the Center for Brain Science at Harvard, about the implications for society if and when brain science can identify with confidence a propensity for violence, or for lying. He bats it right back at them. “You tell me,” Dr. Sanes said. “It’s a huge issue. I wish I had something smart to say.” Last year, President Obama announced that the federal government would create a Brain Initiative to speed up the development of tools that can track how the brain works and how it breaks. It is not hard to imagine the benefits, beginning with more carefully targeted treatments for people afflicted with psychiatric ailments. “There has not been a brand new type of drug for antidepression or autism or schizophrenia, bipolar disorder or O.C.D. in something like 25 years,” Dr. Sanes said. “This is where we have to make a long-term investment and come up with some new types of help because what we are doing isn’t working.” Work on animals has shown in broad strokes how information gets into the head and processed, but current imaging tools cannot keep up with the brain’s processing speed, or are not powerful enough to follow the molecular transactions involved in passing information and creating thought. © 2013 The New York Times Company
Link ID: 18666 - Posted: 09.18.2013
By Sarah Amandolare Decades of research and billions of dollars go into developing and marketing drugs. Here's the life span of a typical brain drug—Cymbalta, a popular antidepressant Tuberculosis researchers discover that a drug that treats infections, called iproniazid, also boosts patients' mood. They learn that iproniazid slows the breakdown of three chemicals in the brain— serotonin, norepinephrine and dopamine. These molecules take center stage in the next two decades, as scientists search for antidepressants. 1974 Eli Lilly researchers develop fluoxetine (Prozac), the first selective serotonin reuptake inhibitor. Fluoxetine thwarts the absorption, or “reuptake,” of serotonin. This boosts levels of the chemical in the pockets of space between neurons. Prozac does not hit drugstore shelves until 1988. 1980s Scientists start tinkering with the reuptake of norepinephrine and dopamine, which, in addition to elevating mood, can relieve muscle and joint pain. They dub this new class of antidepressants serotonin-norepinephrine reuptake inhibitors (SNRIs). At Eli Lilly, scientists begin developing an SNRI with a special focus on norepinephrine. One of their molecules becomes known as duloxetine, later branded Cymbalta. 1986 © 2013 Scientific American
Link ID: 18660 - Posted: 09.18.2013
By PAULINE W. CHEN, M.D. One afternoon at a school not far from the hospital where I was working, a teacher opened a utility closet and found a staff member passed out on the floor. He was clutching a small bloody mass in one hand, a sharp knife in the other, she reported, a red stain spreading rapidly at his middle. He had amputated his genitals. Once he’d been brought to our emergency room and resuscitated, the man refused further treatment. Doctors and nurses, concerned that if they waited any longer to reattach the severed part the surgery might not work, took the necessary steps to deem him mentally incompetent to make such decisions. “The guy was seriously nuts,” I remember one of the doctors saying afterward. “He kept screaming that he didn’t want ‘it’ back.” For days after the successful operation, the gruesome story was all anyone at the hospital could discuss. Most of us chalked it up to his being “certifiable,” and several wondered if maybe they should have skipped the surgery. “After all,” said one clinician, “isn’t that what he wanted?” But in all the chatter none of us mentioned a key part of the patient’s story: the unbearable suffering that must have pushed him to commit so brutal an act. In fact, anyone overhearing our conversations might have been hard pressed to find any of the warmth and sensitivity we routinely displayed toward patients with cancer, AIDS or heart disease. I remembered the man and our reactions this past week while reading “Falling Into the Fire: A Psychiatrist’s Encounters With the Mind in Crisis,” a thought-provoking new book by Dr. Christine Montross. Of all the afflictions that fall upon us, few remain as misunderstood and stigmatized as those that affect the mind. Copyright 2013 The New York Times Company
