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by Sara Reardon As suicide rates climb steeply in the US a growing number of psychiatrists are arguing that suicidal behaviour should be considered as a disease in its own right, rather than as a behaviour resulting from a mood disorder. They base their argument on mounting evidence showing that the brains of people who have committed suicide have striking similarities, quite distinct from what is seen in the brains of people who have similar mood disorders but who died of natural causes. Suicide also tends to be more common in some families, suggesting there may be genetic and other biological factors in play. What's more, most people with mood disorders never attempt to kill themselves, and about 10 per cent of suicides have no history of mental disease. The idea of classifying suicidal tendencies as a disease is being taken seriously. The team behind the fifth edition of the Diagnostic Standards Manual (DSM-5) – the newest version of psychiatry's "bible", released at the American Psychiatric Association's meeting in San Francisco this week – considered a proposal to have "suicide behaviour disorder" listed as a distinct diagnosis. It was ultimately put on probation: put into a list of topics deemed to require further research for possible inclusion in future DSM revisions. Another argument for linking suicidal people together under a single diagnosis is that it could spur research into the neurological and genetic factors they have in common. This could allow psychiatrists to better predict someone's suicide risk, and even lead to treatments that stop suicidal feelings. © Copyright Reed Business Information Ltd.

Related chapters from BP7e: Chapter 16: Psychopathology: Biological Basis of Behavior Disorders; Chapter 15: Emotions, Aggression, and Stress
Related chapters from MM:Chapter 12: Psychopathology: Biological Basis of Behavioral Disorders; Chapter 11: Emotions, Aggression, and Stress
Link ID: 18165 - Posted: 05.18.2013

20:00 13 May 2013 by Douglas Heaven Genes in cells throughout the body switch on and off throughout the day in a coordinated way. Or at least they should. In people with clinical depression, genes in their brain tissues appear to be significantly out of sync – a finding that could lead to new treatments for the condition. We know from previous studies that genes in cells elsewhere, such as the skin, follow a 24-hour cycle of activity. But identifying patterns of genetic activity in a living brain isn't easy to do. "We always assumed we would have a clock [in our brain]," says Huda Akil at the University of Michigan in Ann Arbor. "But it had never been shown before." Akil and her colleagues examined the brains of 55 people with a known time of death, looking at around 12,000 genes in tissues from six brain regions. By matching the time of death with molecular signs of genetic activity – whether each gene was actively expressing itself or not – the team identified hundreds of genes that follow a daily cycle. Sudden death Akil says it was important to look at the brains of individuals who had died suddenly – through a heart attack or car accident, for example. Slower deaths can cause dramatic changes in the brain that would have obscured what they were looking for, but sudden death freezes the genetic activity. "We can capture an instant," she says. © Copyright Reed Business Information Ltd.

Related chapters from BP7e: Chapter 16: Psychopathology: Biological Basis of Behavior Disorders; Chapter 14: Biological Rhythms, Sleep, and Dreaming
Related chapters from MM:Chapter 12: Psychopathology: Biological Basis of Behavioral Disorders; Chapter 10: Biological Rhythms and Sleep
Link ID: 18158 - Posted: 05.14.2013

By Samyukta Mullangi A recent article in NYTimes [1] declared that the rising rate of suicides among our baby boomer generation now made suicides, by raw numbers alone, a bigger killer than motor vehicle accidents! Researchers quoted within the article pointed to complex reasons like the economic downturn over the past decade, the widespread availability of opioid drugs like oxycodone, and changes in marriage, social isolation and family roles. Then I scrolled down, as I always do, to peruse some of the readers’ comments, and that’s when I paused. I suppose in hindsight that I had expected readers to exclaim at the shocking statistics (suicide rates now stand at 27.3 per 100,000 for middle aged men, 8.1 per 100,000 for women), or lament over personal stories of relatives or friends who took their own lives. While I certainly saw a few such comments, I was amazed to discover the number of readers who were sympathetic to the idea of suicide. “Molly” wrote “Why is suicide usually looked upon as a desperate and forbidden act? Can’t we accept that in addition to poverty, loneliness, alienation, ill health, life in world [sic] that is sometimes personally pointless means that death is a relief? I believe the right to die, in a time and place (and wishfully peacefully without violence) is a basic human right.” This post was ‘recommended’ by 351 other readers at the time of this essay being written. © 2013 Scientific American

