Chapter 16. Psychopathology: Biological Basis of Behavior Disorders
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By Melissa Healy contact the reporter Schizophrenia is one of psychiatry's most puzzling afflictions, with a complex of symptoms that goes far beyond its hallmark hallucinations and delusional thinking. But new research has found connections among several of schizophrenia's peculiar collection of symptoms -- including agitation and memory problems -- and linked them to a single genetic variant among the hundreds thought to heighten risk of the disorder. The findings offer new insights into the molecular basis for schizophrenia and could lead to treatments for the disease that are more targeted and more comprehensive. Published Monday in the journal Nature Neuroscience, the study looks at how a gene variant called Arp2/3 contributes to psychosis, agitation and problems of short- and long-term memory. Mice that were genetically modified to lack the Arp2/3 gene variant showed all three symptoms (although to measure psychosis in mice, scientists looked instead for an abnormal startle response that is also seen in humans in the grips of psychosis). The study's authors, led by Duke University neurobiologist Scott Soderling, then dug below those behaviors to see whether brain abnormalities linked to such behaviors had anything in common. Mice that lacked the Arp2/3 gene variant, they discovered, had not only symptoms of schizophrenia, but also several of the underlying brain abnormalities most closely linked to psychosis, agitation and memory problems seen in those with schizophrenia.
Link ID: 20895 - Posted: 05.06.2015
|By Michele Solis An individual with obsessive-compulsive disorder (OCD) is overcome with an urge to engage in unproductive habits, such as excessive hand washing or lock checking. Though recognizing these behaviors as irrational, the person remains trapped in a cycle of life-disrupting compulsions. Previous studies found that OCD patients have abnormalities in two different brain systems—one that creates habits and one that plays a supervisory role. Yet whether the anomalies drive habit formation or are instead a consequence of doing an action over and over remained unclear. To resolve this question, a team at the University of Cambridge monitored brain activity while people were actually forming new habits. Lapses in supervision are to blame, the researchers reported in a study published online in December 2014 in the American Journal of Psychiatry. They scanned 37 people with OCD and 33 healthy control subjects while they learned to avoid a mild shock by pressing on a foot pedal. Pressing the pedal became a habit for everyone, but people with OCD continued to press even when the threat of shock was over. Those with OCD showed abnormal activity in the supervisory regions important for goal-directed behavior but not in those responsible for habit formation. The finding suggests that shoring up the goal-directed systems through cognitive training might help people with OCD. The growing understanding of OCD's roots in the brain may also help convince individuals to engage in standard habit-breaking treatments, which expose a person to a trigger but prevent his or her typical response. “It's hard for people to not perform an action that their whole body is telling them to do,” says first author Claire Gillan, now at New York University. “So if you have an awareness that the habit is just a biological slip, then it makes OCD a lot less scary and something you can eventually control.” © 2015 Scientific American
By Tina Hesman Saey People with depression have more mitochondrial DNA and shorter telomeres than nondepressed people do, an international team of researchers reports online April 23 in Current Biology. Mitochondria are organelles that produce energy for cells. Mitochondria seem to become inefficient under stress, the team found, so more mitochondria may be needed to produce enough energy. Telomeres are the DNA endcaps on chromosomes that prevent the genetic material from unraveling. Short telomeres are associated with shorter life spans. The altered DNA may reflect metabolic changes associated with depression, the researchers say. Experiments with mice showed that these DNA changes are brought on by stress or by stress hormones. Four weeks after scientists stopped stressing the mice, their mitochondrial and telomere DNA had returned to normal. Those results indicate that the molecular changes are reversible. Researchers also studied DNA from more than 11,000 people to learn whether past stress was responsible for the molecular changes seen in people with depression. Depression was associated with the DNA changes, but having a stressful life was not. For instance, people who had experienced childhood sexual abuse but were not depressed did not have statistically meaningful changes to their DNA compared with people who had no history of abuse. The findings suggest that stress can change DNA but many people can bounce back. Depressed people may have a harder time recovering from the molecular damage. © Society for Science & the Public 2000 - 2015.