By Philip Yam New Hampshire health officials announced last week that hospitals in three New England states may have accidentally exposed 15 people to prions, the infectious protein that ravages the brain and leaves it full of holes. Evidently, the hospitals involved used surgical tools that had previously been deployed on a patient who officials suspect later died from a particular prion infection called sporadic Creutzfeldt-Jakob disease (CJD). As disturbing as the revelation was, it pales in comparison with the announcement in 2002, when the University of Pittsburgh Medical Center Presbyterian announced that up to 4,000 patients might have been exposed to the prion. Both incidents show that the hospital transmission of prion diseases remains an ever-present possibility, if thankfully a very unlikely one. Prions are unusual pathogens distinct from parasites, fungi, bacteria and viruses. They are misfolded proteins that can transform healthy proteins into sickly versions, leading to the death of cells. Particularly abundant in the brain, they took center stage in the late 1980s, during the mad cow outbreak in the U.K. People who ate beef from infected cows ran the risk of contracting a variant of CJD. The panic brought to light the range of prion diseases that can affect humans and animals, including one that develops spontaneously. Called sporadic CJD, this spontaneous form strikes about one in every million people each year for no apparent reason. What’s more, the brain tissue from the unlucky few can infect healthy brains—hence, the worry over surgical transmission. © 2013 Scientific American
Link ID: 18643 - Posted: 09.14.2013
By Gary Stix New types of drugs for schizophrenia, depression and other psychiatric disorders are few and far between—and a number of companies have scaled back or dropped development of this class of pharmaceuticals. One exception stands out. Ketamine, the anesthetic and illegal club drug, is now being repurposed as the first rapid-acting antidepressant drug and has been lauded as possibly the biggest advance in the treatment of depression in 50 years. A few trials by large pharma outfits are now underway on a new, purportedly improved and, of course, more profitable variant of ketamine, which in its current generic drug form does not make pharmaceutical marketing departments salivate. Some physicians have decided they simply can’t wait for the lengthy protocols of the drug approval process to be sorted out. They have read about experimental trials in which a low-dose, slow-infusion of ketamine seems to produce what no Prozac-like pill can achieve, lifting the black cloud in hours, not weeks. With nothing to offer desperate, sometimes suicidal patients, physicians have decided against waiting for an expensive, ketamine lookalike to arrive and have started writing scripts for the plain, vanilla generic version that has been used for decades as an anesthetic. Ketamine, it seems, has captivated a bunch of white coats with the same grassroots energy that has propelled the medical marijuana movement. © 2013 Scientific American
By ERIC R. KANDEL THESE days it is easy to get irritated with the exaggerated interpretations of brain imaging — for example, that a single fMRI scan can reveal our innermost feelings — and with inflated claims about our understanding of the biological basis of our higher mental processes. Such irritation has led a number of thoughtful people to declare that we can never achieve a truly sophisticated understanding of the biological foundation of complex mental activity. In fact, recent newspaper articles have argued that psychiatry is a “semi-science” whose practitioners cannot base their treatment of mental disorders on the same empirical evidence as physicians who treat disorders of the body can. The problem for many people is that we cannot point to the underlying biological bases of most psychiatric disorders. In fact, we are nowhere near understanding them as well as we understand disorders of the liver or the heart. But this is starting to change. Consider the biology of depression. We are beginning to discern the outlines of a complex neural circuit that becomes disordered in depressive illnesses. Helen Mayberg, at Emory University, and other scientists used brain-scanning techniques to identify several components of this circuit, two of which are particularly important. One is Area 25 (the subcallosal cingulate region), which mediates our unconscious and motor responses to emotional stress; the other is the right anterior insula, a region where self-awareness and interpersonal experience come together. These two regions connect to the hypothalamus, which plays a role in basic functions like sleep, appetite and libido, and to three other important regions of the brain: the amygdala, which evaluates emotional salience; the hippocampus, which is concerned with memory; and the prefrontal cortex, which is the seat of executive function and self-esteem. All of these regions can be disturbed in depressive illnesses. © 2013 The New York Times Company
