Chapter 12. Psychopathology: Biological Basis of Behavioral Disorders
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Nancy Shute Powerful antipsychotic medications are being used to treat children and teenagers with ADHD, aggression and behavior problems, a study finds, even though safer treatments are available and should be used first. "There's been concern that these medications have been overused, particularly in young children," says Mark Olfson, a professor of psychiatry at Columbia University who led the study. It was published Wednesday in JAMA Psychiatry. "Guidelines and clinical wisdom suggest that you really should be using a high degree of caution and only using them when other treatments have failed, as a last resort." Olfson and his colleagues looked at prescription data from about 60 percent of the retail pharmacies in the United States in 2006, 2008 and 2010. That included almost 852,000 children, teenagers and young adults. Teens were most likely to be prescribed antipsychotics, with 1.19 percent getting the drugs in 2010, compared to 0.11 percent in younger children. Boys were more likely to be given the medications. Antipsychotic medications like clozapine and olanzapine are used to treat schizophrenia, bipolar disorder and some symptoms of autism. They have not been approved by the Food and Drug Administration to treat aggression and ADHD, but are prescribed off label to reduce disruptive behavior. FDA Debates Safety Of Antipsychotic Drugs In Kids Use of antipsychotics in children has been questioned because the drugs can have serious side effects, including tremors, weight gain, increased diabetes risk and elevated cholesterol. © 2015 NPR
Boys are more likely than girls to receive a prescription for antipsychotic medication regardless of age, researchers have found. Approximately 1.5 percent of boys ages 10-18 received an antipsychotic prescription in 2010, although the percentage falls by nearly half after age 19. Among antipsychotic users with mental disorder diagnoses, attention deficit hyperactivity disorder (ADHD) was the most common among youth ages 1-18, while depression was the most common diagnosis among young adults ages 19-24 receiving antipsychotics. Despite concerns over the rising use of antipsychotic drugs to treat young people, little has been known about trends and usage patterns in the United States before this latest research, which was funded by the National Institute of Mental Health (NIMH), part of the National Institutes of Health. Mark OlfsonExternal Web Site Policy, M.D., M.P.H., of the Department of Psychiatry, College of Physicians and Surgeons and Columbia University and New York State Psychiatric Institute, New York City, and colleagues Marissa King, Ph.D., Yale, New Haven, Connecticut, and Michael Schoenbaum, Ph.D., NIMH, report their findings on July 1 in JAMA Psychiatry. “No prior study has had the data to look at age patterns in antipsychotic use among children the way we do here,” said co-author Michael Schoenbaum, Ph.D., senior advisor for mental health services, epidemiology and economics at NIMH. “What’s especially important is the finding that around 1.5 percent of boys aged 10-18 are on antipsychotics, and then this rate abruptly falls by half, as adolescents become young adults.” “Antipsychotics should be prescribed with care,” says Schoenbaum. “They can adversely affect both physical and neurological function and some of their adverse effects can persist even after the medication is stopped.”