By Smitha Mundasad Health reporter, BBC News A mindfulness-based therapy could offer a "new choice for millions of people" with recurrent depression, a Lancet report suggests. Scientists tested it against anti-depressant pills for people at risk of relapse and found it worked just as well. The therapy trains people to focus their minds and understand that negative thoughts may come and go. In England and Wales doctors are already encouraged to offer it. Patients who have had recurrent clinical depression are often prescribed long-term anti-depressant drugs to help prevent further episodes. And experts stress that drug therapy is still essential for many. In this study, UK scientists enrolled 212 people who were at risk of further depression on a course of mindfulness-based cognitive therapy (MBCT) while carefully reducing their medication. Patients took part in group sessions where they learned guided meditation and mindfulness skills. The therapy aimed to help people focus on the present, recognise any early warning signs of depression and respond to them in ways that did not trigger further reoccurrences. Researchers compared these results to 212 people who continued to take a full course of medication over two years. By the end of the study, a similar proportion of people had relapsed in both groups. And many in the MBCT group had been tapered off their medication. Scientists say these findings suggest MBCT could provide a much-needed alternative for people who cannot or do not wish to take long-term drugs. In their report, they conclude it "may be a new choice for millions of people with recurrent depression on repeat prescriptions." © 2015 BBC
By KATIE THOMAS Last fall, an article in the American Journal of Psychiatry caught the attention of specialists who treat borderline personality disorder, an intractable condition for which no approved drug treatment exists. The article seemed to offer a glimmer of hope: The antipsychotic drug Seroquel XR reduced some of the disorder’s worst symptoms in a significant number of patients. “It was an exciting development,” recalled Mark F. Lenzenweger, a professor at Binghamton University and Weill Cornell Medical College and an expert in borderline personality disorder. In the realm of clinical trials, however, reality is sometimes far messier than the tidy summaries in medical journals. A closer look at the Seroquel XR study shows just how complicated things can get when a clinical trial involves psychiatric disorders and has its roots in intersecting and sometimes competing interests: a drug company looking to hold onto sales of a best-selling drug, a prominent academic with strong ties to the pharmaceutical industry and a university under fire for failing to protect human study subjects. The trial was paid for by AstraZeneca, the maker of Seroquel XR, and was conducted by Dr. S. Charles Schulz, the head of psychiatry at the University of Minnesota. Two of the study participants were living in a residential treatment facility for sex offenders and may have lied about their diagnosis to qualify for the trial. One of those men slipped the drugs to unwitting treatment center residents and staff, an alarming development that nevertheless did not seem to ruffle the university oversight board that is charged with looking into such episodes. The University of Minnesota’s clinical trial practices are now under intense scrutiny. In February, a panel of outside experts excoriated the university for failing to properly oversee clinical trials and for paying inadequate attention to the protection of vulnerable subjects. The review, commissioned by the university after years of criticism of its research practices, singled out Dr. Schulz and his department of psychiatry, describing “a culture of fear” that pervaded the department. © 2015 The New York Times Company
Link ID: 20814 - Posted: 04.18.2015
Michaeleen Doucleff It began with anxiety and depression. A few months later, hallucinations appeared. Then the Texas man, in his 40s, couldn't feel the left side of his face. He thought the symptoms were because of a recent car accident. But the psychiatric problems got worse. And some doctors thought the man might have bipolar disorder. Cattle feeding practices have been changed in an effort to halt the spread of mad cow disease. Eventually, he couldn't walk or speak. He was hospitalized. And about 18 months after symptoms began, the man died. An autopsy confirmed what doctors had finally suspected: the human version of mad cow disease, called variant Creutzfeldt-Jakob disease.* The case, published Wednesday in the journal Emerging Infectious Diseases, is only the fourth one diagnosed in the U.S. In those previous cases, people caught the disease in another country. Right away the man's diagnosis raised a new question: How did a rare disease linked to contaminated beef in the U.K. more than a decade ago get to a Texas man? Back in the early '80s, British ranchers noticed some of their cows were dying of a strange neurological disease. The cows became aggressive. They couldn't walk. Eventually, scientists figured out the culprit. A rogue protein formed large clumps in the brain and spinal cord. Over time, the clumps spread throughout the brain and damaged tissue. © 2015 NPR
Link ID: 20812 - Posted: 04.18.2015
