Chapter 12. Psychopathology: The Biology of Behavioral Disorders

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By Jocelyn Kaiser HOUSTON, TEXAS—Schizophrenia tends to run in families, which suggests it’s largely inherited. But a long-running search for genes underlying this severe psychiatric condition has yielded only indirect clues. Now, by scouring the DNA of tens of thousands of people, gene hunters have for the first time nabbed a handful of rare genes that, when mutated, appear to be direct contributors to the disease—and may shed light on what goes awry in a schizophrenia patient’s brain. “These are concrete genes with mutations with a clear molecular mechanism,” says Mark Daly of the Broad Institute in Cambridge, Massachusetts, and the University of Helsinki, who is principal investigator for a consortium that presented the work last week at the annual meeting of the American Society of Human Genetics (ASHG) here. “It was a fabulous talk,” says Jennifer Mulle of Emory University in Atlanta, who studies the genetics of psychiatric disorders. “We don’t understand anything about the biological pathways [in schizophrenia]. Now, these genes give us an avenue.” People with schizophrenia, which afflicts about 0.7% of the U.S. population, have a distorted sense of reality and confused thinking; they may have hallucinations and delusions. Some patients share similar genetic abnormalities, such as missing specific chunks of DNA, but how those gaps may contribute to disease isn’t known. © 2019 American Association for the Advancement of Science

Keyword: Schizophrenia; Genes & Behavior
Link ID: 26756 - Posted: 10.26.2019

Researchers have discovered in mice how one of the few genes definitively linked to schizophrenia, called SETD1A, likely confers risk for the illness. Mice genetically engineered to lack a functioning version of the enzyme-coding gene showed abnormalities in working memory, mimicking those commonly seen in schizophrenia patients. Restoring the gene’s function corrected the working memory deficit. Counteracting the gene’s deficiencies also repaired neuronal circuit deficits in adult mice – suggesting clues for potential treatment strategies. A team of scientists led by Joseph Gogos, M.D., Ph.D., of Columbia University, New York City, reported on their research – supported by the National Institutes of Health – in Neuron. “You could call SETD1A a master regulator,” explained David Panchision Ph.D., of the NIH’s National Institute of Mental Health (NIMH), which co-funded the study. “This schizophrenia risk gene codes for an enzyme that influences the expression of many other genes. In mice, a hobbled version of SETD1A disrupted gene expression in a network harboring other genomic suspects in schizophrenia. Remarkably, the resulting abnormalities were reversible.” Researchers have identified both common and rare genetic variations that contribute to risk for schizophrenia. Mutant SETD1A is one of just a few rare genes known to unequivocally confer risk for schizophrenia. While common genetic variations linked to schizophrenia individually exert only tiny effects on risk, having just one mutant copy of SETD1A is sufficient to confer a large increase in disease risk. SETD1A plays a key role in epigenomic regulation – the switching on-and-off of genes in response to experience – a molecular process widespread in the brain. Mutations in SETD1A have primarily been found in people with schizophrenia, suggesting that this rare gene variation might hold important clues to the underlying disease process.

Keyword: Schizophrenia; Genes & Behavior
Link ID: 26750 - Posted: 10.25.2019

By Jonathan Lambert Prozac, a commonly prescribed medication for kids and teens with autism, is no more effective than a placebo at treating obsessive-compulsive behaviors, a small study finds. The results of the randomized clinical trial, published October 22 in JAMA, cast further doubt on the widespread practice of prescribing a class of antidepressants known as selective serotonin reuptake inhibitors, or SSRIs, to treat children with autism who have these behaviors, says pediatric neurologist Ann Neumeyer. “We really don’t have any good medications that have yet been studied in children with autism for these behaviors,” says Neumeyer, the medical director of the Massachusetts General Hospital Lurie Center for Autism in Lexington, who wasn’t involved in the study. “That’s a problem.” Autism spectrum disorders encompass a diversity of symptoms, but common among them are obsessive-compulsive behaviors (SN: 10/16/18). Individuals with autism can become hyperfocused on specific ideas or objects and can engage in ritualistic “tics,” such as rocking or hand-waving. For many individuals, these symptoms interfere with everyday functioning. SSRI antidepressants account for a quarter to a third of all prescriptions to children and teens with autism, according to pediatrician Dinah Reddihough at the Murdoch Children’s Research Institute in Melbourne, Australia. “Despite their widespread use, there is no evidence of effectiveness of SSRIs for autism spectrum disorders in children,” she says. © Society for Science & the Public 2000–2019.