Related chapters from BP7e: Chapter 16: Psychopathology: Biological Basis of Behavior Disorders; Chapter 14: Biological Rhythms, Sleep, and Dreaming
Related chapters from MM:Chapter 12: Psychopathology: Biological Basis of Behavioral Disorders; Chapter 10: Biological Rhythms and Sleep
Link ID: 18157 - Posted: 05.14.2013

By NICHOLAS BAKALAR Two studies have found that depression and the use of certain antidepressants are both associated with increased risk for Clostridium difficile infection, an increasingly common cause of diarrhea that in the worst cases can be fatal. Researchers studied 16,781 men and women, average age 68, using hospital records and interviews to record cases of the infection, often called C. diff, and diagnoses of depression. The interviews were conducted biennially from 1991 to 2007 to gather self-reports of feelings of sadness and other emotional problems. There were 404 cases of C. difficile infection. After adjusting for other variables, the researchers found that the risk of C. diff infection among people with a history of depression or depressive symptoms was 36 to 47 percent greater than among people without depression. A second study, involving 4,047 hospitalized patients, average age 58, found a similar association of infection with depression. In addition, it found an association of some antidepressants — Remeron, Prozac and trazodone — with C. diff infection. There was no association with other antidepressants. “We have known for a long time that depression is associated with changes in the gastrointestinal system,” said the lead author, Mary A.M. Rogers, a research assistant professor at the University of Michigan, “and this interaction between the brain and the gut deserves more study.” Both reports appeared in the journal BMC Medicine. Copyright 2013 The New York Times Company

Related chapters from BP7e: Chapter 16: Psychopathology: Biological Basis of Behavior Disorders; Chapter 15: Emotions, Aggression, and Stress
Related chapters from MM:Chapter 12: Psychopathology: Biological Basis of Behavioral Disorders; Chapter 11: Emotions, Aggression, and Stress
Link ID: 18136 - Posted: 05.09.2013

By TARA PARKER-POPE Suicide rates among middle-aged Americans have risen sharply in the past decade, prompting concern that a generation of baby boomers who have faced years of economic worry and easy access to prescription painkillers may be particularly vulnerable to self-inflicted harm. More people now die of suicide than in car accidents, according to the Centers for Disease Control and Prevention, which published the findings in Friday’s issue of its Morbidity and Mortality Weekly Report. In 2010 there were 33,687 deaths from motor vehicle crashes and 38,364 suicides. Suicide has typically been viewed as a problem of teenagers and the elderly, and the surge in suicide rates among middle-aged Americans is surprising. From 1999 to 2010, the suicide rate among Americans ages 35 to 64 rose by nearly 30 percent, to 17.6 deaths per 100,000 people, up from 13.7. Although suicide rates are growing among both middle-aged men and women, far more men take their own lives. The suicide rate for middle-aged men was 27.3 deaths per 100,000, while for women it was 8.1 deaths per 100,000. The most pronounced increases were seen among men in their 50s, a group in which suicide rates jumped by nearly 50 percent, to about 30 per 100,000. For women, the largest increase was seen in those ages 60 to 64, among whom rates increased by nearly 60 percent, to 7.0 per 100,000. Suicide rates can be difficult to interpret because of variations in the way local officials report causes of death. But C.D.C. and academic researchers said they were confident that the data documented an actual increase in deaths by suicide and not a statistical anomaly. While reporting of suicides is not always consistent around the country, the current numbers are, if anything, too low. © 2013 The New York Times Company

