Chapter 12. Psychopathology: Biological Basis of Behavioral Disorders
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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
By Dr. Mitesh Popat It’s common knowledge that eating better, exercising more, limiting alcohol intake and not smoking can lead to a healthier, longer life. For many, sustaining healthy behaviors is not easy. For diabetics, maintaining healthy behaviors is even more challenging, although it is critical. If well managed, the disease can be held in check; if not, it can be devastating, leading to kidney failure, blindness, stroke and even death. It may be a surprise that there is strong association between depression, anxiety and diabetes. Not only can depression and anxiety seriously affect the ability to manage the disease, but there also is evidence that, for some, depression plays a role in actually causing diabetes. Research indicates that depression is unrecognized and untreated in approximately two-thirds of patients with diabetes. Whether cause or effect, the medical profession needs to do more to address the psychological issues associated with the disease. As a family medicine physician, I see the association on daily basis. Some patients are so overwhelmed by the necessary daily self-care that comes with diabetes that they become highly anxious and depressed. Others who are suffering from complications or are having trouble managing their blood sugar levels may feel a loss of control and get anxious or depressed. These symptoms are often compounded in people who live in poverty, including the low-income Latinos, African Americans and seniors whom we care for at Marin Community Clinics. Diabetes has become an epidemic in these groups. Working three jobs and constantly worrying about making ends meet can trigger depression and anxiety in anyone. Add to that the need to adopt a disciplined healthy lifestyle, and it can be a real struggle.
Link ID: 20410 - Posted: 12.13.2014
By ANDREW POLLACK It is either the most exciting new treatment for depression in years or it is a hallucinogenic club drug that is wrongly being dispensed to desperate patients in a growing number of clinics around the country. It is called ketamine — or Special K, in street parlance. While it has been used as an anesthetic for decades, small studies at prestigious medical centers like Yale, Mount Sinai and the National Institute of Mental Health suggest it can relieve depression in many people who are not helped by widely used conventional antidepressants like Prozac or Lexapro. And the depression seems to melt away within hours, rather than the weeks typically required for a conventional antidepressant. But some psychiatrists say the drug has not been studied enough to be ready for use outside of clinical trials, and they are alarmed that clinics are springing up to offer ketamine treatments, charging hundreds of dollars for sessions that must be repeated many times. “We don’t know what the long-term side effects of this are,” said Dr. Anthony J. Rothschild, a professor of psychiatry at the University of Massachusetts Medical School. Some psychiatrists say the drug has not been studied enough to be ready for use outside of clinical trials. Credit Sandy Huffaker for The New York Times Pharmaceutical companies hope to solve the problem by developing drugs that work like ketamine but without the side effects, which are often described as out-of-body experiences. © 2014 The New York Times Company
By Tina Rosenberg When Ebola ends, the people who have suffered, who have lost loved ones, will need many things. They will need ways to rebuild their livelihoods. They will need a functioning health system, which can ensure that future outbreaks do not become catastrophes. And they will need mental health care. Depression is the most important thief of productive life for women around the world, and the second-most important for men. We sometimes imagine it is a first-world problem, but depression is just as widespread, if not more so, in poor countries, where there is a good deal more to be depressed about. And it is more debilitating, as a vast majority of sufferers have no safety net. Health care for all must include mental health care. It’s hard to believe but both Liberia and Sierra Leone have only a single psychiatrist. The Ebola crisis has exposed these countries’ malignant neglect of their health systems. People can’t get care for diarrhea and malaria. How will these countries take care of an epidemic of depression? This isn’t really a medical question. We know how to treat depression. What we don’t know yet is how to make effective treatment cheap, culturally appropriate, convenient and non-stigmatizing — all needed to get treatment out to millions and millions of people. But some researchers are finding out. They are doing so despite the fact that growing attention to this issue hasn’t been accompanied by money. The U.S. National Institute of Mental Health last year provided just $24.5 million for global mental health efforts, and the Canadian government’s Grand Challenges Canada, which is said to have the largest portfolio of mental health innovation in developing countries, has spent only $28 million on them since it began in 2010. © 2014 The New York Times Company
