Chapter 16. Psychopathology: Biological Basis of Behavior Disorders
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By ROBERT PEAR WASHINGTON — Federal investigators say they have found evidence of widespread overuse of psychiatric drugs by older Americans with Alzheimer’s disease, and are recommending that Medicare officials take immediate action to reduce unnecessary prescriptions. The findings will be released Monday by the Government Accountability Office, an arm of Congress, and come as the Obama administration has already been working with nursing homes to reduce the inappropriate use of antipsychotic medications like Abilify, Risperdal, Zyprexa and clozapine. But in the study, investigators said officials also needed to focus on overuse of such drugs by people with dementia who live at home or in assisted living facilities. The Department of Health and Human Services “has taken little action” to reduce the use of antipsychotic drugs by older adults living outside nursing homes, the report said. Doctors sometimes prescribe antipsychotic drugs to calm patients with dementia who display disruptive behavior like hitting, yelling or screaming, the report said. Researchers said this was often the case in nursing homes that had inadequate numbers of employees. Dementia is most commonly associated with a decline in memory, but doctors say it can also cause changes in mood or personality and, at times, agitation or aggression. Experts have raised concern about the use of antipsychotic drugs to address behavioral symptoms of Alzheimer’s and other forms of dementia. The Food and Drug Administration says antipsychotic drugs are often associated with an increased risk of death when used to treat older adults with dementia who also have psychosis. © 2015 The New York Times Company
Anti-depressants are the most commonly-prescribed medication in the U.S., with one in 10 Americans currently taking pills like Zoloft and Lexapro to treat depression. But these pharmaceuticals are only fully effective roughly 30 percent of the time, and often come with troublesome side effects. In a controversial new paper published in the journal Neuroscience & Biobehavioral Reviews, psychologist Paul Andrews of McMaster University in Ontario argues that this failure of medication may be based in a misunderstanding of the underlying chemistry related to depression. Andrews surveyed 50 years' worth of research supporting the serotonin theory of depression, which suggests that the disease is caused by low levels of the "happiness" neurotransmitter, serotonin. But Andrews argues that depression may actually be caused by elevated levels of serotonin. And this fundamental misunderstanding may be responsible for inappropriate treatment: The most common form of antidepressants are selective serotonin re-uptake inhibitors (SSRIs), which operate by targeting serotonin receptors in the brain in an effort to amplify serotonin production. Currently, scientists are unable to measure precisely how the brain releases and uses serotonin, because it can't be safely observed in a human brain. But Andrews points to research on animals which suggests that serotonin might work just the opposite from what we've assumed. ©2015 TheHuffingtonPost.com, Inc.
Link ID: 20636 - Posted: 03.02.2015
Distinct changes in the immune systems of patients with ME or chronic fatigue syndrome have been found, say scientists. Increased levels of immune molecules called cytokines were found in people during the early stages of the disease, a Columbia University study reported. It said the findings could help improve diagnosis and treatments. UK experts said further refined research was now needed to confirm the results. People with ME (myalgic encephalopathy) or CFS (chronic fatigue syndrome) suffer from exhaustion that affects everyday life and does not go away with sleep or rest. They can also have muscle pain and difficulty concentrating. ME can also cause long-term illness and disability, although many people improve over time. It is estimated that around 250,000 people in the UK have the disease. Disease pattern The US research team, who published their findings in the journal Science Advances, tested blood samples from nearly 300 ME patients and around 350 healthy people. They found specific patterns of immune molecules in patients who had the disease for up to three years. These patients had higher levels of of cytokines, particularly one called interferon gamma, which has been linked to the fatigue that follows many viral infections. Healthy patients and those who had the disease for longer than three years did not show the same pattern. Lead author Dr Mady Hornig said this was down to the way viral infections could disrupt the immune system. "It appears that ME/CFS patients are flush with cytokines until around the three-year mark, at which point the immune system shows evidence of exhaustion and cytokine levels drop."