Keyword: Autism
Link ID: 26738 - Posted: 10.23.2019

By Marlene Cimons In 1991, Karestan Koenen was a recent college graduate and Peace Corps volunteer who arrived in a village in Niger eager to help local women start small businesses. When her sister came to visit during Christmas, the two decided to travel north to Agadez, a city in the Sahara. There, on the morning of Dec. 27, two male traders stopped by, trying to sell them jewelry. Koenen’s sister went to the market with one of men to have a look. While she was gone, the second man grabbed Koenen, held her down and raped her. Traumatized by the experience, Koenen was medically evacuated to the United States two days later and resigned from the Peace Corps. She returned to New Jersey to live with her parents, but the assault continued to haunt her. Increasingly, she became depressed. A psychologist diagnosed Koenen with post-traumatic stress disorder, or PTSD, a condition triggered by a traumatic, scary or dangerous event, and, for reasons still unclear, seems to disproportionately afflict women. These assaults can include combat, sexual assault, gun violence, accidents, natural disasters, even the death of a loved one. “I lay in bed, unable to sleep, thinking of ways to kill myself,” she recalls. “When I did sleep, I had nightmares. I lost interest in everything. I couldn’t read and was too jumpy to sit through a movie or watch TV. I was irritable with my family. I was always on guard — angry — and couldn’t stop thinking about what had happened. I felt like I was stuck in a dark tunnel, moving more and more quickly, but it only got darker.”

Keyword: Stress; Sexual Behavior
Link ID: 26726 - Posted: 10.21.2019

Dean Burnett It’s a damp, midweek afternoon. Even so, Cardiff’s walk-in stress management course has pulled in more than 50 people. There are teenagers, white-haired older people with walking aids, people from Caucasian, Asian and Middle Eastern backgrounds. There is at least one pair who look like a parent and child – I’m unsure who is there to support whom. The course instructor makes it clear that she is not going to ask people to speak out about their own stress levels in this first class: “We know speaking in public is stressful in itself.” She tells us a bit about previous attendees: a police officer whose inexplicable and constant worrying prevented him from functioning; a retired 71-year-old unable to shake the incomprehensible but constant fatigue and sadness that blighted his life; a single mother unable to attend her daughter’s school concert, despite the disappointment it would cause. What is the common theme that links these people – and the varied group sitting there this afternoon and listening? Stress may once just have been a kind of executive trophy – “I’m so stressed!” – but recent research suggests it is a key element in developing mental health problems such as depression and anxiety. The constant, stress-induced stimulation of key brain regions seems to be a major contributor to anxiety. And, in turn, vital brain regions becoming unresponsive and inflexible is believed to be a fundamental element of depressive disorders. Why do these regions become unresponsive? Possibly because they’re overworked, exhausted, by the effects of stress. This would explain why anxiety and depression regularly occur together. © 2019 Guardian News & Media Limited

Keyword: Depression; Stress
Link ID: 26701 - Posted: 10.15.2019

Allison Aubrey There's fresh evidence that eating a healthy diet, one that includes plenty of fruits and vegetables and limits highly processed foods, can help reduce symptoms of depression. A randomized controlled trial published in the journal PLOS ONE finds that symptoms of depression dropped significantly among a group of young adults after they followed a Mediterranean-style pattern of eating for three weeks. Participants saw their depression "score" fall from the "moderate" range down to the "normal" range, and they reported lower levels of anxiety and stress too. Alternatively, the depression scores among the control group of participants — who didn't change their diets — didn't budge. These participants continued to eat a diet higher in refined carbohydrates, processed foods and sugary foods and beverages. Their depression scores remained in the "moderate severity" range. "We were quite surprised by the findings," researcher Heather Francis, a lecturer in clinical neuropsychology at Macquarie University in Sydney, Australia, told NPR via email. "I think the next step is to demonstrate the physiological mechanism underlying how diet can improve depression symptoms," Francis said. In this study, participants in the "healthy eating" arm of the study ate about six more servings of fruits and vegetables per week, compared with the control group. Participants "who had a greater increase in fruit and vegetable intake showed the greatest improvement in depression symptoms," Francis said. © 2019 npr