Related chapters from BP7e: Chapter 16: Psychopathology: Biological Basis of Behavior Disorders; Chapter 15: Emotions, Aggression, and Stress
Related chapters from MM:Chapter 12: Psychopathology: Biological Basis of Behavioral Disorders; Chapter 11: Emotions, Aggression, and Stress
Link ID: 18118 - Posted: 05.04.2013

by Andy Coghlan and Sara Reardon The world's biggest mental health research institute is abandoning the new version of psychiatry's "bible" – the Diagnostic and Statistical Manual of Mental Disorders, questioning its validity and stating that "patients with mental disorders deserve better". This bombshell comes just weeks before the publication of the fifth revision of the manual, called DSM-5. On 29 April, Thomas Insel, director of the US National Institute of Mental Health (NIMH), advocated a major shift away from categorising diseases such as bipolar disorder and schizophrenia according to a person's symptoms. Instead, Insel wants mental disorders to be diagnosed more objectively using genetics, brain scans that show abnormal patterns of activity and cognitive testing. This would mean abandoning the manual published by the American Psychiatric Association that has been the mainstay of psychiatric research for 60 years. The DSM has been embroiled in controversy for a number of years. Critics have said that it has outlasted its usefulness, has turned complaints that are not truly illnesses into medical conditions, and has been unduly influenced by pharmaceutical companies looking for new markets for their drugs. There have also been complaints that widened definitions of several disorder have led to over-diagnosis of conditions such as bipolar disorder and attention deficit hyperactivity disorder. Now, Insel has said in a blog post published by the NIMH that he wants a complete shift to diagnoses based on science not symptoms. © Copyright Reed Business Information Ltd.

Related chapters from BP7e: Chapter 16: Psychopathology: Biological Basis of Behavior Disorders
Related chapters from MM:Chapter 12: Psychopathology: Biological Basis of Behavioral Disorders
Link ID: 18117 - Posted: 05.04.2013

The short answer is no. But your question gets to the heart of an important problem that we have in this country: that all medications are approved by the Food and Drug Administration on the basis of relatively short-term studies, even though many are used long-term for medical and psychiatric disorders that are chronic, if not lifelong. The F.D.A. approves antidepressants like selective serotonin re-uptake inhibitors, or S.S.R.I.’s, if the drug beats a placebo in two randomized clinical trials that typically last 4 to 12 weeks and involve a few hundred patients. Longer-term maintenance studies, usually lasting one to two years, indicate that S.S.R.I.’s do not cause any serious harm, though they have plenty of side effects, like weight gain and sexual dysfunction. Once a drug hits the market, we have only a voluntary system of reporting adverse effects in the United States; there are no systematic long-term studies of any drug lasting 10 or more years. Still, S.S.R.I.’s have been used since the late 1980s and given to more than 40 million Americans, so it’s reasonable to say that if these drugs caused any significant toxic effects, we would have seen many such reports. Instead, we have some anecdotal reports claiming a wide range of S.S.R.I.-related toxicity, but one cannot know from these reports whether the symptoms are related to S.S.R.I. use or to medical illnesses that happen to develop over time in people taking these drugs. Copyright 2013 The New York Times Company

Related chapters from BP7e: Chapter 16: Psychopathology: Biological Basis of Behavior Disorders; Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Related chapters from MM:Chapter 12: Psychopathology: Biological Basis of Behavioral Disorders; Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Link ID: 18116 - Posted: 05.04.2013

By David Levine Sleep deprivation is a quick and efficient way to treat depression. It works 60 to 70 percent of the time—far better than existing drugs—but the mood boost usually lasts only until the patient falls asleep. As an ongoing treatment, sleep deprivation is impractical, but researchers have been studying the phenomenon in an effort to uncover the cellular mechanisms behind depression and remission. Now a team at Tufts University has pinpointed glia as the key players. The researchers previously found that astrocytes, a star-shaped type of glial cell, regulate the brain chemicals involved in sleepiness. During our waking hours, astrocytes continuously release the neurotransmitter adenosine, which builds up in the brain and causes “sleep pressure,” the feeling of sleepiness and its related memory and attention impairments. The neurotransmitter causes this pressure by binding to adenosine receptors on the outside of neurons like a key fitting into a lock. As more adenosine builds up, more receptors are triggered, and the urge to sleep gets stronger. In the new study, published online January 15 in the journal Translational Psychiatry, the scientists investigated whether this process is responsible for the antidepressant effects of sleep deprivation. Mice with depressivelike symptoms were administered three doses of a compound that triggers adenosine receptors, thus mimicking sleep deprivation. Although the mice continued to sleep normally, after 12 hours they showed a rapid improvement in mood and behavior, which lasted for 48 hours. © 2013 Scientific American