By ABIGAIL ZUGER, M.D. On an early summer night in 1944, on the wooded shoulder of a rural Massachusetts highway, a man in a rumpled brown suit wandered in the shadows. Whenever a car passed, he dropped to the ground and lay flat. His hair was matted, his face smeared with mud. He was a respectable Boston doctor on the lam, hungry, lost and ill. He was Mimi Baird’s father, Dr. Perry Baird, a Texas-born, Harvard-trained physician whose severe bipolar disease ultimately destroyed his life and scarred his family with the usual wide-ranging cruelties of mental illness. Dr. Baird vanished from Ms. Baird’s life when she was a little girl. She saw him once, briefly, when she was a teenager, then never again. He died in his mid-50s, in 1959. More than 30 years later, when Ms. Baird herself was in her 50s, a large package arrived on her doorstep and her father re-entered her world. The box contained a manuscript long forgotten in a relative’s garage, written in smudged pencil on onionskin paper, a memoir her father had composed of five terrible months in his life. The story began the very day Dr. Baird said goodbye to 5-year-old Mimi and her sister, and permanently left the household. Stunned and bereft all over again, Ms. Baird then spent two decades chasing down the rest of the story, talking to neighbors, colleagues and relatives about long-ago events and obtaining her father’s medical records. Now in her late 70s, a retired medical administrator, she has, with the help of a co-author, woven all this material into “He Wanted the Moon,” an extraordinary Möbius strip of a book. (Read an excerpt.) Its core is the full text of her father’s manuscript, deftly annotated and explained. Around it she layers the voices of caretakers, friends, relatives and medical authorities. Events are revisited and reframed, turned inside out, then right side up again. The book is autobiography, biography, science, history and literature all in one, as instructive as any textbook and utterly impossible to put down. © 2015 The New York Times Company
Link ID: 20600 - Posted: 02.24.2015
By Kate Baggaley A buildup of rare versions of genes that control the activity of nerve cells in the brain increases a person’s risk for bipolar disorder, researchers suggest in a paper posted online the week of February 16 in Proceedings of the National Academy of Sciences. “There are many different variants in many different genes that contribute to the genetic risk,” says coauthor Jared Roach, a geneticist at the Institute for Systems Biology in Seattle. “We think that most people with bipolar disorder will have inherited several of these…risk variants.” The bulk of a person’s risk for bipolar disorder comes from genetics, but only a quarter of that risk can be explained by common variations in genes. Roach’s team sequenced the genomes of 200 people from 41 families with a history of bipolar disorder. They then identified 164 rare forms of genes that show up more often in people with the condition. People with bipolar disorder had, on average, six of these rare forms, compared with just one, on average, found in their healthy relatives and the general population. The identified genes control the ability of ions, or charged particles, to enter or leave nerve cells, or neurons. This affects neurons’ ability to pass information through the brain. Some of the gene variants probably increase how much neurons fire while others decrease it, the researchers say. Future research will need to explain what role these brain changes play in bipolar disorder. Citations S.A. Ament et al. Rare variants in neuronal excitability genes influence risk for bipolar disorder. Proceedings of the National Academy of Sciences. Published online the week of February 16, 2015. doi:10.1073/pnas.1424958112. © Society for Science & the Public 2000 - 2015
|By Gary Stix Implantation of electrodes deep within the brain is now commonly performed for treatment of the neurological disorders Parkinson’s disease and essential tremor. But the use of deep-brain stimulation, as it is known, is expanding. It is now being assessed in as many as 200 patients for major depression—and is being considered for other disorders such as anorexia. Helen Mayberg, a neurologist from Emory University, has pioneered the use of imaging techniques to understand the functioning of different brain circuits to determine how to tailor various treatments for depression, including deep-brain stimulation, to a patient’s needs. Learn about her work below in “Deep-Brain Stimulation: A Decade of Progress with Helen Mayberg,” a Webinar put on by the Brain & Behavior Research Foundation. © 2015 Scientific American
Link ID: 20584 - Posted: 02.16.2015