By Bret Stetka Plenty of us have known a dog on Prozac. We have also witnessed the eye rolls that come with the mention of canine psychiatry. Doting pet owners—myself included—ascribe all kinds of questionable psychological ills to our pawed companions. But in fact, the science suggests that numerous nonhuman species do suffer from psychiatric symptoms. Birds obsess; horses on occasion get pathologically compulsive; dolphins and whales, especially those in captivity, self-mutilate. And that thing when your dog woefully watches you pull out of the driveway from the window—that might be DSM-certified separation anxiety. “Every animal with a mind has the capacity to lose hold of it from time to time,” wrote science historian and author Laurel Braitman in her 2014 book Animal Madness. But at least one mental malady, while common in humans, seems to have spared other animals: schizophrenia, which affects an estimated 0.4 to 1 percent of adults. Although animal models of psychosis exist in laboratories, and odd behavior has been observed in creatures confined to cages, most experts agree that psychosis has not typically been seen in other species, whereas depression, obsessive-compulsive disorder and anxiety traits have been reported in many nonhuman species. This raises the question of why such a potentially devastating, often lethal disease is still hanging around plaguing humanity. We know from an abundance of recent research that schizophrenia is heavily genetic in origin. One would think that natural selection would have eliminated the genes that predispose to psychosis. A study published earlier this year in Molecular Biology and Evolution provides clues as to how the potential for schizophrenia may have arisen in the human brain and, in doing so, suggests possible treatment targets. It turns out that psychosis may be an unfortunate cost of having a big brain that is capable of complex cognition. © 2015 Scientific American
Link ID: 21101 - Posted: 06.27.2015
Matthew C Keller & Peter M Visscher Epidemiological studies and anecdotal evidence show overlap between psychiatric disorders and creativity, but why? A new study uses genome-wide association data from schizophrenia and bipolar disorder to show that genetics are part of the explanation. Thinkers contemplating the human condition have long associated creativity with psychiatric illness—the 'mad genius' archetype. According to Aristotle, “no great genius was without a mixture of insanity.” And there are the oft-repeated anecdotes: the psychotic breaks of Vincent van Gogh and John Nash, the manic and depressive episodes of Virginia Woolf and Ernest Hemingway. There is, in fact, some empirical evidence that the psychological factors underlying psychiatric disorders are linked to increased creativity. Unaffected relatives of those with bipolar disorder (BD) have greater creativity1 and are over-represented in creative professions2, and similar findings have been reported for schizophrenia (SCZ)2, 3. What these studies have not shown is whether this overlap is a result of genetic variation that influences both creativity and BD/SCZ or whether some environmental factor explains the association. For example, highly unstructured rearing environments might contribute to both creativity and risk of the disorders. Understanding whether shared gene variants are responsible for the overlap is important. It can help to elucidate the biological underpinnings of these disorders and shine light on the puzzle of why psychiatric diseases persist in the population. Power et al.4, in work reported in this issue of Nature Neuroscience, asked whether creativity and psychiatric disorders might be associated through common variation in the genome. They used a large discovery sample of 86,292 adults from Iceland and four replication samples totaling over 27,000 adults from Sweden and the Netherlands. All had genome-wide SNP genotyping and their professions were known. None of them knowingly suffered from a psychiatric illness. About 1% of them were artists, including actors, dancers, musicians and writers. © 2015 Macmillan Publishers Limited
By JAIME LOWE The manila folder is full of faded faxes. The top sheet contains a brief description of my first medically confirmed manic episode, more than 20 years ago, when I was admitted as a teenager to U.C.L.A.’s Neuropsychiatric Institute: “Increased psychomotor rate, decreased need for sleep (about two to three hours a night), racing thoughts and paranoid ideation regarding her parents following her and watching her, as well as taping the phone calls that she was making.” I believed I had special powers, the report noted; I knew ‘‘when the end of the world was coming due to toxic substances’’ and felt that I was the only one who could stop it. There was also an account of my elaborate academic sponsorship plan so I could afford to attend Yale — some corporation would pay for a year of education in exchange for labor or repayment down the line. (Another grand delusion. I was a B-plus student, at best.) After I was admitted to the institute's