Link ID: 20404 - Posted: 12.08.2014
By Neuroskeptic | An important new study could undermine the concept of ‘endophenotypes’ – and thus derail one of the most promising lines of research in neuroscience and psychiatry. The findings are out now in Psychophysiology. Unusually, an entire special issue of the journal is devoted to presenting the various results of the study, along with commentary, but here’s the summary paper: Knowns and unknowns for psychophysiological endophenotypes by Minnesota researchers William Iacono, Uma Vaidyanathan, Scott Vrieze and Stephen Malone. In a nutshell, the researchers ran seven different genetic studies to try to find the genetic basis of a total of seventeen neurobehavioural traits, also known as ‘endophenotypes’. Endophenotypes are a hot topic in psychiatric neuroscience, although the concept is somewhat vague. The motivation behind interest in endophenotypes comes mainly from the failure of recent studies to pin down the genetic cause of most psychiatric syndromes: endophenotypes_A Essentially an endophenotype is some trait, which could be almost anything, which is supposed to be related to (or part of) a psychiatric disorder or symptom, but which is “closer to genetics” or “more biological” than the disorder itself. Rather than thousands of genes all mixed together to determine the risk of a psychiatric disorder, each endophenotype might be controlled by only a handful of genes – which would thus be easier to find.
Close to 8 percent of Americans have depression of some kind, but only about a third of those are getting treated for it, a major federal survey finds. The most depressed group? Women ages 40 to 59. More than 12 percent of women that age say they're depressed. The least? Teenage boys. Just 4 percent of them have been diagnosed with depression. "During 2009-2012, 7.6 percent of Americans aged 12 and over had depression (moderate or severe depressive symptoms in the past 2 weeks)," Laura Pratt and Debra Brody of the National Center for Health Statistics wrote. "About 3 percent of Americans aged 12 and over had severe depressive symptoms," they added. "Of those with severe symptoms, 35 percent reported having contact with a mental health professional in the past year." This is troubling, because depression is difficult to treat and does best when people are given a combination of drugs and counseling. People living below the poverty level were more than twice as likely to have depression than people making more money. Almost 43 percent of people with severe depressive symptoms reported serious difficulties in work, home and social activities.
Link ID: 20383 - Posted: 12.03.2014
By Nicholas Bakalar Short-term psychotherapy may be an effective way to prevent repeated suicide attempts. Using detailed Danish government health records, researchers studied 5,678 people who had attempted suicide and then received a program of short-term psychotherapy based on needs, including crisis intervention, cognitive therapy, behavioral therapy, and psychodynamic and psychoanalytic treatment. They compared them with 17,034 people who had attempted suicide but received standard care, including admission to a hospital, referral for treatment or discharge with no referral. They were able to match the groups in more than 30 genetic, health, behavioral and socioeconomic characteristics. The study is online in Lancet Psychiatry. Treatment focused on suicide prevention and comprised eight to 10 weeks of individual sessions. Over a 20-year follow-up, 16.5 percent of the treated group attempted suicide again, compared with 19.1 percent of the untreated group. In the treated group, 1.6 percent died by suicide, compared with 2.2 percent of the untreated. “Suicide is a rare event,” said the lead author, Annette Erlangsen, an associate professor at the Johns Hopkins Bloomberg School of Public Health, “and you need a huge sample to study it. We had that, and we were able to find a significant effect.” The authors estimate that therapy prevented 145 suicide attempts and 30 deaths by suicide in the group studied. © 2014 The New York Times Company
Link ID: 20379 - Posted: 12.02.2014