Related chapters from BP7e: Chapter 14: Biological Rhythms, Sleep, and Dreaming; Chapter 16: Psychopathology: Biological Basis of Behavior Disorders
Related chapters from MM:Chapter 10: Biological Rhythms and Sleep; Chapter 12: Psychopathology: Biological Basis of Behavioral Disorders
Link ID: 18083 - Posted: 04.27.2013

By Shaunacy Ferro When David Nichols earned a Ph.D in medicinal chemistry from the University of Iowa in 1973 by studying psychedelics, he thought he would continue studying hallucinogens indefinitely. "I thought I would work on it for the rest of my life," he says. His timing was less than fortuitous. In 1970, the year after Nichols started grad school, Richard Nixon signed into law the Controlled Substances Act, designed to clamp down on the manufacture and distribution of drugs in the U.S. The act classified hallucinogenic substances like LSD, DMT, psilocybin (the psychedelic alkaloid in mushrooms) and mescaline as Schedule I substances--the most restrictive use category, reserved for drugs with high potential for abuse and no accepted medical use. Marijuana was also placed in this category, and 15 years later when ecstasy came onto the scene, MDMA was emergency-classified as a Schedule I substance as well. By contrast, cocaine, opium and morphine are Schedule II substances, meaning they can be prescribed by a doctor. Despite some promising results from trials of psychedelics in treating alcoholism, psychiatric conditions and modeling mental illness, by the early '70s, the government had tightened control of Schedule I substances, even for research. It's only now that we're starting to return to the notion that these drugs could be medicine. © 2012 Popular Science

Related chapters from BP7e: Chapter 15: Emotions, Aggression, and Stress; Chapter 16: Psychopathology: Biological Basis of Behavior Disorders
Related chapters from MM:Chapter 11: Emotions, Aggression, and Stress; Chapter 12: Psychopathology: Biological Basis of Behavioral Disorders
Link ID: 18056 - Posted: 04.22.2013

By STEPHEN CASTLE LONDON — British antitrust authorities on Friday accused the pharmaceuticals giant GlaxoSmithKline of paying three rivals to delay the introduction of a generic version of an antidepressant drug. It is the latest so-called pay-for-delay case drawing scrutiny from regulators on both sides of the Atlantic. The Office of Fair Trading in Britain contended that Glaxo had abused its dominant position in the market, kept prices artificially high and denied “significant cost savings” to Britain’s state-run health provider, the National Health Service. The British case centers on efforts by three companies, Alpharma, Generics (U.K.) and Norton Healthcare, to market an alternative to Seroxat, GlaxoSmithKline’s brand of paroxetine. The company sells it in the United States under the brand name Paxil. In recent years, regulators in Europe and the United States have paid greater attention to pay-for-delay deals, suspecting that they may allow pharmaceutical companies to make big profits by exploiting a brief but lucrative period of monopoly over the supply of a product. “These are blockbuster drugs,” said Farasat Bokhari, a senior lecturer in economics at the University of East Anglia, “so if they are on the market without generics challenging them then companies can maintain high, monopoly profits. “As soon as generic entry takes place,” Mr. Bokhari added, “prices drop significantly, sometimes by up to 70 to 80 percent.” GlaxoSmithKline, according to British authorities, warned the three companies that their generic equivalents would infringe a patent. To resolve the dispute, each of the rivals concluded one or more agreements with GlaxoSmithKline, the Office of Fair Trading said. © 2013 The New York Times Company

Related chapters from BP7e: Chapter 16: Psychopathology: Biological Basis of Behavior Disorders
Related chapters from MM:Chapter 12: Psychopathology: Biological Basis of Behavioral Disorders
Link ID: 18050 - Posted: 04.20.2013