adolescent ward, I thought the nurses and doctors and therapists were trying to poison me. So was the TV in the rec room. I warned my one friend in the ward that its rays were trying to kill him. The generator outside my window was pumping in gas. The place, I was sure, was a death camp. I refused meds because they were obviously agents of annihilation. It took four orderlies to medicate me: They pinned me to the floor while a nurse plunged a syringe into my left hip. Over time, I became too tired to refuse medication. Or perhaps the cocktail of antipsychotics started working. The Dixie cup full of pills included lithium, which slowly took hold of my mania. After a few weeks, I stopped whispering to the other patients that we were all about to be killed. Eventually, I stopped believing it myself. Mark DeAntonio, the U.C.L.A. psychiatrist who was treating me, said I had bipolar disorder. Here’s the phrasing from the National Institute of Mental Health: ‘‘unusually intense emotional states that occur in distinct periods called ‘mood episodes.’ Each mood episode represents a drastic change from a person’s usual mood and behavior. An overly joyful or overexcited state is called a manic episode, and an extremely sad or hopeless state is called a depressive episode.’’ The generic definition doesn’t quite cover the extremes of the disease or its symptoms, which include inflated self-esteem, sleeplessness, loquaciousness, racing thoughts and doing things that, according to the Mayo Clinic, ‘‘have a high potential for painful consequences — for example, unrestrained buying sprees, sexual indiscretions or foolish business investments.’’ © 2015 The New York Times Company
Link ID: 21094 - Posted: 06.25.2015
By Nellie Bowles One recent Friday night, at a software-development firm’s warehouse in San Francisco, Mikey Siegel called to order the hundred and fifty or so meditators, video gamers, and technocrats who had gathered for one of the city’s biweekly Consciousness Hacking meet-ups. Siegel, the primary organizer of the event and the founder of a Santa Cruz–based biofeedback startup called Bio Fluent, asked the crowd, men and women of widely varied ages, to go around the room introducing themselves in three words. Everyone laughed, but took the task seriously. The introductions moved quickly through the room in a brisk beat: “Me Technological Cartoon” “Heather Curious About Brains” “Neuromore Singularity Atom Here” “Dan Thoughtful Helpful Software” “Harry Self-Modification Exploration” “David Psychiatrist Technological Retarded Curious” “Jordan Moving Meditation Butts” “Juliana Joel’s Aunt” “Ben Existence Existence Existence” “Zohara Chocolate Maker Meditation Awareness” “Lila Awake Empath Warrior” San Francisco’s Consciousness Hacking meet-ups are an opportunity for engineers, entrepreneurs, and enthusiasts to test the fleet of still experimental self-examination technologies emerging largely from Silicon Valley. The region’s tech community is a body culture, obsessed with monitoring and perfecting its food (Soylent), fitness (Fitbit), and physiology (23andMe). As brain-wave technologies get cheaper and more popular, some company founders hope that consumers, who seem to be acclimating to devices like the increasingly ubiquitous Fitbit, will consider other, more cumbersome devices and procedures. Consciousness Hackers are a kind of self-selected early market-research group. Tonight, that was especially clear.
By John Horgan Transcranial magnetic stimulation is becoming an increasingly popular treatment for depression in spite of a lack of objective evidence of effectiveness. Illustration: National Institute of Mental Health. Delving into the history of treatments for mental illness can be depressing. Rather than developing ever-more-potent therapies, psychiatrists and others in the mental-health industry seem merely to recycle old ones. Consider, for example, therapies that stimulate the brain with electricity. In 1901, H. Lewis Jones, a physician, stated in the Journal of Mental Science: "The employment of electricity in medicine has passed through many vicissitudes, being at one time recognized and employed at the hospitals, and again being neglected, and left for the most part in the hands of ignorant persons, who continue to perpetrate the grossest impositions in the name of electricity. As each fresh important discovery in electric science has been reached, men’s minds have been turned anew to the subject, and interest in its therapeutic properties has been stimulated. Then after extravagant hopes and promises of cure, there have followed failures, which have thrown the employment of this agent into disrepute, to be again after time revived and brought into popular favor." Jones’s concerns could apply to our era, when electro-cures for mental illness have once again been "brought into popular favor." Below I briefly review the evidence—or lack thereof--for five electrotherapies: transcranial magnetic stimulation, cranial electrotherapy stimulation, vagus-nerve stimulation, deep-brain stimulation and electroconvulsive therapy.