By EUGENIA BONE I TRIED magic mushrooms out of curiosity and in middle age. I’d been on the amateur mycological circuit for a couple of years, but hallucinogenic species were rarely mentioned at the foraging expeditions and conferences I attended. It’s almost as if they were the black sheep of mycology: embarrassing to serious taxonomy jocks. I read some books on the subject, but most were tripper’s guides that didn’t utilize, um, specific language or current science. Psychoactive mushrooms had been in a kind of scientific ghetto ever since they were criminalized in 1968. But now the drug derived from the mushroom, psilocybin, is finally being re-examined for its medical applications. A study published last month in the Journal of the Royal Society Interface compared M.R.I.s of the brains of subjects injected with psilocybin with scans of their normal brain activity. The brains on psilocybin showed radically different connectivity patterns between cortical regions (the parts thought to play an important role in consciousness). The researchers mapped out these connections, revealing the activity of new neural networks between otherwise disconnected brain regions. The researchers suspect that these unusual connections may be responsible for the synesthetic experience trippers describe, of hearing colors, for example, and seeing sounds. The part of the brain that processes sound may be connecting to the part of the brain that processes sight. The study’s leader, Paul Expert at King’s College London, told me that his team doubted that this psilocybin-induced connectivity lasted. They think they are seeing a temporary modification of the subject’s brain function. © 2014 The New York Times Company
By Anna North What is depression? Anyone who has dealt with the condition knows what it can feel like — but what causes it, what sustains it, and what’s the best way to make it subside? Despite the prevalence of the disorder — in one Centers for Disease Control and Prevention study, 9.1 percent of adults met the criteria for depression — experts haven’t fully answered these questions. And to fully do so, some say we need new ways of thinking about depression entirely. For Turhan Canli, a professor of integrative neuroscience at Stony Brook University, that means looking at the possibility that depression could be caused by an infection. “I’ve always been struck by the fact that the treatment options did not seem to have dramatically improved over the course of decades,” Dr. Canli told Op-Talk. “I always had a feeling that somehow we seem to be missing the actual treatment of the disease.” He was intrigued by research showing a connection between depression and inflammation in the body, and he started to think about the known causes of inflammation — among them pathogens like bacteria, viruses and parasites. In a paper published in the journal Biology of Mood and Anxiety Disorders, he lays out his case for rethinking depression as a response to infection. He notes that the symptoms of depression are similar to those of infection: “Patients experience loss of energy; they commonly have difficulty getting out of bed and lose interest in the world around them. Although our Western conceptualization puts affective symptoms front-and-center, non-Western patients who meet DSM criteria for major depression report primarily somatic symptoms.” © 2014 The New York Times Company
Daniel Freeman and Jason Freeman “Although it is a waste of time to argue with a paranoid patient about his delusions, he may still be persuaded to keep them to himself, to repress them as far as possible and to forgo the aggressive action they might suggest, in general to conduct his life as if they did not exist.” This quote from Clinical Psychiatry, a hugely influential textbook in the 1950s and 1960s, epitomises the way in which unusual mental states were generally understood for much of the 20th century. Delusions (such as paranoid thoughts) and hallucinations (hearing voices, for example) were of interest purely as symptoms of psychosis, or what used to be called madness. Apart from their utility in diagnosis, they were deemed to be meaningless: the incomprehensible effusions of a diseased brain. Or in the jargon: “empty speech acts, whose informational content refers to neither world nor self”. There’s a certain irony here, of course, in experts supposedly dedicated to understanding the way the mind works dismissing certain thoughts as unworthy of attention or explanation. The medical response to these phenomena, which were considered to be an essentially biological problem, was to eradicate them with powerful antipsychotic drugs. This is not to say that other strategies weren’t attempted: in one revealing experiment in the 1970s, patients in a ward for “paranoid schizophrenics” in Vermont, US, were rewarded with tokens for avoiding “delusional talk”. These tokens could be exchanged for items including “meals, extra dessert, visits to the canteen, cigarettes, time off the ward, time in the TV and game room, time in bedroom between 8am and 9pm, visitors, books and magazines, recreation, dances on other wards.” (It didn’t work: most patients modified their behaviour temporarily, but “changes in a patient’s delusional system and general mental status could not be detected by a psychiatrist”.) © 2014 Guardian News and Media Limited
Link ID: 20369 - Posted: 11.29.2014