Kristoffer Famm, et al. Imagine a day when electrical impulses are a mainstay of medical treatment. Your clinician will administer 'electroceuticals' that target individual nerve fibres or specific brain circuits to treat an array of conditions. These treatments will modulate the neural impulses controlling the body, repair lost function and restore health. They could, for example, coax insulin from cells to treat diabetes, regulate food intake to treat obesity and correct balances in smooth-muscle tone to treat hypertension and pulmonary diseases. All this is within reach if researchers from disparate disciplines in academia and industry work together. Here, we outline what needs to be done to bring about electroceuticals and unveil a public–private research initiative and an award that we hope will catalyse the field. Electrical impulses — action potentials — are the language of the body's nervous system. Virtually all organs and functions are regulated through circuits of neurons communicating through such impulses1. Two features make these circuits excellent targets for therapeutic intervention. First, they comprise discrete components — interconnected cells, fibre tracts and nerve bundles — allowing for pinpoint intervention. Second, they are controlled by patterns of action potentials, which can be altered for treatment. Already, devices that harness electrical impulses are used to treat disease. Pacemakers and defibrillators save millions of lives each year; deep-brain stimulation dramatically improves the quality of life for people with Parkinson's disease and depression; sacral-nerve stimulation restores some bladder control in people with paraplegia, and vagus-nerve stimulation shows clinical benefits in diseases ranging from epilepsy to rheumatoid arthritis2. But these devices do not target specific cells within circuits. © 2013 Nature Publishing Group

Related chapters from BP7e: Chapter 16: Psychopathology: Biological Basis of Behavior Disorders; Chapter 3: Neurophysiology: The Generation, Transmission, and Integration of Neural Signals
Related chapters from MM:Chapter 12: Psychopathology: Biological Basis of Behavioral Disorders; Chapter 3: Neurophysiology: The Generation, Transmission, and Integration of Neural Signals
Link ID: 18032 - Posted: 04.13.2013

By Steven E. Hyman During the past three years the global pharmaceutical industry has significantly decreased its investment in new treatments for depression, bipolar disorder, schizophrenia, and other psychiatric disorders.1 Some large companies, such as GlaxoSmithKline, have closed their psychiatric laboratories entirely. Others, such as Pfizer, have markedly decreased the size of their research programs. Yet others, such as AstraZeneca, have brought their internal research to a close and are experimenting with external collaborations on a smaller scale. This retreat has occurred despite the fact that mental disorders are not only common worldwide, but also increasingly recognized by healthcare systems. There is, moreover, vast unmet medical need, meaning that many individuals with mental disorders remain symptomatic and often disabled despite existing treatments. For example, people suffering with the depressed phase of bipolar disorder often continue to experience severe symptoms even when they take multiple medications with serious side effects. For some significantly disabling conditions, such as the core social deficits of autism and the cognitive impairments of schizophrenia, there simply are no effective treatments. Because mental disorders are highly prevalent and our ability to treat them remains limited, these illnesses cause enormous societal burden. In aggregate, they are the world’s leading cause of disability.2 In addition, this retreat has happened despite the fact that different classes of psychiatric drugs have been among the industry’s most profitable products during the last several decades—and despite the fact that, according to Medco Health Solutions, one in five American adults now takes at least one psychiatric drug. Among the earliest commercial successes were the Valium-like benzodiazepines, used both as tranquilizers and as sleeping pills. These were followed by the Prozac-like selective serotonin reuptake inhibitor (SSRI) antidepressants. Most recently, “second-generation” antipsychotic drugs have been among the global revenue leaders for the pharmaceutical industry, serious side effects notwithstanding. That’s why it’s surprising that almost all industry research dollars are invested in cancer, metabolism, autoimmunity, and other disease areas. Copyright 2013 The Dana Foundation

Related chapters from BP7e: Chapter 16: Psychopathology: Biological Basis of Behavior Disorders; Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Related chapters from MM:Chapter 12: Psychopathology: Biological Basis of Behavioral Disorders; Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Link ID: 18031 - Posted: 04.13.2013