By ERICA GOODE He was described, in the immediate aftermath of the Germanwings crash, as a cheerful and careful pilot, a young man who had dreamed of flying since boyhood. But in the days since, it has seemed increasingly clear that Andreas Lubitz, 27, the plane’s co-pilot, was something far more sinister: the perpetrator of one of the worst mass murder-suicides in history. If what researchers have learned about such crimes is any indication, this notoriety may have been just what Mr. Lubitz wanted. The actions now attributed to Mr. Lubitz — taking 149 unsuspecting people with him to a horrifying death — seem in some ways unfathomable, and his full motives may never be fully understood. But studies over the last decades have begun to piece together characteristics that many who carry out such violence seem to share, among them a towering narcissism, a strong sense of grievance and a desire for infamy. Adam Lankford, an associate professor of criminal justice at the University of Alabama, said that in his research on mass killers who also took their own lives, he has found “a significant number of cases where they mention a desire for fame, glory or attention as a motive.” Before Adam Lanza, 20, the Sandy Hook Elementary School shooter, killed 20 children, six adults and himself in 2012, he wrote in an online forum, “Just look at how many fans you can find for all different types of mass murderers.” Robert Hawkins, 19, who committed suicide after killing eight people at a shopping mall in Omaha in 2007, left a note saying “I’m gonna be famous,” punctuating the sentence with an expletive. And Dylan Klebold, 17, of Columbine High School fame, bragged that the goal was to cause “the most deaths in U.S. history…we’re hoping. We’re hoping.” “Directors will be fighting over this story,” Mr. Klebold said in a video made before the massacre. © 2015 The New York Times Company
Arran Frood A psychedelic drink used for centuries in healing ceremonies is now attracting the attention of biomedical scientists as a possible treatment for depression. Researchers from Brazil last month published results from the first clinical test of a potential therapeutic benefit for ayahuasca, a South American plant-based brew1. Although the study included just six volunteers and no placebo group, the scientists say that the drink began to reduce depression in patients within hours, and the effect was still present after three weeks. They are now conducting larger studies that they hope will shore up their findings. The work forms part of a renaissance in studying the potential therapeutic benefits of psychedelic or recreational drugs — research that was largely banned or restricted worldwide half a century ago. Ketamine, which is used medically as an anaesthetic, has shown promise as a fast-acting antidepressant; psilocybin, a hallucinogen found in ‘magic mushrooms’, can help to alleviate anxiety in patients with advanced-stage cancer2; MDMA (ecstasy) can alleviate post-traumatic stress disorder; and patients who experience debilitating cluster headaches have reported that LSD eases their symptoms. Ayahuasca, a sacramental drink traditionally brewed from the bark of a jungle vine (Banisteriopsis caapi) and the leaves of a shrub (Psychotria viridis), contains ingredients that are illegal in most countries. But a booming ayahuasca industry has developed in South America, where its religious use is allowed, and where thousands of people each year head to rainforest retreats to sample its intense psychedelic insights. © 2015 Nature Publishing Group,
By Anne Skomorowsky Because Germanwings pilot Andreas Lubitz killed himself when he purposefully drove a plane carrying 149 other people into a mountain in the Alps, there has been an assumption that he suffered from “depression”—an assumption strengthened by the discovery of antidepressants in his home and reports that he had been treated in psychiatry and neurology clinics. Many patients and other interested parties are rightly concerned that Lubitz’s murderous behavior will further stigmatize the mentally ill. It is certainly true that stigma may lead those in need to avoid treatment. When I was a psychiatrist at an HIV clinic, I was baffled by the shame associated with a visit to see me. Patients at the clinic had advanced AIDS, often contracted through IV drug use or sex work, and many had unprotected sex despite their high viral loads. Some were on parole. Many had lost custody of their children. Many lived in notorious single-room occupancy housing and used cocaine daily. But these issues, somehow, were less embarrassing than the suggestion that they be evaluated by a psychiatrist. Even doctors invoke “depression” to explain anything a reasonable adult wouldn’t do. For my clinic patients, it was shameful to be mentally ill. But to engage in antisocial behavior as a way of life? Not so bad. I think my patients were on to something. Bad behavior—even suicidal behavior—is not the same as depression. It is a truism in psychiatry that depression is underdiagnosed. But as a psychiatrist confronted daily with “problem” patients in the general hospital where I work, I find that depression is also overdiagnosed. Even doctors invoke “depression” to explain anything a reasonable adult wouldn’t do. © 2014 The Slate Group LLC.