By Brian Mossop A fine line separates creativity and madness. Bipolar disorder teeters along that line, with patients experiencing moments of impulsive thought, which can yield bold insights or quickly descend into confusion or rage. In her new book, Haldol and Hyacinths, Iranian-American author and activist Moezzi presents a captivating autobiographical account of her struggle with bipolar disorder. Using a series of vignettes, she reconstructs her downward spiral into psychosis, which eventually led to a suicide attempt and multiple stays in mental health facilities. From seemingly innocuous bouts of insomnia to full-blown hallucinations, Moezzi describes how she descended into madness. Moezzi's medical issues first emerged in her sophomore year of college, when she began to experience severe abdominal pain, later diagnosed as pancreatitis. Doctors decided to remove her pancreas to save her life and prevent a cyst from festering. Everyone she knew rallied alongside her during this time. Things were much different when Moezzi's bipolar disorder took hold in the years following her physical illness. She soon discovered that mental illness has no heroes, no celebrity spokesperson, no champions. Relying solely on the support of her immediate family and a devoted husband, Moezzi saw that the disorder carries a stigma, exacerbated by inaccurate media portrayals. Even worse is the plight of patients in places such as Moezzi's homeland of Iran, where mental illness is simply ignored. Despite bipolar disorder being the sixth leading cause of disability in the world, there is not even a word for the disease in Farsi. © 2013 Scientific American
Link ID: 18559 - Posted: 08.26.2013
Linda Carroll TODAY contributor Whether it’s “One Flew Over the Cuckoo’s Nest,” “Girl Interrupted,” or “Homeland,” Hollywood’s portrayals of electroconvulsive therapy have never been pretty. And the images from those movies and TV shows have only added to a stigma that keeps many desperate patients from opting for a therapy that might turn their lives around, experts say. “We can’t get past the stigma of all the visuals we’ve seen from movies and the fact that it seems so antiquated when you consider modern medicine,” NBC chief medical editor Dr. Nancy Snyderman told TODAY’s Matt Lauer. “But time and time and time again if you look at patients who have severe depression who don’t respond to medications, they will tell you that ECT works.” That’s certainly true in Denise Stewart’s case. Stewart, a mother of two, suffers from schizoaffective disorder. Her hallucinations were pushing her closer and closer to suicide each day. “There would be voices in my head that would sit there and say, ‘Denise, see the knife in the kitchen? Cut your wrists. Denise, see those pills over there? Take all those pills,’” she told TODAY. After antidepressants made Stewart’s condition worse, her doctors suggested ECT. And the change was dramatic. “If it hadn’t been for the electroconvulsive therapy, I wouldn’t be alive right now,” Stewart said. These days an estimated 100,000 Americans undergo ECT each year – and the process is a lot different from what you see in the media, experts say.
By RICHARD A. FRIEDMAN, M.D. Fully 1 in 5 Americans take at least one psychiatric medication. Yet when it comes to mental health, we are facing a crisis in drug innovation. Sure, we have many antidepressants, antipsychotics, hypnotic medications and the like. But their popularity masks two serious problems. First, each of these drug classes is filled with “me too” drugs, which are essentially just copies of one another; we have six S.S.R.I. antidepressants that essentially do the same thing, and likewise for the 10 new atypical antipsychotic drugs. Second, the available drugs leave a lot to be desired: patients with illnesses like schizophrenia, major depression and bipolar disorder often fail to respond adequately to these medications or cannot tolerate their side effects. Yet even though 25 percent of Americans suffer from a diagnosable mental illness in any year, there are few signs of innovation from the major drug makers. After a series of failed clinical trials in which novel antidepressants and antipsychotics did little or no better than placebos, the companies seem to have concluded that developing new psychiatric drugs is too risky and too expensive. This trend was obvious at the 2011 meeting of the American Society for Clinical Pharmacology and Therapeutics, where only 13 of 300 abstracts related to psychopharmacology and none related to novel drugs. Instead, they are spending most of their research dollars on illnesses like cancer, heart disease and diabetes, which have well-defined biological markers and are easier to study than mental disorders. © 2013 The New York Times Company
