Chapter 16. Psychopathology: Biological Basis of Behavior Disorders

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By Elissa Welle Many of the physicians who worked on the current diagnostic and treatment guidelines for psychiatric conditions in the United States have financial ties to pharmaceutical companies, according to a study published today in The BMJ. Nearly 60 percent of the 92 U.S.-based physicians who shepherded the Diagnostic and Statistical Manual of Mental Disorders, fifth edition, text revision (DSM-5-TR) accepted industry payments totaling $14.2 million during the three years prior to working on the manual, the study shows. The results raise questions about systemic “economies of influence” over a document used by public health officials, health insurance plans and drug regulators, says lead investigator Lisa Cosgrove, professor of counseling and school psychology and a faculty fellow at the Applied Ethics Center at the University of Massachusetts, Boston. “Financial conflicts of interest, industry ties don’t point to wrongdoing — we’re not saying that people did anything wrong consciously,” Cosgrove says. “It’s just implicit bias.” DSM-5-TR decision-makers were not allowed to receive more than $5,000 from industry, according to a statement to The Transmitter by a spokesperson for the American Psychiatric Association (APA), which published the DSM-5-TR in March 2022. And an independent committee reviewed financial and non-financial disclosures for all other contributors to the revision. The text revision centered on literature searches to incorporate new scientific findings since the publication of the DSM-5 in 2013, the spokesperson wrote. “Any rare, minor instances of content that connected a diagnosis to a therapy were omitted from DSM-5-TR,” the spokesperson wrote. “No content was found in the submitted text that related to a specific treatment for which industry funding may have been provided for related research.” © 2023 Simons Foundation.

Keyword: Depression; Schizophrenia
Link ID: 29096 - Posted: 01.13.2024

By Tim Vernimmen It is increasingly well understood that the countless microbes in our guts help us to digest our food, to absorb and produce essential nutrients, and to prevent harmful organisms from settling in. Less intuitive — perhaps even outlandish — is the idea that those microbes may also affect our mood, our mental health and how we perform on cognitive tests. But there is mounting evidence that they do. For nearly two decades, neuroscientist John Cryan of University College Cork in Ireland has been uncovering ways in which intestinal microbes affect the brain and behavior of humans and other animals. To his surprise, many of the effects he’s seen in rodents appear to be mirrored in our own species. Most remarkably, research by Cryan and others has shown that transplanting microbes from the guts of people with psychiatric disorders like depression to the guts of rodents can cause comparable symptoms in the animals. These effects may occur in several ways — through the vagus nerve connecting the gut to the brain, through the influence of gut bacteria on our immune systems, or by microbes synthesizing molecules that our nerve cells use to communicate. Cryan and coauthors summarize the science in a set of articles including “Man and the Microbiome: A New Theory of Everything?,” published in the Annual Review of Clinical Psychology. Cryan told Knowable Magazine that even though it will take much more research to pin down the mechanisms and figure out how to apply the insights, there are some things we can do already. This conversation has been edited for length and clarity.

Keyword: Depression; Stress
Link ID: 29091 - Posted: 01.11.2024

Pam Belluck A research team analyzed records of nearly a million women in Sweden’s national medical registries from 2001 through 2017, comparing 86,551 women who had perinatal depression with 865,510 women who did not. The groups were matched by age and year they gave birth. In two studies, the team found that depression that begins in pregnancy or soon after can have troubling implications for as long as 18 years. One study, published on Tuesday in JAMA Network Open, found that women with perinatal depression had three times the risk of suicidal behavior, defined as attempted or completed suicide, than women who did not experience perinatal depression. Risks were greatest in the year following their diagnosis, but, while they lessened over time, years later the risks were still twice as high compared with women without the disorder. The other study, published on Wednesday in BMJ, found that women with perinatal depression were more than six times at risk of dying by suicide as those without that diagnosis. The number of suicides was small, but it accounted for a large share of the deaths of women diagnosed with perinatal depression: 149 of the 522 deaths in that group, or 28.5 percent. For women without perinatal depression, there were 117 suicides out of 1,568 deaths or 7.5 percent. Suicide was a major reason women with perinatal depression were twice as likely to die from any cause over the 18-year period of the study compared with women without the disorder. The researchers also compared more than 20,000 women with perinatal depression to their biological sisters who gave birth during the same time frame and did not have the disorder. The risk of suicidal behavior for the sisters with perinatal depression was nearly three times that of their sisters without the diagnosis — almost as high as the difference between women with the illness and those without it to whom they were not related. That suggests depression plays a greater role in these outcomes than genetics or childhood environment, the researchers wrote. © 2024 The New York Times Company