Keyword: Depression; Obesity
Link ID: 26693 - Posted: 10.11.2019

Between 1999 and 2017, the United States experienced a 10-fold increase in the number of people who died from overdoses of Valium and other benzodiazepines. For years, scientists thought that these powerful sedatives, which are used to treat anxiety, muscle spasms, and sleeping disorders, worked alone to calm nerves. Now, in an article published in Science, researchers from the National Institutes of Health show that this view of the drugs and the neural circuits they affect may have to change. In a study of mice, scientists discovered that both may need the assistance of a ‘sticky’ gene, named after a mythological figure, called Shisa7. “We found that Shisa7 plays a critical role in the regulation of inhibitory neural circuits and the sedative effects some benzodiazepines have on circuit activity,” said Wei Lu, Ph.D., a Stadtman Investigator at NIH’s National Institute of Neurological Disorders and Stroke (NINDS) and the senior author of the study. “We hope the results will help researchers design more effective treatments for a variety of neurological and neuropsychiatric disorders that are caused by problems with these circuits.” Dr. Lu’s lab studies the genes and molecules used to control synapses; the trillions of communications points made between neurons throughout the nervous system. In this study, his team worked with researchers led by Chris J. McBain, Ph.D., senior investigator at NIH’s Eunice Kennedy Shriver National Institute of Child Health and Human Development (NICHD), to look at synapses that rely on the neurotransmitter gamma-aminobutyric acid (GABA) to calm nerves. Communication at these synapses happens when one neuron fires off packets of GABA molecules that are then quickly detected by proteins called GABA type A (GABAA) receptors on neighboring neurons.

Keyword: Drug Abuse; Stress
Link ID: 26692 - Posted: 10.11.2019

Bianca Nogrady As droughts go, the one plaguing the antidepressant drug development landscape for the past few decades has been noteworthy. Since the advent of serotonin and norepinephrine reuptake inhibitors in the 1980s and 1990s, there has been a dearth of new pharmacological therapies for mood disorders, says psychiatrist Samantha Meltzer-Brody, director of the University of North Carolina’s Perinatal Psychiatry Program. “The same medications largely that were there when I went to medical school a long time ago were still the ones we’ve been using.” Given this state of affairs, Meltzer-Brody says she had the “most modest” of expectations a few years ago when she got involved in the first clinical trial testing a new drug, SAGE-547, for postpartum depression. Developed by Massachusetts-based Sage Therapeutics, SAGE-547 is a solution of allopregnanolone, a neuroactive metabolite of the sex hormone progesterone, which plays key roles in the female reproductive system. Progesterone and allopregnanolone levels peak during the third trimester of pregnancy, then crash immediately after delivery. Preclinical data suggested the drop in allopregnanolone could be a trigger for postpartum depression in some women. The company-funded trial involved administering SAGE-547 to a handful of patients with postpartum depression as an intravenous infusion over 48 hours. The response in the first patient treated with SAGE-547 was dramatic. From being withdrawn and depressed with no appetite before treatment, she began smiling, talking, eating, and interacting, Meltzer-Brody says. “After that first patient, we thought either that’s one heck of a placebo or maybe there’s a signal.” Three more patients were treated, with similar results. Known by the generic name brexanolone, the drug sped through Phase 2 and Phase 3 trials before being approved by the US Food and Drug Administration (FDA) on March 19. © 1986–2019 The Scientist