By Kathryn Doyle Despite concerns that antidepressant use during pregnancy might affect infants’ growth and development, a small new study finds no size differences in the first year of life between babies exposed and not exposed to the drugs. The medications — known as selective serotonin reuptake inhibitors, or SSRIs, which include fluoxetine (marketed as Prozac) and citalopram (Celexa) — have been tied to premature births and lower birth weight. But their effect on growth during infancy had not been studied. The agency will lift a requirement that the products carry a strict limit on how long they can be used. “It’s a reassuring finding in that when you have an illness during pregnancy, you want to know what is the impact of the illness and what is the impact of the medication,” Katherine Wisner, the study’s lead author, said. Untreated depression also didn’t seem to influence infant growth, according to Wisner, the director of Northwestern University’s Asher Center for the Study and Treatment of Depressive Disorders. That’s important because a baby’s most rapid growth happens in the first year, which sets the stage for growth patterns for the whole life span, she added. Wisner and her colleagues tracked 97 pregnant women without depression, 46 on antidepressants and 31 with depression that was not treated with medication. Their babies were measured and weighed four times over the first year of life. © 1996-2013 The Washington Post

Related chapters from BP7e: Chapter 16: Psychopathology: Biological Basis of Behavior Disorders; Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 12: Psychopathology: Biological Basis of Behavioral Disorders; Chapter 13: Memory, Learning, and Development
Link ID: 17981 - Posted: 04.02.2013

by Niall Firth Automatic systems that analyse gestures and facial expressions may soon be helping psychologists pick up the easily missed symptoms of depression The interviewee shifts uncomfortably in his seat before stumbling over his answer. The movement, hesitation and telltale gaze aversion are noted: this person may be depressed. The probing questioner is SimSensei, a digital avatar that interviews humans to judge their state of mind. SimSensei is one of several new initiatives designed to partially automate one of the medical profession's trickiest tasks: diagnosing depression. SimSensei is more than an astute questioner. Behind the scenes, it uses face recognition technology and depth-sensing cameras built into Microsoft's Kinect to record and interpret the interviewee's body language. The animated psychologist can then respond appropriately. In work to be presented at the Automatic Face and Gesture Recognition conference in Shanghai, China, next month, Stefan Scherer of the University of Southern California and colleagues used the system to identify characteristic movements that indicate someone may be depressed. To extract the right features, his team interviewed a mixture of healthy volunteers and those who had previously been diagnosed with depression or post-traumatic stress disorder. © Copyright Reed Business Information Ltd

Related chapters from BP7e: Chapter 16: Psychopathology: Biological Basis of Behavior Disorders
Related chapters from MM:Chapter 12: Psychopathology: Biological Basis of Behavioral Disorders
Link ID: 17957 - Posted: 03.28.2013

By HARRIET BROWN Mental-health care has come a long way since the remedy of choice was trepanation — drilling holes into the skull to release “evil spirits.” Over the last 30 years, treatments like cognitive-behavioral therapy, dialectical behavior therapy and family-based treatment have been shown effective for ailments ranging from anxiety and depression to post-traumatic stress disorder and eating disorders. The trouble is, surprisingly few patients actually get these kinds of evidence-based treatments once they land on the couch — especially not cognitive behavioral therapy. In 2009, a meta-analysis conducted by leading mental-health researchers found that psychiatric patients in the United States and Britain rarely receive C.B.T., despite numerous trials demonstrating its effectiveness in treating common disorders. One survey of nearly 2,300 psychologists in the United States found that 69 percent used C.B.T. only part time or in combination with other therapies to treat depression and anxiety. C.B.T. refers to a number of structured, directive types of psychotherapy that focus on the thoughts behind a patient’s feelings and that often include exposure therapy and other activities. Instead, many patients are subjected to a kind of dim-sum approach — a little of this, a little of that, much of it derived more from the therapist’s biases and training than from the latest research findings. And even professionals who claim to use evidence-based treatments rarely do. The problem is called “therapist drift.” “A large number of people with mental health problems that could be straightforwardly addressed are getting therapies that have very little chance of being effective,” said Glenn Waller, chairman of the psychology department at the University of Sheffield and one of the authors of the meta-analysis. Copyright 2013 The New York Times Company