Keyword: Depression; Hormones & Behavior
Link ID: 29089 - Posted: 01.11.2024

By Christina Jewett and Benjamin Mueller In early 2020, the Food and Drug Administration responded to decades of escalating concerns about a commonly prescribed drug for asthma and allergies by deploying one of its most potent tools: a stark warning on the drug’s label that it could cause aggression, agitation and even suicidal thoughts. The agency’s label, which was primarily aimed at doctors, was supposed to sound an alert about the 25-year-old medication, Singulair, also known by its generic name, montelukast. But it barely dented use: The drug was still prescribed to 12 million people in the United States in 2022. Children face the greatest risks of the drug’s ill effects, and while usage by minors did decline, it was still taken by 1.6 million of them — including Nicole Sims’s son. Ms. Sims had no idea why, at 6, her son started having nightmares and hallucinations of a woman in the window. When he told her that he wanted to die, Ms. Sims went online, desperate for answers. Only then did she learn about the F.D.A. warning. She also found a Facebook support group with 20,000 members for people who had experienced side effects of the drug. Members of the group recounted a haunting toll that they linked to the drug with the help of peers, not their doctors. “It’s a mental health crisis that nobody is recognizing,” said Anna Maria Rosenberg, an administrator of the group. The F.D.A.’s handling of Singulair illustrates systemic gaps in the agency’s approach to addressing troubling side effects from medicines approved long ago — and to warning the public and doctors when serious issues arise. The agency had flagged the 2020 warning label, known as a “boxed warning,” to physicians’ groups, but it had not required that doctors be educated about the drug’s side effects. Federal regulators in 1998 initially dismissed evidence that emerged during the approval process about the drug’s potential to affect the brain and did not revise their assessment until two decades later. The F.D.A. was slow to alert the public as reports of psychiatric problems surfaced, highlighting deficiencies of a drug-monitoring system that puts the onus on drugmakers to report problems. © 2024 The New York Times Company

Keyword: Depression
Link ID: 29087 - Posted: 01.09.2024

By Bill Sullivan Schizophrenia can produce persistent delusions, hallucinations, and disorganized thinking. The precise cause is unknown but seems to involve a combination of genetics and environmental risk factors. One environmental factor may be an infectious agent, such as the common parasite Toxoplasma gondii, which causes toxoplasmosis. Since cats can transmit Toxoplasma to humans, scientists have been investigating whether there is a link between cat ownership and schizophrenia. Many studies have tried to answer this question over the past 50 years; some studies show an association, but others do not. Researchers at the University of Queensland in Australia recently reanalyzed all these studies to determine the current consensus. What Is Toxoplasma? Toxoplasma is a single-celled parasite that infects all warm-blooded animals, including up to one-third of the human population. Cats are the only animals that support the sexual stage of the parasite’s life cycle, which culminates in the expulsion of infectious parasites in the feces. These fecal parasites are housed in sturdy containers called oocysts, which are stable in the environment for years and can spread the infection to a new individual if inhaled or ingested. In addition to litter boxes, people can pick up oocysts wherever a cat may have defecated, for example in the yard, sandbox, or garden (including unwashed fruits and vegetables). Oocysts have also made their way into streams and seawater, where they can infect people though shellfish. Up to 40 million people in the U.S. are infected with Toxoplasma. While a healthy immune system can control the parasite’s growth, it cannot get rid of the infection entirely. Toxoplasma parasites remain in the brain and other tissues as latent cysts, which can resume growth if the immune system is weakened.

Keyword: Schizophrenia
Link ID: 29084 - Posted: 01.09.2024

By Max Kozlov Shredded iboga root, the main ingredient in the psychedelic drug ibogaine, is prepared for use in a traditional ceremony in Gabon.Credit: Rachel Nuwer Psychedelic drugs such as MDMA and psilocybin, the hallucinogenic compound found in magic mushrooms, have promised to revolutionize psychiatric treatments. Now, a small trial in military veterans suggests that a lesser-known, potent psychedelic drug called ibogaine could be used to treat traumatic brain injury (TBI). One month after ibogaine treatment, the veterans reported that TBI symptoms such as post-traumatic stress disorder (PTSD) and depression had decreased by more than 80%, on average1. “The drug seems to have a broad, dramatic and consistent effect,” says Nolan Williams, a neuroscientist at Stanford University in California and a co-author of the study. The results of the trial, which did not include a control group, are published today in Nature Medicine. These data support launching rigorous trials to test the drug, says Alan Davis, a clinical psychologist at the Ohio State University in Columbus. However, they note that MDMA and psilocybin, which are already in late-stage trials, will be “much better candidates for meeting the needs of this community”. Ibogaine will require years of study to determine its efficacy and safety, Davis says. Warfare’s lasting effects Ibogaine is made from the bark of a shrub (Tabernanthe iboga) native to Central Africa, where it is used for ceremonial purposes. Researchers have tended to shy away from exploring the use of ibogaine for the treatment of conditions other than opioid dependence and withdrawal2, because it is tightly regulated in many countries and can cause fatal heartbeat irregularities, says Maria Steenkamp, a clinical psychologist who studies PTSD in veterans at the NYU Grossman School of Medicine in New York City. But the available therapies for PTSD and other conditions don’t help everybody, Steenkamp says. “We are desperately in need of new interventions.” © 2024 Springer Nature Limited