Keyword: Depression
Link ID: 26689 - Posted: 10.10.2019

By Benedict Carey For more than a decade, doctors have been using brain-stimulating implants to treat severe depression in people who do not benefit from medication, talk therapy or electroshock sessions. The treatment is controversial — any psychosurgery is, given its checkered history — and the results have been mixed. Two major trials testing stimulating implant for depression were halted because of disappointing results, and the approach is not approved by federal health regulators. Now, a team of psychiatric researchers has published the first long-term results, reporting Friday on patients who had stimulating electrodes implanted as long ago as eight years. The individuals have generally fared well, maintaining their initial improvements. The study, appearing in the American Journal of Psychiatry, was small, with just 28 subjects. Even still, experts said the findings were likely to extend interest in a field that has struggled. “The most impressive thing here is the sustained response,” Dr. Darin Dougherty, director of neurotherapeutics at Massachusetts General Hospital, said. “You do not see that for anything in this severe depression. The fact that they had this many people doing well for that long, that’s a big deal.” The implant treatment is known as deep brain stimulation, or D.B.S., and doctors have performed it for decades to help people control the tremors of Parkinson’s disease. In treating depression, surgeons thread an electrode into an area of the brain that sits beneath the crown of the head and is known to be especially active in people with severe depression. Running electrical current into that region, known as Brodmann Area 25, effectively shuts down its activity, resulting in relief of depression symptoms in many patients. The electrode is connected to a battery that is embedded in the chest. The procedure involves a single surgery; the implant provides continuous current from then on. © 2019 The New York Times Company

Keyword: Consciousness
Link ID: 26673 - Posted: 10.04.2019

By Liz Eavey My brother Roland’s Facebook post set off a flurry of concern throughout his social network. He’d been assaulted, he wrote, by “old-world mentality Agent Smiths who are threatening our ability to bring natural plant-based Medicine and intelligent health care to the world.” In caps, he told his followers to ALERT THE PRESS AND BRING SIGNS OF PROTEST. The yogis sent positive vibes; the rebels cried fight the man; the good Samaritans offered to jump in their cars and rescue him. Except that Roland hadn’t exactly been assaulted. He’d been placed under an involuntary psychiatric hold and forcibly subdued in an emergency room at the same institution where he was training to become a psychiatrist. And, with that, four years ago, Facebook snitched our big family secret: Roland, the literary prodigy, the tenderhearted musician, the Ivy League grad, was bipolar. Roland — who read and approved this essay — is the effortlessly brilliant middle child who takes up a disproportionate amount of space in a room, with a booming voice and the charisma of a megachurch pastor. After college, he moved to Hollywood and landed, with zero experience or connections, a coveted job with an A-list director. Then, he decided to become a doctor, enrolling in a top-tier M.D./M.B.A. program. Everything about my brother is superlative, including his demons: crippling insomnia, legendary alcoholism and a chemical imbalance that has repeatedly imploded his life. I, the firstborn, am diplomatic and obedient, less concerned with standing out than blending in. Just 17 months apart, Roland and I constantly butted heads trying to assert our individuality growing up. In seventh grade, I wrote “An Older Sister’s Guide to Having Younger Brothers,” which began: “A smart idea, which would prevent use of this guide, would be to just not have younger brothers.” Yet, when we weren’t vying for sibling dominance, we were always looking out for each other. © 2019 The New York Times Company

Keyword: Schizophrenia
Link ID: 26652 - Posted: 09.27.2019

By Jill Halper, M.D. Depression is not cancer. It’s a completely different disease. Yet when I look back on my husband’s depression and death by suicide three years ago, it sure looks a lot like cancer to me. As an adolescent medicine physician in Los Angeles, I have cared for many patients with depression and mental illness, and as a pediatric resident in training, I also cared for many children with cancer. But the difference in how people view these illnesses is astounding. Before we met, my husband’s first marriage had ended, and his ex-wife told him that he did not deserve love. Primed by genetics and an abusive childhood, he was convinced he would always be alone. He attempted suicide with an overdose of pills. When he unexpectedly woke up in the morning, he drove to U.C.L.A. and was checked into the psychiatric unit. He was treated, started on medication and improved. Six months later we met, and soon felt that we were soul mates. He realized he did deserve love. We never took the suicide attempt lightly and always had professional support and treatment. We were married for nearly 20 years. We had two children, purchased a home and negotiated our marriage as best we could. We communicated well, and had the support of a couples’ therapist. It seemed his horrible disease was cured — until it wasn’t. He wasn’t cured; as with some cancers, his disease was simply in remission. And while his first suicide attempt was about the fear of never finding love, his second fear, equally unwarranted, was that he was a complete failure as a provider. My husband’s father was not trained in any skill or profession. He was laid off in his 50s, and never worked again. When he died in his 60s, he left behind a financial mess. © 2019 The New York Times Company