Link ID: 21092 - Posted: 06.25.2015
By Tina Rosenberg Elle is a mess. She’s actually talented, attractive and good at her job, but she feels like a fraud — convinced that today’s the day she’ll flunk a test, lose a job, mess up a relationship. Her colleague Moody also sabotages himself. He’s a hardworking, nice person, but loses friends because he’s grumpy, oversensitive and gets angry for no reason. If you suffer from depression or anxiety as Elle and Moody do, spending time with them could help. They are characters in a free online program of cognitive behavioral therapy called MoodGYM, which leads users through quizzes and exercises — therapy without the therapist. Cognitive behavioral therapy is a commonly used treatment for depression, anxiety and other conditions. With it, the therapist doesn’t ask you about your mother — or look at the past at all. Instead, a cognitive behavioral therapist aims to give patients the skills to manage their moods by helping them identify unhelpful thoughts like “I’m worthless,” “I’ll always fail” or “people will always let me down.” Patients learn to analyze them and replace them with constructive thoughts that are more accurate or precise. For example, a patient could replace “I fail at everything” with “I succeed at things when I’m motivated and I try hard.” That new thought in turn changes feelings and behaviors. The success of cognitive behavioral therapy is well known; many people consider it the most effective therapy for depression. What is not widely known, at least in the United States, is that you don’t need a therapist to do it. Scores of studies have found that online C.B.T. works as well as conventional face-to-face cognitive behavioral therapy – as long a there is occasional human support or coaching. “For common mental disorders like anxiety and depression, there is no evidence Internet-based treatment is less effective than face-to-face therapy,” said Pim Cuijpers, professor of clinical psychology at the Vrije Universiteit Amsterdam and a leading researcher on computer C.B.T. © 2015 The New York Times Company
Link ID: 21076 - Posted: 06.20.2015
By Michael Hedrick I’ve had a little success dating in the nearly 10 years I’ve lived with schizophrenia. But there are a lot of obstacles. Schizophrenia is a terrifying word for many people. It conjures up ideas of murderous intent, lack of control and a host of other scary things. I live with this word, though; I am the word. But it is not a word you can just drop into a conversation and follow with “It’s not a big deal, though.” I seem to fall in love easily, but it’s always with girls who don’t feel the same way about me. I have seen more rejection than I care to admit, putting myself on the line like that, and it’s been a chore for me not to let my emotions get the best of me. If it’s not outright rejection, it seems to be something else that always seems to happen. I can remember one date I went on some months back. She was a big girl with blonde hair and eyes that had that squinty “I’m up to no good” look. We met over Match.com, and I was struck by how much time she spent going to Phish shows. Her profile was scattered with a number of bands that I had loved at different points in my life. She was a teacher, and she mentioned in her profile something along the lines that because of her love of sparkles, arts-and- crafts, and rainbows, she was a 6-year-old in a woman’s body. Before I knew it, I was asking if she wanted to go get a beer. She said yes, a little too eagerly I thought. I got to the restaurant about 15 minutes early and ordered a beer, apprehensive knowing that eventually I would have to tell her about my illness. Soon enough she walked in, and I was struck by the fact that she seemed a little disappointed to be there. There was no smile as she sat down to join me. © 2015 The New York Times Company
Link ID: 21051 - Posted: 06.15.2015
Sara Reardon Traumatic experiences, such as those encountered during warfare, can cause long-lasting stress. Tweaking the immune system could be key to treating, or even preventing, post-traumatic stress disorder (PTSD). Research in rodents suggests that immunizing animals can lessen fear if they are later exposed to stress. Researchers have known for some time that depression and immune-system health are linked and can affect each other. Early clinical trials have shown that anti-inflammatory drugs can reduce symptoms of depression1, raising hopes that such treatments might be useful in other types of mental illness, such as PTSD. “I think there’s kind of a frenzy about inflammation in psychiatry right now,” says Christopher Lowry, a neuroscientist at the University of Colorado Boulder. He presented results of experiments probing the link between fearful behaviour and immune response at a meeting in Victoria, Canada, last week of the International Behavioral Neuroscience Society. Studies of military personnel suggest that immune function can influence the development of PTSD. Soldiers whose blood contains high levels of the inflammatory protein CRP before they are deployed2, or who have a genetic mutation that makes CRP more active3, are more likely to develop the disorder. To directly test whether altering the immune system affects fear and anxiety, Lowry and colleagues injected mice with a common bacterium, Mycobacterium vaccae, three times over three weeks to modulate their immune systems. The scientists then placed these mice, and a control group of unimmunized mice, in cages with larger, more aggressive animals. © 2015 Nature Publishing Group