Related chapters from BP7e: Chapter 16: Psychopathology: Biological Basis of Behavior Disorders
Related chapters from MM:Chapter 12: Psychopathology: Biological Basis of Behavioral Disorders
Link ID: 17952 - Posted: 03.26.2013

Arran Frood Two studies have decoded the structure of two of the brain's serotonin receptors. Here shown is a receptor known as 1B with the migraine drug ergotamine (pink) locked into one of its binding pockets. Researchers have deciphered the molecular structures of two of the brain's crucial lock-and-key mechanisms. The two molecules are receptors for the natural neurotransmitter serotonin — which regulates activities such as sleep, appetite and mood — and could provide targets for future drugs to combat depression, migraines or obesity. “This is huge,” says Bryan Roth, a neuropharmacologist at the University of North Carolina Chapel Hill Medical School, and a co-author of the two studies published in Science today1, 2. “Before this there was no crystal structure for any serotonin receptor. A lot of what was theoretical is now known with a great degree of certainty,” he says. Scientists have been trying to decipher serotonin receptors for years. Armed with information on the atomic level, they might now be able to make breakthroughs in drug discovery and in understanding how the physical structures of the brain produce consciousness, says Roth. Christoph Anacker, a neuropharmacologist at King's College London, agrees that the findings are important for drug discovery. “These receptors are involved in so many conditions, especially depression, and knowing the molecular structures will help to develop more specific drugs and avoid the expression of undesired side effects.” © 2013 Nature Publishing Group,

Related chapters from BP7e: Chapter 16: Psychopathology: Biological Basis of Behavior Disorders; Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Related chapters from MM:Chapter 12: Psychopathology: Biological Basis of Behavioral Disorders; Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Link ID: 17937 - Posted: 03.23.2013

By Neuroskeptic When does sadness cease to be a normal emotional response, and become a mental disorder? Can psychiatrists ‘draw the line’ between healthy and sick moods, and if so, where? An important new study offers an answer: When does depression become a disorder? Using recurrence rates to evaluate the validity of proposed changes in major depression diagnostic thresholds (free pdf). The authors, Jerome Wakefield and Mark Schmitz of New York, made use of the ECA survey, a 1980s study of almost 20,000 American adults. Participants were surveyed twice each, approximately one year apart. On each occasion, they were asked questions about their mood, emotions, and mental health symptoms. Some people reported a history of depression at the first visit. Wakefield & Schmitz wanted to find a way of predicting which of those people were most likely to end up depressed at the time of the second interview, a year later – the recurrence rate. To do this, they examined the particular patterns of symptoms reported at the first visit. It turned out that there was a strong predictor of recurrence, which the authors call “complicated” depression. People with a history of complicated depression had a 15% chance of being depressed at follow up. Only 3.4% of those who’d had “uncomplicated” symptoms, however, were depressed a year later. Given that 1.7% of people with no depression history had become unwell by Time 2, this means that “uncomplicated” depression was almost never recurrent.

Related chapters from BP7e: Chapter 16: Psychopathology: Biological Basis of Behavior Disorders
Related chapters from MM:Chapter 12: Psychopathology: Biological Basis of Behavioral Disorders
Link ID: 17911 - Posted: 03.18.2013

By ANAHAD O'CONNOR Depression may lower the effectiveness of the shingles vaccine, a new study found. The research showed that adults with untreated depression who received the vaccine mounted a relatively weak immune response. But those who were taking antidepressants showed a normal response to the vaccine, even when symptoms of depression persist. Shingles, an acute and painful rash, strikes a million Americans each year, mostly older adults. Health officials recommend that those over 60 get vaccinated against the condition, which is caused by reactivation of the same virus that causes chickenpox, varicella-zoster. In the new study, published in the journal Clinical Infectious Diseases, researchers followed a group of 92 older men and women for two years. Forty of the subjects had a major depressive disorder; they were matched with 52 control subjects of similar age. The researchers measured their immune responses to the shingles vaccine and a placebo shot. Compared with the control patients, those with depression were poorly protected by the vaccine. But the patients who were being treated for their depression showed a boost in immunity — what the researchers called a “normalization” of the immune response. It is unclear why that was the case. The authors of the study speculated that treatment of older people with depression might increase the effectiveness of the flu shot and other vaccines as well. Copyright 2013 The New York Times Company