Keyword: Depression
Link ID: 26650 - Posted: 09.27.2019

By Nicholas Bakalar Sleep apnea may increase the risk for mood disorders, researchers have found. Obstructive sleep apnea, or O.S.A., is a sleep-related breathing disorder that has been linked to many other conditions, including cardiovascular disease, asthma exacerbation, glaucoma, erectile dysfunction and neurocognitive problems. For the new study, in JAMA Otolaryngology—Head & Neck Surgery, researchers enrolled 197 Korean men and women diagnosed with O.S.A. and 788 people without the syndrome matched for age, sex, and health and socioeconomic characteristics. None of the 985 participants had been diagnosed with depression, bipolar illness or an anxiety disorder before the start of the study. The researchers followed them for an average of nine years. Over the course of the study, people with O.S.A. were nearly three times as likely to be diagnosed with depression, and almost twice as likely to be diagnosed with anxiety as those in the control group. Women with O.S.A. were more likely than men to develop a mood disorder. The reason for the association is unknown. The researchers had no information about the use of positive airway pressure devices or oral appliances used to treat sleep apnea, so they could not determine whether treatment would reduce the risk. Still, they write, “studies that investigate O.S.A. management and the risk of developing affective disorders may yield strategies for effective prevention and intervention practices.” © 2019 The New York Times Company

Keyword: Sleep; Depression
Link ID: 26645 - Posted: 09.25.2019

Researchers have discovered that gene expression regulators work together to raise an individual’s risk of developing schizophrenia. Schizophrenia-like gene expression changes modeled in human neurons matched changes found in patients’ brains. The researchers, led by Kristen Brennand, of the Icahn School of Medicine at Mount Sinai, New York City, report on their findings in Nature Genetics. The work was funded by the National Institute of Mental Health (NIMH), part of the National Institutes of Health. Genome-wide association studies have revealed at least 143 chromosomal sites associated with risk for schizophrenia. However, individually, each of these sites can explain only a small fraction of the risk. Even when the effects of disease-linked rare genetic variants are factored in, most of schizophrenia’s known high inheritance remains unexplained. One possible clue: more than 40% of the suspect chromosomal sites contain regulators, called expression quantitative trait loci, or eQTLs, that govern the expression of multiple genes. “Individually, these gene regulators have a modest effect on the brain. Working in concert, they exert different and more significant effects on the brain — effects that boost schizophrenia risk,” explained David Panchision, chief of the Developmental Neurobiology Program at NIMH. “Learning more about the downstream cellular and molecular effects of such synergy holds hope for advances in precision psychiatry and more personalized medicine.” To explore the role of these regulators, Brennand and colleagues studied them in induced neurons using a molecular modeling technology. This induced pluripotent stem cell method makes it possible to grow a person’s unique neurons in a petri dish using stem cells derived from their skin cells.

Keyword: Schizophrenia; Genes & Behavior
Link ID: 26643 - Posted: 09.24.2019

By Maureen O'Hagan, Kaiser Health News Hanging on Kimberly Repp’s office wall in Hillsboro, Ore., is a sign in Latin: “Hic locus est ubi mors gaudet succurrere vitae,” meaning “This is a place where the dead delight in helping the living.” For medical examiners, it is a mission. Their job is to investigate deaths and learn from them, for the benefit of us all. Repp, however, is not a medical examiner; she is a microbiologist. She is also an epidemiologist for Oregon’s Washington County, where she had been accustomed to studying infectious diseases such as flu or norovirus outbreaks among the living. But in 2012 she was asked by county officials to look at suicide. The request introduced her to the world of death investigations and also appears to have led to something remarkable: in this suburban county of 600,000, just west of Portland, the suicide rate now is going down. That result is remarkable because national suicide rates have risen, despite decades-long efforts to reverse the deadly trend. Advertisement While many factors contribute to suicide, officials here believe they have chipped away at this problem through Repp’s initiative to use data—very localized data that any jurisdiction could collect. Now her mission is to help others learn how to gather and use them. New York State has just begun testing a system like Repp’s. Humboldt County in California is implementing it. She has gotten inquiries from Utah and Kentucky. Colorado, meanwhile, is using its own brand of data collection to try to achieve the same kind of turnaround. © 2019 Scientific American