By Rachel Ehrenberg SAN JOSE, Calif. — New moms suffering from postpartum depression change their activity on Facebook, suggesting that the social media site could help detect the onset of the baby blues. Many new parents share pictures and videos of their babies on Facebook and use the site to interact with friends they might be too busy to see in person. But compared with most typical new moms, those suffering from postpartum depression are less active on the social media site, Munmun De Choudhury of Georgia Tech reported February 14 at the annual meeting of the American Association for the Advancement of Science. She and her colleagues at Microsoft Research in Redmond, Wash., conducted an elaborate study that included a depression screening questionnaire, interviews and an analysis of Facebook activity and interactions of 165 mothers both before and after they had their babies. These women also tend to keep a stiff upper lip on the site, refraining from reporting on their emotional well-being and instead posting objective content geared toward getting feedback or advice on a specific matter, De Choudhury and her colleagues discovered. The scientists also found they could train a computer program to identify which moms had the blues. Such research might help with designing interventions, whereby moms could be warned that they might be sinking into depression and encouraged to reach out for social support or medical attention. M. De Choudhury. Online Social Dynamics and Emotional Wellbeing. American Association for the Advancement of Science Annual Meeting, San Jose, Calif., February 14, 2015. © Society for Science & the Public 2000 - 2015
Smoking potent cannabis was linked to 24% of new psychosis cases analysed in a study by King's College London. The research suggests the risk of psychosis is three times higher for users of potent "skunk-like" cannabis than for non-users. The study of 780 people was carried out by KCL's Institute of Psychiatry, Psychology and Neuroscience. A Home Office spokesman said the report underlines the reasons why cannabis is illegal. Scientists found the risk of psychosis was five times higher for those who use it every day compared with non-users. They also concluded the use of hash, a milder form of the drug, was not associated with increased risk of psychosis. Psychosis refers to delusions or hallucinations that can be present in certain psychiatric conditions such as schizophrenia and bipolar disorder. "Compared with those who had never tried cannabis, users of high potency skunk-like cannabis had a threefold increase in risk of psychosis,' said Dr Marta Di Forti, lead author on the research. She added: "The results show that psychosis risk in cannabis users depends on both the frequency of use and cannabis potency." Dr Di Forti told BBC Radio 4's Today programme that the availability of skunk-like cannabis was becoming more widespread. "In London, it's very difficult to find anything else," she said. "There were lots of reports from police across the UK saying we have become a great producer of skunk. And not only do we use it locally but we export, so this is a Made in England product." Someone suffering from psychosis would often be "extremely paranoid and become very suspicious" about the people around them, she added. She has called for "a clear public message" to cannabis users, comparable to medical advice on alcohol and tobacco. © 2015 BBC
By Jane E. Brody Bereavement — how one responds and adjusts to the death of a loved one — is a very individual matter. It is natural to experience a host of negative reactions in the weeks and months following the loss of a loved one: among them, sadness, difficulty sleeping, painful reminders of the person, difficulty enjoying activities once shared, even anger. Grief is a normal human reaction, not a disease, and there is no one right way to get through it. Most often, within six months of a death, survivors adjust and are more or less able to resume usual activities, experience joy, and remember their loved ones without intense pain. But sometimes, even when the loss is neither sudden nor unexpected, as is true in the majority of deaths in the United States, survivors close to the deceased can experience extremely disruptive grief reactions that persist far longer. In a report last month in The New England Journal of Medicine, Dr. M. Katherine Shear presents a composite portrait of what is known as complicated grief, an extreme, unrelenting reaction to loss that persists for more than six months and can result in a serious risk to health. She describes a 68-year-old widow who continued to be seriously impaired by grief four years after her husband died. The woman slept on