Boer Deng A genetic variant protected some practitioners of cannibalism from prion disease. Scientists who study a rare brain disease that once devastated entire communities in Papua New Guinea have described a genetic variant that appears to stop misfolded proteins known as prions from propagating in the brain1. Kuru was first observed in the mid-twentieth century among the Fore people of Papua New Guinea. At its peak in the late 1950s, the disease killed up to 2% of the group's population each year. Scientists later traced the illness to ritual cannibalism2, in which tribe members ate the brains and nervous systems of their dead. The outbreak probably began when a Fore person consumed body parts from someone who had sporadic Creutzfeldt-Jakob disease (CJD), a prion disease that spontaneously strikes about one person in a million each year. Scientists have noted previously that some people seem less susceptible to prion diseases if they have an amino-acid substitution in a particular region of the prion protein — codon 1293. And in 2009, a team led by John Collinge — a prion researcher at University College London who is also the lead author of the most recent analysis — found another protective mutation among the Fore, in codon 1274. The group's latest work, reported on 10 June in Nature1, shows that the amino-acid change that occurs at this codon, replacing a glycine with a valine, has a different and more powerful effect than the substitution at codon 129. The codon 129 variant confers some protection against prion disease only when it is present on one of the two copies of the gene that encodes the protein. But transgenic mice with the codon-127 mutation were completely resistant to kuru and CJD regardless of whether they bore one or two copies of it. The researchers say that the mutation in codon 127 appears to confer protection by preventing prion proteins from becoming misshapen. © 2015 Nature Publishing Group,
Link ID: 21043 - Posted: 06.13.2015
Owning a cat as a kid could put you at risk for schizophrenia and bipolar disorder later on because of parasites found in feline feces, new research says. Previous studies have linked the parasite toxoplasma gondii (T. gondii) to the development of mental disorders, and two more research papers published recently provide further evidence. Researchers from the Academic Medical Centre in Amsterdam looked at more than 50 studies and found that a person infected with the parasite is nearly twice as likely to develop schizophrenia. The other study, led by Dr. Robert H. Yolken of Johns Hopkins University School of Medicine in Baltimore, confirmed the results of a 1982 questionnaire that found half of people who had a cat as a kid were diagnosed with mental illnesses later in life compared to 42% of those who didn't grow up with a cat. "Cat ownership in childhood has now been reported in three studies to be significantly more common in families in which the child is later diagnosed with schizophrenia or another serious mental illness," the authors said in a press release. The findings were published in Schizophrenia Research and Acta Psychiatrica Scandinavica. T. gondii, which causes the disease toxoplasma, is especially risky for pregnant women and people with weak immune symptoms. The parasite can also be found in undercooked meat and unwashed fruits and vegetables.
Angus Chen The genetic underpinnings of psychosis are elusive and diffuse. There are hundreds of common genetic mutations scattered throughout the human genome that each bump up by just a tiny bit the risk of developing a mental illness like schizophrenia. Many people carry some set of those genes, but most don't end up with a psychotic disorder. Instead, a study suggests, they might be getting a small creative boost. Meghan, 23, began experiencing hallucinations at 19. "Driving home, cars' headlights turned into eyes. The grills on the cars turned into mouths and none of them looked happy. It would scare the crap out of me," Meghan says. Those genetic changes may persist in human DNA because they confer benefits, according Dr. Kári Stefánsson, a neurologist and CEO of a biological research company called deCODE Genetics, which conducted the study published in Nature Neuroscience Monday. "They are found in most of us, and they're common because they either confer or in the past conferred some reproductive advantage," he says. The advantage of having a more creative mind, he suggests, might help explain why these genes persist, even as they increase the risk of developing debilitating disorders, such as schizophrenia. It's an idea from the ancients. The philosopher Aristotle famously opined that genius and madness go hand in hand. Psychiatric studies have to some degree supported the adage. Studies of more than 1 million Swedish people in 2011 and 2013 found that people who had close relatives with schizophrenia or bipolar disorder were much more likely to become creative professionals. (The patients with mental illness were not themselves more creative, with the exception of some who had bipolar disorder.) What's more, studies that looked at healthy people who carry genetic markers associated with a psychotic disorder found their brains work slightly differently than others who lack those genetic markers. © 2015 NPR
by Helen Thomson For the first time, scientists have discovered a mechanism in humans that could explain how your lifestyle choices may impact your children and grandchildren's genes. Mounting evidence suggests that environmental factors such as smoking, diet and stress, can leave their mark on the genes of your children and grandchildren. For example, girls born to Dutch women who were pregnant during a long famine at the end of the second world war had twice the usual risk of developing schizophrenia. Likewise, male mice that experience early life stress give rise to two generations of offspring that have increased depression and anxiety, despite being raised in a caring environment. This has puzzled many geneticists, as genetic information contained in sperm and eggs is not supposed to be affected by the environment, a principle called the August Weismann barrier. But we also know the activity of our own genes can be changed by our environment, through epigenetic mechanisms . These normally work by turning a gene on or off by adding or subtracting a methyl group to or from its DNA. These methyl groups can inactivate genes by making their DNA curl up, so that enzymes can no longer access the gene and read its instructions. Such epigenetic mechanisms are high on the list of suspects when it comes to explaining how environmental factors that affect parents can later influence their children, such as in the Dutch second world war study, but just how these epigenetic changes might be passed on to future generations is a mystery. © Copyright Reed Business Information Ltd.