What if a psychiatrist could tell whether someone was about to commit suicide simply by taking a sample of their blood? That’s the promise of new research, which finds increased amounts of a particular protein in the bloodstream of those contemplating killing themselves. The test was conducted on only a few people, however, and given that such “biomarkers” often prove unreliable in the long run, it’s far from ready for clinical use. Suicide isn’t like a heart attack. People typically don’t reveal early symptoms to their doctor—morbid thoughts, for example, instead of chest pain—and there’s no equivalent of a cholesterol or high blood pressure test to identify those at most risk of killing themselves. "We are dealing with something more complex and less accessible," says Alexander Niculescu III, a psychiatrist at the Indiana University School of Medicine in Indianapolis. So some researchers are eager to find physical signs, called biomarkers, that can be measured in the bloodstream to signal when a person is at a high likelihood of committing suicide. Over the past decade, Niculescu and his colleagues have been refining a method for identifying biomarkers that can distinguish psychological states. The technique depends on blood samples taken from individuals in different mental states over time—for example, from people with bipolar disorder as they swing between the disorder’s characteristic high and low moods. The researchers test those samples for differences in the activity, or expression, of genes for of different proteins. After screening the blood samples, the scientists “score” a list of candidate biomarker genes by searching for related results in a large database of studies by other groups using a program that Niculescu compares to the Google page-ranking algorithm. In previous published studies, Niculescu and other groups have used the technique to probe for biomarkers in disorders such as bipolar disorder, psychosis, and alcoholism. © 2012 American Association for the Advancement of Science.
Link ID: 18530 - Posted: 08.20.2013
By Bruce Bower NEW YORK CITY — Psychiatrists regularly get criticized for turning typical life problems into medical disorders. But in an odd reversal, many mental health clinicians are trying to transform one certified mental illness, borderline personality disorder, into a label for needy, manipulative people who don’t need treatment, a sociologist reported at the American Sociological Association’s annual meeting on August 11. Patients with borderline personality disorder, unlike people with schizophrenia or other serious mental conditions, are often viewed by mental health providers as having cynically planned out rash acts and even suicide attempts, sociologist Sandra Sulzer of the University of North Carolina at Chapel Hill found in extensive interviews with 22 psychiatrists and psychologists in the United States. The condition includes difficulty controlling emotions, intense but unstable relationships, recklessness, cutting and other acts of self-harm, along with attempted and completed suicides. Before Sulzer’s study, little was known about how mental health professionals discuss and deal with this troubling set of symptoms. “Clinicians frequently view borderline personality disorder symptoms as signs of badness, not sickness, and as a code to route patients out of mental health care,” Sulzer said. That finding goes a long way toward explaining why many borderline personality disorder patients receive no treatment despite the availability of effective forms of psychotherapy (SN: 6/16/07, p. 374), she suggested. © Society for Science & the Public 2000 - 2013
Link ID: 18511 - Posted: 08.15.2013