Related chapters from BP7e: Chapter 16: Psychopathology: Biological Basis of Behavior Disorders; Chapter 15: Emotions, Aggression, and Stress
Related chapters from MM:Chapter 12: Psychopathology: Biological Basis of Behavioral Disorders; Chapter 11: Emotions, Aggression, and Stress
Link ID: 17836 - Posted: 02.23.2013

By PAM BELLUCK A type of brain stimulation caused by a mild electric current that appears to have minimal negative side effects is showing promise as a potential treatment for major depression, according to several studies. The experimental therapy, known as transcranial direct current stimulation, or tDCS, involves a low-level charge about one-400th of that used in electroshock treatment. Unlike electroshock (also called electroconvulsive therapy or ECT), which is administered for a few seconds to patients under anesthesia, tDCS is given for 20 to 30 minutes continuously while patients are conscious. While doctors do not see it replacing electroshock, considered the most effective approach for major depression that has been treatment-resistant and requires urgent attention, tDCS does not appear to cause memory loss as electroshock can. Because it is inexpensive and easily administered, scientists say it might become an alternative or additional treatment for people whose depression is not completely helped by medication. “I think tDCS could be tried before ECT,” said Dr. Andre R. Brunoni, a psychiatrist at the University of São Paulo in Brazil and an author of a study published last week in The Journal of the American Medical Association-Psychiatry. Or, he said, it could be used “for avoiding drug treatment in patients that cannot use drugs.” Researchers said Dr. Brunoni’s study is the largest to date of about half a dozen studies in recent years. It is the first comparing tDCS with another treatment — in this case, sertraline, or Zoloft. The study, involving 120 patients, found that tDCS appeared to work about as well as a low dose of Zoloft, and that combined with Zoloft, it worked better than the drug or the stimulation alone. Zoloft and tDCS were equally safe. A few patients became manic, and some developed redness where electrodes were applied. Copyright 2013 The New York Times Company

Related chapters from BP7e: Chapter 16: Psychopathology: Biological Basis of Behavior Disorders
Related chapters from MM:Chapter 12: Psychopathology: Biological Basis of Behavioral Disorders
Link ID: 17789 - Posted: 02.12.2013

A telltale boost of activity at the back of the brain while processing emotional information predicted whether depressed patients would respond to an experimental rapid-acting antidepressant, a National Institutes of Health study has found. “We have discovered a potential neuroimaging biomarker that may eventually help to personalize treatment selection by revealing brain-based differences between patients,” explained Maura Furey, Ph.D., of NIH’s National Institute of Mental Health (NIMH). Furey, NIMH’s Carlos Zarate, M.D., and colleagues, reported on their functional magnetic resonance imaging (fMRI) study of a pre-treatment biomarker for the antidepressant response to scopolamine, Jan. 30, 2013, online in JAMA Psychiatry. Scopolamine, better known as a treatment for motion sickness, has been under study since Furey and colleagues discovered its fast-acting antidepressant properties in 2006. Unlike ketamine, scopolamine works through the brain’s acetylcholine chemical messenger system. The NIMH team’s research has demonstrated that by blocking receptors for acetylcholine on neurons, scopolamine can lift depression in many patients within a few days; conventional antidepressants typically take weeks to work. But not all patients respond, spurring interest in a predictive biomarker. The acetylcholine system plays a pivotal role in working memory, holding information in mind temporarily, but appears to act by influencing the processing of information rather than through memory. Imaging studies suggest that visual working memory performance can be enhanced by modulating acetylcholine-induced activity in the brain’s visual processing area, called the visual cortex, when processing information that is important to the task.

Related chapters from BP7e: Chapter 16: Psychopathology: Biological Basis of Behavior Disorders; Chapter 2: Functional Neuroanatomy: The Nervous System and Behavior
Related chapters from MM:Chapter 12: Psychopathology: Biological Basis of Behavioral Disorders; Chapter 2: Cells and Structures: The Anatomy of the Nervous System
Link ID: 17754 - Posted: 02.05.2013