Link ID: 20736 - Posted: 03.31.2015
|By Roni Jacobson As intangible as they may seem, memories have a firm biological basis. According to textbook neuroscience, they form when neighboring brain cells send chemical communications across the synapses, or junctions, that connect them. Each time a memory is recalled, the connection is reactivated and strengthened. The idea that synapses store memories has dominated neuroscience for more than a century, but a new study by scientists at the University of California, Los Angeles, may fundamentally upend it: instead memories may reside inside brain cells. If supported, the work could have major implications for the treatment of post-traumatic stress disorder (PTSD), a condition marked by painfully vivid and intrusive memories. More than a decade ago scientists began investigating the drug propranolol for the treatment of PTSD. Propranolol was thought to prevent memories from forming by blocking production of proteins required for long-term storage. Unfortunately, the research quickly hit a snag. Unless administered immediately after the traumatic event, the treatment was ineffective. Lately researchers have been crafting a work-around: evidence suggests that when someone recalls a memory, the reactivated connection is not only strengthened but becomes temporarily susceptible to change, a process called memory reconsolidation. Administering propranolol (and perhaps also therapy, electrical stimulation and certain other drugs) during this window can enable scientists to block reconsolidation, wiping out the synapse on the spot. The possibility of purging recollections caught the eye of David Glanzman, a neurobiologist at U.C.L.A., who set out to study the process in Aplysia, a sluglike mollusk commonly used in neuroscience research. Glanzman and his team zapped Aplysia with mild electric shocks, creating a memory of the event expressed as new synapses in the brain. The scientists then transferred neurons from the mollusk into a petri dish and chemically triggered the memory of the shocks in them, quickly followed by a dose of propranolol. © 2015 Scientific American
By Gary Stix One of the most intriguing new areas of research in neuroscience has to do with the discovery that proteins involved with Alzheimer’s, Parkinson’s and other neurodegenerative illnesses can contort into the wrong shape. The misshapen molecules can spread throughout the brain in a manner akin to prion diseases—the most notorious of which is variant Creutzfeldt-Jakob disease, better known as Mad Cow. Misfolded proteins can lead to a buildup of cellular gunk that then causes damage inside or outside cells. If the process of misfolding observed in Alzheimer’s and Parkinson’s is similar to the one in Mad Cow, the next question is whether these misshapen proteins are transmissible from one organism to another. Last month, an article appeared in Acta Neuropathologica Communications from researchers at the Centre for Biological Threats and Special Pathogens at the Robert Koch-Institut in Berlin that raised questions about whether medical instruments need to be decontaminated if they come into contact with post-mortem brain tissue from Alzheimer’s or Parkinson’s patients. The case for putting in place such prophylaxis is rooted in lab studies that show that injecting deposits of these proteins into an animal brain can initiate a “seeding” process in which one protein causes another to misfold. “Whether those harmful effects can be also caused by transmitted protein particles in humans who express mutated or normal alpha-synuclein, A-beta or tau is still unknown,” the article says. But then it goes on: “…the ability to decontaminate medical instruments from aggregated A-beta, tau and alpha-synuclein may potentially add to patient safety.” © 2015 Scientific American
Jon Hamilton A new understanding of the brain's cerebellum could lead to new treatments for people with problems caused by some strokes, autism and even schizophrenia. That's because there's growing evidence that symptoms ranging from difficulty with abstract thinking to emotional instability to psychosis all have links to the cerebellum, says Jeremy Schmahmann, a professor of neurology at Harvard and Massachusetts General Hospital. "The cerebellum has all these functions we were previously unaware of," Schmahmann says. Scientists once thought the cerebellum's role was limited to balance and coordinating physical movements. In the past couple of decades, though, there has been growing evidence that it also plays a role in thinking and emotions. As described in an earlier post, some of the most compelling evidence has come from people like Jonathan Keleher, people born without a cerebellum. "I'm good at routine (activities) and (meeting) people," says Keleher, who is 33. He also has good long-term memory. What he's not good at is strategizing and abstract thinking. But remarkably, Keleher's abilities in these areas have improved dramatically over time. "I'm always working on how to better myself," he says. "And it's a continuous struggle." © 2015 NPR