the couch because she could not bear to sleep in the bed she had shared with him. She found it too painful to engage in activities they used to do together. She no longer ate regular meals because preparing them was a too-distressing reminder of her loss. And she remained alternately angry with the medical staff who cared for him and with herself for not recognizing his illness earlier. Symptoms of complicated grief commonly include intense yearning, longing or emotional pain; frequent preoccupying, intrusive thoughts and memories of the person lost; a feeling of disbelief or inability to accept the loss; and difficulty imagining a meaningful life without that person. © 2015 The New York Times Company
By David Tuller The Institute of Medicine on Tuesday proposed a new name and new diagnostic criteria for the condition that many still call chronic fatigue syndrome. Experts generally agree that the disease has a physical basis, but they have struggled for decades to characterize its symptoms. The new report may help improve diagnosis, but the recommendations are unlikely to end the long, contentious debate over who has the condition and what may be causing it. An institute panel recommended that the illness be renamed “systemic exertion intolerance disease,” a term that reflects what patients, clinicians and researchers all agree is a core symptom: a sustained depletion of energy after minimal activity, called postexertional malaise. The new name “really describes much more directly the key feature of the illness, which is the inability to tolerate both physical and cognitive exertion,” said Dr. Peter Rowe, a member of the panel and a pediatrician at Johns Hopkins who treats children with the condition. An alternate name for the illness, myalgic encephalomyelitis, meaning “brain and spinal cord inflammation with muscle pain,” was coined decades ago. Many experts now refer to the condition as M.E./C.F.S. About one million people in the United States are believed to have the syndrome. Many say they have been accused of imagining or exaggerating their symptoms, and many doctors have long viewed it as a psychological illness. The authors urged that doctors take patients’ physical complaints seriously. “This is not a figment of their imagination,” said Dr. Ellen Wright Clayton, the chairwoman of the Institute of Medicine panel and a professor of pediatrics and law at Vanderbilt University. Patients attribute much of their mistreatment to the name “chronic fatigue syndrome,” chosen by the Centers for Disease Control in 1988. © 2015 The New York Times Company
Link ID: 20573 - Posted: 02.13.2015
By ALAN SCHWARZ High numbers of students are beginning college having felt depressed and overwhelmed during the previous year, according to an annual survey released on Thursday, reinforcing some experts’ concern about the emotional health of college freshmen. The survey of more than 150,000 students nationwide, “The American Freshman: National Norms Fall 2014,” found that 9.5 percent of respondents had frequently “felt depressed” during the past year, a significant rise over the 6.1 percent reported five years ago. Those who “felt overwhelmed” by schoolwork and other commitments rose to 34.6 percent from 27.1 percent. Conducted by the Cooperative Institutional Research Program at the University of California, Los Angeles’s Higher Education Research Institute for almost 50 years, the survey assesses hundreds of matters ranging from political views to exercise habits. It is considered one of the most comprehensive snapshots of trends among recent high school seniors and is of particular interest to people involved in mental well-being. “It’s a public health issue,” said Dr. Anthony L. Rostain, a psychiatrist and co-chairman of a University of Pennsylvania task force on students’ emotional health. “We’re expecting more of students: There’s a sense of having to compete in a global economy, and they think they have to be on top of their game all the time. It’s no wonder they feel overwhelmed.” Other survey results indicated that students were spending more time on academics and socializing less — trends that would normally be lauded. But the lead author of the study, Kevin Eagan, cautioned that the shift could result in higher levels of stress. © 2015 The New York Times Company