By RONI CARYN RABIN Over the past two decades, the use of antidepressants has skyrocketed. One in 10 Americans now takes an antidepressant medication; among women in their 40s and 50s, the figure is one in four. Experts have offered numerous reasons. Depression is common, and economic struggles have added to our stress and anxiety. Television ads promote antidepressants, and insurance plans usually cover them, even while limiting talk therapy. But a recent study suggests another explanation: that the condition is being overdiagnosed on a remarkable scale. The study, published in April in the journal Psychotherapy and Psychosomatics, found that nearly two-thirds of a sample of more than 5,000 patients who had been given a diagnosis of depression within the previous 12 months did not meet the criteria for major depressive episode as described by the psychiatrists’ bible, the Diagnostic and Statistical Manual of Mental Disorders (or D.S.M.). The study is not the first to find that patients frequently get “false positive” diagnoses for depression. Several earlier review studies have reported that diagnostic accuracy is low in general practice offices, in large part because serious depression is so rare in that setting. Elderly patients were most likely to be misdiagnosed, the latest study found. Six out of seven patients age 65 and older who had been given a diagnosis of depression did not fit the criteria. More educated patients and those in poor health were less likely to receive an inaccurate diagnosis. Copyright 2013 The New York Times Company
Link ID: 18499 - Posted: 08.13.2013
By D. D. GUTTENPLAN LONDON — With its battered desks, fluorescent lights and interactive whiteboard showing an odd creature that, depending on how you look at it, could be either a duck or a rabbit, this could be a class in any university philosophy department. But this is a class with a difference. It is the Maudsley Philosophy Group, a seminar that meets regularly on the grounds of the Maudsley Hospital, Britain’s largest mental health teaching hospital, which is affiliated with the Institute of Psychiatry at King’s College London. Participants at the last session included psychiatrists, psychologists, philosophers and an actor who had just finished working as a chaplain in a locked men’s ward at the hospital and who was about to organize a storytelling group there. “We started out as a reading group for trainee psychiatrists,” said Gareth S. Owen, a researcher at the Institute of Psychiatry who co-founded the group in 2002. “Then, gradually, we developed and started inviting philosophers — at first it was quite low key. We would talk about our clinical experiences and then they would relate those experiences to their way of thinking.” Robert Harland, another co-founder of the group, said he had known Dr. Owen since they “cut up a corpse together at medical school.” “The analytic philosophers brought a real clarity to our discussions,” Dr. Harland said. “We were looking at various models to help us understand what we were doing as psychiatrists. “There is lots of applied science now in psychiatry: neuroimaging, genetics, epidemiology. But they don’t have much to say about sitting with a patient and trying to understand that person’s experiences.” © 2013 The New York Times Company
Some colors humans are exposed to late at night could cause symptoms of clinical depression. That is the conclusion of a study that builds on previous findings that individuals exposed to dim levels of light overnight, such as from a glowing television set, can develop signs of clinical depression. Investigators, curious as to whether the color of light contributed to depressive symptoms in humans, designed an experiment that exposed hamsters to different colors. They chose hamsters because they are nocturnal, meaning they sleep during the day and are active at night. One group of hamsters was kept in the dark during their nighttime period. Another group of rodents was exposed to blue light and a third group slept in the presence of white light. A fourth group of hamsters was exposed to glowing red light. After four weeks, researchers noted how much sugary water the hamsters drank. The more depressed rodents consumed the least amount of water. Randy Nelson, chair of Ohio State University’s Department of Neuroscience and co-author of the study, said animals that slept in blue and white light appeared to be the most depressed. “What we saw is these animals didn’t show any sleep disruptions at all but they did have mucked up circadian clock genes and they did show depressive phenotypes whereas if they were in the dim red light, they did not,” Nelson said. Nelson explained that photosensitive cells in the retina, which don’t have much to do with vision, detect light and transmit signals to the master circadian clock in the brain that controls the natural sleep-wake cycle.