by Bethany Brookshire We all experience stress, but some handle it better than others. A lot of research has focused on what makes animals and people susceptible to stress and how that, in turn, can trigger depression. It makes sense to study the condition, not the people that don’t experience it. Depression and susceptibility are the broken state. Resilience seems normal by comparison. But resilience is not just the absence of susceptibility. It turns out that a protein called beta-catenin plays an active role in resilience. A new study, from Eric Nestler’s laboratory at the Mount Sinai School of Medicine in New York City, also identifies a large number of new targets that could help scientists understand why some people are susceptible to stress — and how they might be made more resilient. “When people study stress responses, we often just assume that in an animal that’s stressed, there’s an active process that creates these depression-like behaviors,” says Andre Der-Avakian, a neuroscientist at the University of California, San Diego. “But this study and studies from others have shown that resilience is also an active process.” The nucleus accumbens is an area of the brain most often linked with reward and pleasure from items we enjoy, such as food or drugs. But the area also shows changes in people with depression. “It makes sense — here’s a region important in responding to rewards,” Nestler explains. “One of the symptoms of people with depression is that they don’t derive pleasure from things in life.” © Society for Science & the Public 2000 - 2014
By David Tuller Patients with chronic fatigue syndrome are accustomed to disappointment. The cause of the disorder remains unknown; it can be difficult to diagnose, and treatment options are few. Research suggesting that an infection from a mouse virus may cause it raised hopes among patients a few years ago, but the evidence fell apart under closer scrutiny. Many patients are still told to seek psychiatric help. But two recent studies — one from investigators at Stanford a few weeks ago and another from a Japanese research team published earlier this year — have found that the brains of people with chronic fatigue syndrome differ from those of healthy people, strengthening the argument that serious physiological dysfunctions are at the root of the condition. “You’ve got two different groups that have independently said, ‘There’s something going on in the brain that is aberrant,’ ” said Leonard Jason, a psychologist at DePaul University in Chicago who studies the condition, also called myalgic encephalomyelitis and widely known as M.E./C.F.S. “I think you have a growing sense that this illness should be taken seriously.” Both studies were small, however, and their results must be replicated before firm conclusions can be drawn. Still, other studies presented at scientific conferences this year also have demonstrated physiological dysfunctions in these patients. In the most recent study, published by the journal Radiology, researchers at Stanford University compared brain images of 15 patients with the condition to those of 14 healthy people. The scientists found differences in both the white matter, the long, cablelike nerve structures that transmit signals between parts of the brain, and the gray matter, the regions where these signals are processed and interpreted. The most striking finding was that in people with the disorder, one neural tract in the white matter of the right hemisphere appeared to be abnormally shaped, as if the cablelike nerve structures had crisscrossed or changed in some other way. Furthermore, the most seriously ill patients exhibited the greatest levels of this abnormality. © 2014 The New York Times Company
By Michelle Roberts Health editor, BBC News online The brain has a weak spot for Alzheimer's disease and schizophrenia, according to UK scientists who have pinpointed the region using scans. The brain area involved develops late in adolescence and degenerates early during ageing. At the moment, it is difficult for doctors to predict which people might develop either condition. The findings, in the journal PNAS, hint at a potential way to diagnose those at risk earlier, experts say. Although they caution that "much more research is needed into how to bring these exciting discoveries into the clinic". The Medical Research Council team who carried out the study did MRI brain scans on 484 healthy volunteers aged between eight and 85 years. The researchers, led by Dr Gwenaëlle Douaud of Oxford University, looked at how the brain naturally changes as people age. The images revealed a common pattern - the parts of the brain that were the last to develop were also the first to show signs of age-related decline. These brain regions - a network of nerve cells or grey matter - co-ordinate "high order" information coming from the different senses, such as sight and sound. When the researchers looked at scans of patients with Alzheimer's disease and scans of patients with schizophrenia they found the same brain regions were affected. The findings fit with what other experts have suspected - that although distinct, Alzheimer's and schizophrenia are linked. Prof Hugh Perry of the MRC said: "Early doctors called schizophrenia 'premature dementia' but until now we had no clear evidence that the same parts of the brain might be associated with two such different diseases. This large-scale and detailed study provides an important, and previously missing, link between development, ageing and disease processes in the brain. BBC © 2014