By Janice Neumann (Reuters Health) - Moderate-intensity exercise, or even just walking, can improve quality of life for depressed middle-aged women, a large Australian study suggests. Women who averaged 150 minutes of moderate exercise (golf, tennis, aerobics classes, swimming, or line-dancing) or 200 minutes of walking every week had more energy, socialized more, felt better emotionally, and weren't as limited by their depression when researchers followed up after three years. They also had less pain and did better physically, although the psychological benefit was greater. With depression so prevalent, "there is an urgent need" to identify treatments, including non-medical options that people can do themselves, said Kristiann Heesch, who led the study. Heesch, senior lecturer at Queensland University of Technology, and her colleagues point out in a January 13 online article in the American Journal of Preventive Medicine that depression is expected to be the second-leading cause of global disease by 2030 and the leading cause in high-income countries. One in 10 U.S. adults suffers from depression, according to the Centers for Disease Control and Prevention. Women are 70% more likely to be depressed at some point in their lives than men, according to the National Institute of Mental Health. In previous research, Heesch found that exercise and walking could boost physical and emotional health in women who are not depressed. © 2015 Scientific American
Link ID: 20536 - Posted: 01.31.2015
by Jessica Hamzelou WHAT doesn't kill you makes you stronger, at least when it comes to stress and immune cells. Mice that received a cocktail of immune cells from bullied mice appeared to experience a mood boost. The unexpected discovery may have implications for treating depression. We know that prolonged bouts of stress take their toll on the immune system. That leaves us susceptible to illness, which in some cases can lead to depression. Most research on the link between immune health and mood has focused on the innate branch of the immune system – the cells that mount the first response to pathogens, says Miles Herkenham at the National Institutes of Health in Bethesda, Maryland. His team wondered if there might also be a role for the adaptive branch of the immune system, which "learns" about a pathogen in order to respond rapidly the next time it appears. To find out, the team introduced an aggressive competitor mouse into the cages of male mice. "These mice are like bullies," says Herkenham. Two weeks later, the bullied mice seemed depressed: they cowered in dark corners and seemed uninterested in the scent of a female. The team extracted their adaptive immune cells and injected them into another set of mice bred to lack these cells. This meant that the recipient mice essentially acquired the adaptive immune system of the bullied ones. © Copyright Reed Business Information Ltd.
|By Tori Rodriguez Scientists have studied brain structure for decades, so most disease-related structural anomalies have been long known. New findings of this nature are rare—yet last summer one neuroscientist studying depression published just that. Over nine years of sorting through countless brain images, Jerome J. Maller of Monash University and Alfred Hospital in Melbourne noticed a particular type of brain abnormality that seemed to show up more often in depressed patients. Their occipital lobes were often wrapped around each other. Maller and his colleagues investigated further and found that depressed patients are indeed three times as likely to have wraparound lobes. Occipital bending occurred in 35.3 percent of the depressed patients and 12.5 percent of the control subjects, according to their paper, published in Brain. The effect was even more pronounced in women: 45.8 percent of female patients with major depressive disorder exhibited occipital bending versus only 5.9 percent of women without depression, possibly because women's brains fit more snugly in their skulls than men's do. Previous studies have also found that occipital bending is more common in patients with schizophrenia. Maller suggests the lobes may wrap around each other when space for brain growth becomes constricted, perhaps because the brain is not doing enough neural pruning—the process by which the brain gets rid of neurons that are no longer needed. Indeed, many other studies have found that depressed brains are hyperconnected. Maller does not know if the finding will have clinical implications beyond helping to diagnose depression, but experts hope that this avenue of research will eventually lead to a deeper understanding of the disorder. “It really suggests some significant biological basis for at least some forms of depression,” says William Hopkins, a professor of neuroscience at Georgia State University, who was not involved in the study. © 2015 Scientific American