By Fred Guterl Myths can be more harmful than lies, Nobel laureate Harry Kroto has said, because they are more difficult to recognize and often go unexamined. For many years, a diagnosis of schizophrenia was like a prison sentence, because many people (some of them in the medical profession) held to the notion that a schizophrenic could not recover from the illness and was condemned to an inexorable decline into madness. Like any myth, this one had some truth to it. Many people with severe symptoms do not recover. But some can, as Eleanor Longden discovered for herself. Longden began hearing voices when she was an undergraduate. At first they were somewhat benign, making mostly neutral, factual comments, but they grew more troublesome as she struggled to adjust to college life. Longden was diagnosed as schizophrenic and underwent conventional treatment. By her own account, in “Listening to Voices” in the September/October 2013 issue of Scientific American MIND, the label of schizophrenic and the attitudes of those around her to that label exacerbated her own internal struggles. The voices grew more menacing. Longden began her own slide into madness. But then something odd happened: she began to recover. She did so in part, she says, by accepting the voices in her head as an aspect of her own personality. She listened to them, and tried to understand them. In this way she was able to tame them, and she got enough control over her life to attend school and pursue her graduate studies. © 2013 Scientific American
Link ID: 18481 - Posted: 08.10.2013
by Nora Schultz A unique population in northern Finland has helped reveal that schizophrenia, some autism spectrum disorders and other forms of cognitive impairment may all share a common genetic pathway. In Finland, there exist several small communities that used to live for years in isolation. Amongst the descendants of these groups, otherwise rare genes occur more regularly than elsewhere in the country because a level of inbreeding was almost inevitable. Nelson Freimer at the University of California, Los Angeles, and colleagues studied one of these communities, where schizophrenia and other neurological disorders are unusually common. His team first searched for any genetic deletions – chunks of DNA that are missing from a chromosome – that were more common in this group than in the general population. They found a promising candidate on chromosome 22. A deletion on this chromosome was present in 18 of 173 people from this isolated group, but in just one of the 1586 samples taken from people spread throughout the rest of Finland. Tests confirmed that people with schizophrenia or cognitive impairments were more likely to be missing this chunk of DNA. Identifying this deletion as a risk factor for schizophrenia and cognitive impairment puts us one step closer to understanding the biological processes at the root of such complex syndromes, says Freimer. © Copyright Reed Business Information Ltd.
Women living in urban centres in Canada with more than 500,000 inhabitants are at higher risk of postpartum depression than women in other areas, suggests a new study in the Canadian Medical Association Journal. Looking at the experiences of over 6,000 women who lived in rural, semi-rural, semi-urban or urban areas from the 2006 Canadian Maternity Experiences Survey, the study suggests that women in urban areas were at higher risk, with almost 10 per cent reporting postpartum depression compared with six per cent of women in rural areas, almost seven per cent of women in semirural areas and about five per cent in semiurban areas. Urban areas were found to have higher numbers of immigrant populations, and more women in these areas reported lower levels of social support during and after pregnancy. "We found that Canadian women who lived in large urban areas … were at higher risk of postpartum depression than women living in other areas," said Dr. Simone Vigod, psychiatrist at Women's College Hospital and scientist at Women's College Research Institute in Toronto. "The risk factors for postpartum depression [including history of depression, social support and immigration status] that were unequally distributed across geographic regions accounted for most of the variance in the rates of postpartum depression." The reason why immigrant woman appear to be at higher risk is not really known, she said. "Some theories are that it's related to social support or being away from their family." They could also have cultural barriers or needs that are not being met, she added. © CBC 2013
By Scicurious Most current treatments for depression target the serotonin system, a chemical messenger that plays a role in mood (though it also plays a role in many, many other things). Most of the antidepressant drugs on the market (such as Prozac, Celexa, and Zoloft) that target serotonin do it by blocking the recycling of serotonin, keeping it in the spaces between neurons and allowing it to be active for far longer than it might otherwise. The problem is, these drugs take a long time to work. Often many weeks. In that time, patients may grow frustrated as side effects happen and the needed effects don’t. Patients may be in very desperate straights when they first go on medication, and any extra time before the drugs work becomes that much more dangerous. The drugs may not work at all, causing doctors and patients to have to go through the entire, weeks long process over and over again. Scientists are looking for new antidepressant mechanisms, and trying to create more effective drugs. But there are various ways to go about it. You can go looking for an entirely new way of working, but you can also look at ways to make the current drugs work faster. One target that might help antidepressant drugs work faster is one of the many receptors for serotonin, the 5-HT1A receptor. Receptors are proteins that sit on cell surfaces, and bind chemicals. When they bind a chemical, they cause change, maybe by opening a channel, or starting a signal to make a neuron fire more, or less. What a receptor does depends on its type, but also where in the brain it is located and on what type of cell. © 2013 Scientific American
Link ID: 18463 - Posted: 08.06.2013