By Nicholas Bakalar People sometimes take Valium or Ativan to relieve anxiety before surgery, but a new study suggests that these benzodiazepine drugs have little beneficial effect and may even delay recovery. Researchers studied 1,062 patients admitted to French hospitals for surgery requiring general anesthesia. A third took 2.5 milligrams of lorazepam (brand name Ativan), a third received a placebo, and a third were given no premedication. Patients completed questionnaires assessing anxiety, pain levels and quality of sleep before and a day after their operations, while researchers recorded their time to having ventilation tubes removed and to recovering full wakefulness. The study was published in JAMA. Lorazepam was associated with more postsurgery amnesia and a longer time to recover cognitive abilities. Quality of sleep was impaired in the lorazepam group, but not in the others. And ventilation tubes were kept in significantly longer in the lorazepam group. Pain scores did not differ between the lorazepam and the no-medication groups, but there was more pain in the group given the placebo. The lead author, Dr. Axel Maurice-Szamburski, an anesthesiologist at Timone Hospital in Marseille, cited recent surveys showing that benzodiazepines are widely prescribed before surgery. “But until now,” he added, “sedatives have not been evaluated from the patient’s point of view. It’s the patient who should be happy, not the doctor.” © 2015 The New York Times Company
Link ID: 20676 - Posted: 03.10.2015
Jon Hamilton Alzheimer's, Parkinson's and amyotrophic lateral sclerosis ravage the brain in very different ways. But they have at least one thing in common, says Corinne Lasmezas, a neuroscientist and professor at Scripps Research Institute, in Jupiter, Fla. Each spreads from brain cell to brain cell like an infection. "So if we could block this [process], that might prevent the diseases," Lasmezas says. It's an idea that's being embraced by a growing number of researchers these days, including Nobel laureate Dr. Stanley Prusiner, who first recognized in the 1980s the infectious nature of brain proteins that came to be called prions. But the idea that mad cow prions could cause disease in people has its origins in an epidemic of mad cow disease that occurred in Europe and the U.K. some 15 years ago. Back then, Lasmezas was a young researcher in France studying how mad cow, formally known as bovine spongiform encephalopathy, was transmitted. "At that time, nobody knew if this new disease in cows was actually transmissible to humans," she says. In 1996, Lasmezas published a study strongly suggesting that it was. "So that was my first great research discovery," she says. Prions, it turns out, become toxic to brain cells when folded into an abnormal shape. "This misfolded protein basically kills the neurons," Lasmezas says. © 2015 NPR
By CELIA WATSON SEUPEL Every year, nearly 40,000 Americans kill themselves. The majority are men, and most of them use guns. In fact, more than half of all gun deaths in the United States are suicides. Experts and laymen have long assumed that people who died by suicide will ultimately do it even if temporarily deterred. “People think if you’re really intent on dying, you’ll find a way,” said Cathy Barber, the director of the Means Matters campaign at Harvard Injury Control Research Center. Prevention, it follows, depends largely on identifying those likely to harm themselves and getting them into treatment. But a growing body of evidence challenges this view. Suicide can be a very impulsive act, especially among the young, and therefore difficult to predict. Its deadliness depends more upon the means than the determination of the suicide victim. Now many experts are calling for a reconsideration of suicide-prevention strategies. While mental health and substance abuse treatment must always be important components in treating suicidality, researchers like Ms. Barber are stressing another avenue: “means restriction.” Instead of treating individual risk, means restriction entails modifying the environment by removing the means by which people usually die by suicide. The world cannot be made suicide-proof, of course. But, these researchers argue, if the walkway over a bridge is fenced off, a struggling college freshman cannot throw herself over the side. If parents leave guns in a locked safe, a teenage son cannot shoot himself if he suddenly decides life is hopeless. With the focus on who dies by suicide, these experts say, not enough attention has been paid to restricting the means to do it — particularly access to guns. © 2015 The New York Times Company
Link ID: 20674 - Posted: 03.10.2015