|By Simon Makin People with depression process emotional information more negatively than healthy people. They show increased sensitivity to sad faces, for instance, or a weaker response to happy faces. What has been missing is a biological explanation for these biases. Now a study reveals a mechanism: an unusual balance of chemicals in a brain area crucial for the feeling of disappointment. A team led by Roberto Malinow of the University of California, San Diego, studied the lateral habenula, a evolutionarily ancient region deep in the brain [see diagram on bottom]. Neurons in this region are activated by unexpected negative events, such as a punishment out of the blue or the absence of an anticipated reward. For example, studies have shown that primates trained to expect a reward, such as juice, after a visual cue show heightened activity in the lateral habenula if the reward is withheld. Such findings have led to the idea that this area is a key part of a “disappointment circuit.” Past studies have also shown that hyperactivity in the lateral habenula is linked with depressionlike behavior in rodents. In people with depression, low levels of serotonin, the brain chemical targeted by antidepressants, are linked with a rise in lateral habenula activity. The region is unusual because it lacks the standard equipment the brain uses to reduce overactivity: opposing sets of neurons that either increase activity by secreting the chemical glutamate or decrease activity by secreting the chemical GABA. The lateral habenula has very few neurons that decrease activity, so Malinow and his colleagues set out to discover how the brain tamps down activity there. © 2015 Scientific American
Link ID: 20508 - Posted: 01.22.2015
By Consumer Reports The headlines about coffee’s impact on your health seem to change as quickly as the time it takes to drink a cup. Should you savor every drop or try to cut down? Here’s what we know right now: It may lengthen your life. True, coffee drinkers are more likely than nondrinkers to smoke, eat red meat, skimp on exercise and have other life-shortening habits, according to a large 2012 study published in the New England Journal of Medicine. But even after adjusting for such factors, they found that people age 50 to 71 who drank at least one cup of coffee per day had a lower risk than nondrinkers of dying from diabetes, heart disease or other health problems when followed for more than a decade. That may be due to beneficial compounds in coffee such as antioxidants — which might ward off disease — and not caffeine. Decaf drinkers had the same results. It may make you happier. Coffee is not just a pick-me-up; it also has been linked to a lower risk of depression. In a study led by the Harvard School of Public Health that tracked 50,000 women for 10 years, those who drank four or more cups of caffeinated coffee per day were 20 percent less likely to develop depression than nondrinkers. Another study found that adults who drank two to four cups of caffeinated coffee were about half as likely to attempt suicide as decaf drinkers or abstainers. The researchers speculated that long-term coffee drinking may boost the production of “feel good” hormones such as dopamine. It contains many good-for-you chemicals.
By Richard Leiby NEWPORT BEACH, Calif. — The headquarters of Oakley, a maker of recreational and military gear, looks as if it belongs in a war zone. It’s a massive bunker with exposed steel pipes, girders and blast walls. Even the dais in the auditorium is armored. But on a recent afternoon, the talk inside the building, set atop an arid, inland hillside in Orange County, is not about fighting wars but about caring for warriors. Doctors, scientists and veterans approach the podium at a conference to present some of the latest tools to help vets recover from wounds both mental and physical: bionics, virtual reality, magnetic waves. A session called “Healing the Warrior Brain” features a trim, bleach-blond former Army staff sergeant named Jonathan Warren, who recounts on video his struggle with post-traumatic stress disorder after combat in Iraq. His flashbacks, panic attacks and booze benders were well chronicled: For a year, the Los Angeles Times tracked Warren’s efforts to find peace, including via Department of Veterans Affairs therapy. It didn’t work, he says. But now a different Jon Warren is here to say that he is finally free of symptoms, one year after that 2013 story ran. No longer does his worst memory of the Iraq war — failing to rescue his best friend, who nearly burned to death after their Humvee hit a roadside bomb in 2006 — grasp his psyche and inflict guilt. That’s because of a revolutionary new treatment that retuned his brain, he says, and set “my frequencies right.” Now he’s able to proudly embrace his military service, “to keep the memory, to be able to go there,” Warren tells the audience, “and not be controlled by it.”