Steve Connor Scientists have linked the condition with variations in the DNA of genes known to be involved in stimulating or inhibiting the passing of chemical messages across the tiny gaps or “synapses” between nerve cells in the brain. They said the findings are part of a wider body of evidence pointing to the genetic causes of schizophrenia which is known to have a strong inherited component as well as being influenced by a person’s environment and upbringing. “We’re finally starting to understand what goes wrong in schizophrenia. Our study marks a significant step towards understanding the biology underpinning schizophrenia, which is an incredible complex condition and has up until very recently kept scientists largely mystified as to is origins,” said Andrew Pocklington of Cardiff University. “We now have what we hope is a pretty sizeable piece of the jigsaw puzzle that will help us to develop a coherent model of the disease, while helping us to rule out some of the alternatives,” said Dr Pocklington, the lead author of the study published in the journal Neuron. “A reliable model of disease is urgently needed to direct future efforts in developing new treatments, which haven’t really improved a great deal since the 1970s,” he said. © independent.co.uk
By Rachael Rettner and LiveScience Mathematician John Nash, who died May 23 in a car accident, was known for his decades-long battle with schizophrenia—a struggle famously depicted in the 2001 Oscar-winning film "A Beautiful Mind." Nash had apparently recovered from the disease later in life, which he said was done without medication. But how often do people recover from schizophrenia, and how does such a destructive disease disappear? Nash developed symptoms of schizophrenia in the late 1950s, when he was around age 30, after he made groundbreaking contributions to the field of mathematics, including the extension of game theory, or the math of decision making. He began to exhibit bizarre behavior and experience paranoia and delusions, according to The New York Times. Over the next several decades, he was hospitalized several times, and was on and off anti-psychotic medications. But in the 1980s, when Nash was in his 50s, his condition began to improve. In an email to a colleague in the mid-1990s, Nash said, "I emerged from irrational thinking, ultimately, without medicine other than the natural hormonal changes of aging," according to The New York Times. Nash and his wife Alicia died, at ages 86 and 82, respectively, in a crash on the New Jersey Turnpike while en route home from a trip on which Nash had received a prestigious award for his work. © 2015 Scientific American
Link ID: 21018 - Posted: 06.06.2015
By ANDREW SOLOMON At the beginning of spring in 2013, Mary Guest, a lively, accomplished 37-year-old woman, fell in love, became pregnant and married after a short courtship. At the time, Mary taught children with behavioral problems in Portland, Ore., where she grew up. Her supervisor said that he had rarely seen a teacher with Mary’s gift for intuiting students’ needs. “Mary was a powerful person,” he wrote to her mother, Kristin. “Around Mary, one felt compassion, drive, calmness and support.” Mary had struggled with depression for much of her life. Starting in her 20s, she would sometimes say to Kristin that she just wanted to die. “She would always follow up by saying, ‘But you don’t need to worry, Mama,’ ” Kristin told me. “ ‘I don’t have a plan, and I don’t intend to do anything.’ ” In recent years, Mary and her mother went for a walk once a week, and Mary would describe the difficulties she was having. She was helped somewhat by therapy and by antidepressant and antianxiety medications, which blunted her symptoms. Mary’s friends appreciated her wacky sense of humor and her engaging wit. Colleagues said that her moods never impinged on her work; in fact, few of them knew what she was dealing with. Yet for years Mary worried that she would never be in a stable relationship and experience love or a family of her own. She said plaintively to Kristin, “I think I would be a really good mother.” So when she discovered that she was pregnant, she was delighted, and she expected the experience to be blissful. She decided to discontinue her antidepressants, having read about their potential danger for a growing fetus. Given her history of severe depression, she was monitored closely by a psychiatric nurse practitioner, who told her that she could call anytime for an immediate prescription. But Mary elected to stay off medication.