Keyword: Depression
Link ID: 26630 - Posted: 09.21.2019

/ By Gitit Ginat In 1978, at the age of 18, Celine Sabag took a trip to Israel. There, she met a 25-year-old bus driver and spent three weeks touring Jerusalem with him. “He was nice and polite,” she recalls. When the man invited her to his parents’ empty apartment, she accepted the invitation. The pair had been sitting together and laughing for about an hour when the door opened. “I turned to look,” says Sabag, “and my gut told me: ‘Something awful is about to happen.’” Four young men were standing in the doorway. They entered the living room, the fourth locking the door behind him. “I believe they had done it before,” she says. At first, Sabag was dubious. “I said: ‘Fighting? No way. What do I have to do with fighting?’” Sabag returned that night to her hotel, and then fled back to her home in France. She felt guilt and shame, and did not tell anyone that five men had raped her that night in the apartment. Shortly after her homecoming, she tried to commit suicide, the first of many attempts. Desperate for help, Sabag entered therapy. She saw psychiatrists and psychologists and started taking psychiatric medication. She also tried alternative approaches like movement therapy. Though some of the treatments helped, they didn’t eliminate the relentless flashbacks of the rape, her overwhelming fear of unknown men in corridors and on elevators and stairways, and other symptoms of post-traumatic stress disorder (PTSD). Copyright 2019 Undark

Keyword: Stress
Link ID: 26620 - Posted: 09.18.2019

By Ioanna Roumeliotis On any day, at any moment, Toronto’s subway can transform into a tragic stage. It's a place where every year people try to end their lives. Those acts of private despair become public spectacles that force transit workers and commuters to bear horrible witness, a collective trauma that for decades was shrouded in silence. A silence the Toronto Transit Commission is breaking. Talking openly about suicide is incredibly difficult and some consider it nothing short of dangerous. The Toronto Transit Commission (TTC) has a different perspective — that acknowledging what's going on is a crucial part of preventing people from taking their own lives, and showing how simple things can head off tragedy. "We are worried," says John O’Grady, who's been in charge of safety at the TTC for the past 21 years, referring to the fear of a contagion effect if people talk about suicide. "But not talking about it hasn’t worked." It was the death of 27-year-old Michael Padbury three years ago that marked a cautious turning point for the TTC. In a series of tweets, a spokesperson told frustrated commuters the delays were the result of someone’s mental health anguish. It was a nod to the fact Padbury’s death was a deliberate act. And for his mother, it was an acknowledgement that her son existed. ©2019 CBC/Radio-Canada

Keyword: Depression
Link ID: 26615 - Posted: 09.16.2019

By Temma Ehrenfeld One night in her Nashville apartment, Bre Banks read a comment from her boyfriend on Facebook. They were in a shaky spell, and his words seemed proof she would lose him. She put her laptop down on the couch and headed to the bedroom to cry. “My legs seized up, and I fell,” she recalled. With her knees and forehead pressing into the carpet, she heard a voice that said, “Slit your wrists, slit your wrists.” She saw herself in the bathtub with the blood flowing. She was terrified that if she moved she would die. In one study, about a quarter of the suicide attempts were made by people who reported zero suicidal thoughts. Banks, then 25, was a disciplined graduate student with a job and close friends and had no psychiatric history. “I had never considered suicide an option,” she says. But for the next three days, she couldn’t sleep while the voice and disturbing images persisted. After seeing a therapist, she decided to teach herself techniques from dialectical behavior therapy, one of the few treatments shown to reduce suicidality. The voices and images came back over the next few months, but eventually faded. Eight years later, Banks now evaluates suicide prevention programs across Tennessee as a manager at the large mental health provider Centerstone’s research institute, and she and the same boyfriend just celebrated their 10th anniversary. Copyright 2019 Undark