Link ID: 20474 - Posted: 01.13.2015
By Richard A. Friedman, M.D. You’re feeling down, and your doctor or therapist has confirmed it: You have depression. Now what? Until recently, many experts thought that your clinician could literally pick any antidepressant or type of psychotherapy at random because, with a few clinical exceptions, there was little evidence to favor one treatment over another for a given patient. In fact, I used to delight in tormenting the drug company representatives when they asked me how I picked an antidepressant. I would take a quarter out of my pocket, flip the coin and say I’d let chance decide because their drug was no better or worse than their competitors’. Although the holy grail of personalized therapy — be it with psychotropic drugs or psychotherapy — has proved elusive, we’ve learned a lot recently about individual factors that might predict a better response to one type of treatment over another. Dr. Helen Mayberg, a professor of psychiatry at Emory University, recently published a study in JAMA Psychiatry that identified a potential biomarker in the brain that could predict whether a depressed patient would respond better to psychotherapy or antidepressant medication. Using PET scans, she randomized a group of depressed patients to either 12 weeks of treatment with the S.S.R.I. antidepressant Lexapro or to cognitive behavior therapy, which teaches patients to correct their negative and distorted thinking. Over all, about 40 percent of the depressed subjects responded to either treatment. But Dr. Mayberg found striking brain differences between patients who did well with Lexapro compared with cognitive behavior therapy, and vice versa. Patients who had low activity in a brain region called the anterior insula measured before treatment responded quite well to C.B.T. but poorly to Lexapro; conversely, those with high activity in this region had an excellent response to Lexapro, but did poorly with C.B.T. © 2015 The New York Times Company
Link ID: 20468 - Posted: 01.10.2015
Sara Reardon Ketamine, a psychoactive ‘party drug’ better known as Special K, has pharmaceutical companies riding high. Used clinically as an anaesthetic in animals and humans, it has proved an extremely effective treatment for depression, bipolar disorder and suicidal behaviour. It also works incredibly fast. Unlike conventional antidepressants, which generally take weeks to start working, ketamine lifts depression in as little as two hours. “It blew the doors off what we thought we knew about depression treatment,” says psychiatrist James Murrough at Mount Sinai Hospital in New York City. Companies are racing to develop patentable forms of the drug, and researchers are battling to understand how it affects the brain. An increasing number of clinicians are prescribing ketamine off-label for their patients, even as some of their colleagues worry that too little is known about its long-term effects. The excitement over ketamine shows how badly new depression drugs are needed, says Thomas Insel, director of the US National Institute of Mental Health (NIMH) in Bethesda, Maryland. Many drug companies have closed their mental-health divisions in the past five years, and there have been no significant advances in medication for depression in decades. Today’s most common antidepressants target the brain’s serotonin or noradrenaline pathways (some target both). Ketamine blocks the signalling molecule NMDA, a component of the glutamate pathway, which is involved in memory and cognition. Before ketamine was studied, no one even knew that the pathway was involved in depression, Murrough says. © 2015 Nature Publishing Group
Haroon Siddique Research that aims to map the activity of serotonin in the brain could revolutionise the use of antidepressants and behavioural therapy for people with mental illnesses. The neurotransmitter serotonin has long been associated with mood, with drugs that boost the chemical in the brain helping to alleviate the symptoms of common illnesses such as depression and anxiety, but scientists lack a deep understanding of how it mediates different mood disorders. By understanding the biology of serotonin, the hope is that drugs can be created that only target cells relevant to a particular disorder and behavioural therapies can be made more effective, reducing the need for antidepressants. Dr Jeremiah Cohen, an assistant professor at the Johns Hopkins Brain Science Institute in Baltimore, said: “The ultimate aim is to understand the biology of mood and how groups of cells in the brain connect to produce our emotional behaviour. Most antidepressants operate broadly in the entire serotonin system. What we hope to do with this map is use drugs that are available or design new drugs that will target only the components of that system relevant to a particular disorder.” The use of antidepressants in England has soared since the late 1990s, raising concerns in some quarters about over-prescription. Researchers from the Nuffield Trust and the Health Foundation found that 40m prescriptions for antidepressants were made in 2012, compared to 15m in 1998. Doctors write prescriptions for more than one in 10 adults in developed countries, with Iceland, Australia, Canada and European Nordic countries leading the way, according to 2013 data from the Organisation for Economic Co-operation and Development. More than 10% of American adults have used antidepressants.
Link ID: 20455 - Posted: 01.06.2015