By Tori Rodriguez Heart disease and depression often go hand in hand. Long-term studies have found that people with depression have a significantly higher risk of subsequent heart disease, and vice versa. Recent research has revealed that the link begins at an early age and is probably caused by chronic inflammation. A new study in the November 2014 issue of Psychosomatic Medicine by researchers in the U.S., Australia and China examined data from an ongoing study of health among Australians. The researchers looked at the scores of 865 young adults on a questionnaire that assesses depression symptoms and other measures of mental health. They also examined measurements of the internal diameter of the blood vessels of the retina, a possible marker of early cardiovascular disease. After controlling for sex, age, smoking status and body mass index, the investigators found that participants with more symptoms of depression and anxiety had wider retinal arterioles than others, which could reflect the quality of blood vessels in their heart and brain. “We don't know if the association is causal,” explains study co-author Madeline Meier, a psychology professor at Arizona State University. “But our findings suggest that symptoms of depression and anxiety may identify youth at risk for cardiovascular disease.” Other research shows that people with depression have more inflammation throughout their body and nervous system. “One theory is that stress and inflammation could play a causal role in depression,” Meier says. Such chronic inflammation is also a risk factor for cardiovascular disease. The relationship is complex: in some people, inflammation seems to precede depression and heart disease; in others, the disorders seem to cause or exacerbate the inflammation. © 2015 Scientific American
Boer Deng The ability of the bizarre prion protein to cause an array of degenerative brain conditions may help solve a puzzle in Alzheimer's research — why the disease sometimes kills within a few years, but usually causes a slow decline that can take decades. By adopting tools used to study the prion protein, PrP, researchers have found variations in the shape of a protein involved in Alzheimer’s that may influence how much damage it causes in the brain. At the Prion 2015 meeting, held on 26–29 May in Fort Collins, Colorado, neuroscientist Lary Walker described how he has borrowed a technique from prion research to study different ‘strains’ of the amyloid-β protein, which accumulates in clumps in the brains of people with Alzheimer’s. It may be that differences between the strains account for variations in the disease’s symptoms and rate of progression. “The Alzheimer’s field has not been paying enough attention to what’s happening in the prion field,” says Walker, who is based at Emory University in Atlanta, Georgia. Similarities between rare prion diseases and common neurodegenerative diseases such as Alzheimer’s have been noted for decades: both are thought to involve proteins in the nervous system that change shape and clump together. In prion diseases, a misfolded, often foreign, protein induces cascading malformation of the native prion protein in a patient’s brain. In Alzheimer’s, proteins called tau and amyloid-β accumulate within and around nerve cells, though what triggers that process — and the role of the deposits in the disease — is unclear. © 2015 Nature Publishing Group,
Jon Hamilton Antidepressant drugs that work in hours instead of weeks could be on the market within three years, researchers say. "We're getting closer and closer to having really, truly next-generation treatments that are better and quicker than existing ones," says Dr. Carlos Zarate, a researcher at the National Institute of Mental Health. The new drugs are based on the anesthetic ketamine, which is also a popular club drug known as Special K. Unlike current antidepressants, which can take weeks to work, ketamine-like drugs have an immediate effect. They also have helped people with depression who didn't respond to other medications. The drug that is furthest along is esketamine, a chemical variant of ketamine that has been designated a potential breakthrough by the Food and Drug Administration. Esketamine is poised to begin Phase 3 trials, and the drug's maker, Johnson & Johnson, plans to seek FDA approval in 2018. Ketamine, used as a tranquilizer for animals and as an anesthetic in humans, is also being tested as a treatment for depression. Another ketamine-like drug on the horizon is rapastinel. It has completed Phase 2 studies, which showed "rapid, substantial, and sustained reductions in depressive symptoms," according to the drug's maker, Naurex. "I think it's highly probable that we'll see some version of one of these treatments being approved in the relatively near future," says Dr. Gerard Sanacora, director of the Yale Depression Research Program. "In my mind it is the most exciting development in mood disorder treatment in the last 50 years." © 2015 NPR
Link ID: 20999 - Posted: 05.30.2015