By Rachel Rabkin Peachman Many women with a history of depression who take antidepressants assume that once they get pregnant, they should try to wean themselves off their meds to avoid negative side effects for the baby. A new large study published in the journal Pediatrics challenges one reason behind that assumption. The research found that taking selective serotonin reuptake inhibitors (the antidepressants also known as S.S.R.I.s) while pregnant does not increase the risk of asthma in the resulting babies. What is associated with an increased risk of asthma? According to this study and other research, untreated prenatal depression. “The mechanisms underlying the association of prenatal depression and asthma are unknown,” said Dr. Xiaoqin Liu, the lead author of the Pediatrics study and an epidemiologist at Aarhus University in Denmark. An association between prenatal depression and asthma does not mean that prenatal depression causes asthma. There could be other reasons for the correlation, genetic or environmental, or both. For example, people who live in dense, polluted urban areas could be at an increased risk of both asthma and depression. The researchers used Denmark’s national registries to evaluate all singleton babies born from 1996 to 2007, and identify the mothers who had a diagnosis of depression or had used antidepressants, or both, during pregnancy or one year beforehand. Using a statistical model, the study authors found that prenatal depression — with or without the use of antidepressants — was associated with a 25 percent increased risk of asthma in children as compared with children whose mothers did not have a record of depression. © 2015 The New York Times Company
Hannah Devlin, science correspondent Psychedelic drugs could prove to be highly effective treatments for depression and alcoholism, according to a study which has obtained the first brain scans of people under the influence of LSD. Early results from the trial, involving 20 people, are said to be “very promising” and add to existing evidence that psychoactive drugs could help reverse entrenched patterns of addictive or negative thinking. However, Prof David Nutt, who led the study, warned that patients are missing out on the potential benefits of such treatments due to prohibitive regulations on research into recreational drugs. Speaking at a briefing in London, the government’s former chief drugs adviser, said the restrictions amounted to “the worst censorship in the history of science”. After failing to secure conventional funding to complete the analysis of the latest study on LSD, Nutt and colleagues at Imperial College London, are now attempting to raise £25,000 through the crowd-funding site Walacea.com. “These drugs offer the greatest opportunity we have in mental health,” he said. “There’s little else on the horizon.” There has been a resurgence of medical interest in LSD and psilocybin, the active ingredient in magic mushrooms, after several recent trials produced encouraging results for conditions ranging from depression in cancer patients to post-traumatic stress disorder. © 2015 Guardian News and Media Limited
Zoe Cormier Data from population surveys in the United States challenge public fears that psychedelic drugs such as LSD can lead to psychosis and other mental-health conditions and to increased risk of suicide, two studies have found1, 2. In the first study, clinical psychologists Pål-Ørjan Johansen and Teri Suzanne Krebs, both at the Norwegian University of Science and Technology in Trondheim, scoured data from the US National Survey on Drug Use and Health (NSDUH), an annual random sample of the general population, and analysed answers from more than 135,000 people who took part in surveys from 2008 to 2011. Of those, 14% described themselves as having used at any point in their lives any of the three ‘classic’ psychedelics: LSD, psilocybin (the active ingredient in so-called magic mushrooms) and mescaline (found in the peyote and San Pedro cacti). The researchers found that individuals in this group were not at increased risk of developing 11 indicators of mental-health problems such as schizophrenia, psychosis, depression, anxiety disorders and suicide attempts. Their paper appears in the March issue of the Journal of Psychopharmacology1. The findings are likely to raise eyebrows. Fears that psychedelics can lead to psychosis date to the 1960s, with widespread reports of “acid casualties” in the mainstream news. But Krebs says that because psychotic disorders are relatively prevalent, affecting about one in 50 people, correlations can often be mistaken for causations. “Psychedelics are psychologically intense, and many people will blame anything that happens for the rest of their lives on a psychedelic experience.” © 2015 Nature Publishing Group,
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