Keyword: Depression
Link ID: 26605 - Posted: 09.12.2019

Ian Sample Science editor Society must prepare for a technological revolution in which brain implants allow people to communicate by telepathy, download new skills, and brag about their holidays in “neural postcards”, leading scientists say. While such far-fetched applications remain fiction for now, research into brain implants and other neural devices is advancing so fast that the Royal Society has called for a “national investigation” into the technology. “In 10 years’ time this is probably going to touch millions of people,” said Tim Constandinou, director of the next generation neural interfaces lab at Imperial College London, and co-chair of a new Royal Society report called iHuman. “These technologies are not possible today, but we are heading in that direction.” A neuroscientist explains: the need for ‘empathetic citizens’ - podcast The report foresees a “neural revolution” driven by electronic implants that communicate directly with the brain and other parts of the nervous system. By 2040, the scientists anticipate that implants will help the paralysed to walk, with other devices alleviating the symptoms of neurodegenerative diseases and treatment-resistant depression. The new wave of devices will go beyond existing products such as cochlear implant hearing aids and deep brain stimulators for people with Parkinson’s disease, with gadgets that help the healthy. In research labs, scientists are working on ways for people to type with their brains, and share thoughts by connecting their minds. Other teams are developing helmets and headbands to speed up learning and improve memory. “People could become telepathic to some degree, able to converse not only without speaking but without words, through access to each other’s thoughts at a conceptual level. This could enable unprecedented collaboration with colleagues and deeper conversations with friends,” the report states. © 2019 Guardian News & Media Limited

Keyword: Brain imaging; Depression
Link ID: 26595 - Posted: 09.10.2019

Jon Hamilton The depression drug esketamine, marketed as Spravato, appears to offer quick relief to people who are actively considering suicide. Esketamine, a chemical cousin of the anesthetic and party drug ketamine, reduced depression symptoms within hours in two large studies of suicidal patients, the drug's maker announced Monday. The studies, which included 456 patients who were suicidal, found that after 24 hours, patients who got the drug along with standard treatment were less depressed than people who got standard treatment alone. Surprisingly, though, patients who got esketamine were not significantly less suicidal, even though they had fewer symptoms of depression. The finding came from two studies sponsored by the drug's maker, Johnson & Johnson, and presented at the 32nd European College of Neuropsychopharmacology meeting in Copenhagen. Esketamine "showed a benefit in a very high-risk patient population, which is usually excluded from most clinical trials," says Dr. David Hough, a psychiatrist and esketamine compound development team leader at Janssen Research and Development LLC, a part of Johnson & Johnson. © 2019 npr

Keyword: Depression; Drug Abuse
Link ID: 26593 - Posted: 09.10.2019

By Eryn Brown, On March 30, 1981, 25-year-old John W. Hinckley Jr. shot President Ronald Reagan and three other people. The following year, he went on trial for his crimes. Defense attorneys argued that Hinckley was insane, and they pointed to a trove of evidence to back their claim. Their client had a history of behavioral problems. He was obsessed with the actress Jodie Foster, and devised a plan to assassinate a president to impress her. He hounded Jimmy Carter. Then he targeted Reagan. In a controversial courtroom twist, Hinckley’s defense team also introduced scientific evidence: a computerized axial tomography (CAT) scan that suggested their client had a “shrunken,” or atrophied, brain. Initially, the judge didn’t want to allow it. The scan didn’t prove that Hinckley had schizophrenia, experts said—but this sort of brain atrophy was more common among schizophrenics than among the general population. It helped convince the jury to find Hinckley not responsible by reason of insanity. Nearly 40 years later, the neuroscience that influenced Hinckley’s trial has advanced by leaps and bounds—particularly because of improvements in magnetic resonance imaging (MRI) and the invention of functional magnetic resonance imaging (fMRI), which lets scientists look at blood flows and oxygenation in the brain without hurting it. Today neuroscientists can see what happens in the brain when a subject recognizes a loved one, experiences failure, or feels pain. Despite this explosion in neuroscience knowledge, and notwithstanding Hinckley’s successful defense, “neurolaw” hasn’t had a tremendous impact on the courts—yet. But it is coming. Attorneys working civil cases introduce brain imaging ever more routinely to argue that a client has or has not been injured. Criminal attorneys, too, sometimes argue that a brain condition mitigates a client’s responsibility. Lawyers and judges are participating in continuing education programs to learn about brain anatomy and what MRIs and EEGs and all those other brain tests actually show. © 2019 Scientific American

Keyword: Brain imaging
Link ID: 26587 - Posted: 09.09.2019