Keyword: Stress; Drug Abuse
Link ID: 29082 - Posted: 01.06.2024

By Rodrigo Pérez Ortega Politically and ethically fraught, research into what leads to bisexual behavior or exclusive homosexuality typically sparks controversy. The latest study, published today in Science Advances, is no exception. By mining a DNA database of some 450,000 people in the United Kingdom, a research team has concluded that the genes underlying bisexual behavior are distinct from those driving exclusive same-sex behavior, and may be intertwined with a propensity for taking risks. This connection to risk-taking, the authors suggest, may also explain why men with a history of bisexual behavior still have a reasonably high number of offspring, albeit fewer than heterosexual men, possibly explaining why the genes driving such sexual behavior have persisted. The work has drawn a mix of strong reactions. Some scientists called the findings valuable, whereas others found fault with the underlying data. Still others argued the research could potentially stigmatize sexual minorities. The result that bisexuality is tied with risky behavior, some scientists say, could be used by others to discriminate against, and further perpetuate false narratives about, bisexual people. However, study co-author Jianzhi Zhang, an evolutionary geneticist at the University of Michigan (UM), counters that the association between bisexual behavior and risk-taking “is an empirical observation. … We hold no moral judgement on risk-taking and believe [it] has pros and cons (depending on the situation), as almost any trait.” He also pushes back at the idea such research should be taboo or off limits. “We should welcome more studies of bisexuality and homosexuality. … This is partly a biological question, so we should understand it.” From one stark evolutionary perspective, sex without the prospect of producing children could be seen as waste of time and energy—behavior that might be selected against. Yet population surveys have consistently found that about 2% to 10% of people engage in sex with others of the same sex. Studies of twins have suggested such sexual activity is at least partly heritable, and therefore has a genetic component. And scientists have proposed several evolutionary theories explaining why same-sex sexual behavior may persist.

Keyword: Sexual Behavior; Genes & Behavior
Link ID: 29080 - Posted: 01.06.2024

By Gina Kolata People taking the wildly popular drugs Ozempic, to treat diabetes, and Wegovy, to combat obesity, are slightly less likely to have suicidal thoughts than people who are not taking them, researchers reported on Friday. Millions of people take Ozempic and Wegovy, which are considered to be among the biggest blockbusters in medical history. But last year a European drug safety agency said it was investigating whether the drugs cause suicidal thoughts. The new study, published in the journal Nature Medicine, was funded by the National Institutes of Health and used a huge population. The findings provide data that may potentially reassure people who take the drugs. Novo Nordisk, maker of the drugs, had no role in the study, and the study’s investigators had no conflicts of interest. The investigators used anonymized electronic health records from a database of 100.8 million people. That allowed them to look at two groups: 240,618 who were prescribed Wegovy or other weight loss drugs, and 1,589,855 who were prescribed Ozempic or other medicines to lower their blood sugar. Suicidal thoughts were included in patients’ records as part of routine monitoring of their health. The investigators compared the incidence of suicidal thoughts in people who were taking the drugs with the incidence among similar people who were not taking them but were taking other weight loss and anti-diabetes medications. They also asked if there was an increase in the recurrence of suicidal thoughts among those taking the drugs who had previously reported thoughts of suicide. The database’s size allowed the researchers to look at subgroups such as sex, race and age groups. “No matter how hard we tried we did not see any increased risk,” said Rong Xu, director of the Center for Artificial Intelligence in Drug Discovery at Case Western Reserve University in Cleveland. Dr. Xu conceived the study and interpreted the data with Dr. Nora D. Volkow, director of the National Institute on Drug Abuse. But it was an observational study, so it is impossible to draw conclusions about cause and effect. Such studies can only show associations. “More studies are absolutely needed,” Dr. Volkow said. © 2024 The New York Times Company

Keyword: Obesity; Depression
Link ID: 29078 - Posted: 01.06.2024

By April Dembosky Every year, an estimated 100,000 young adults or adolescents in the U.S. experience a psychotic episode. Only 10-20% of them gain access to the holistic treatment approach recommended by the National Institute of Mental Health as the gold standard of care for early psychosis, due to lack of space or because insurance won't cover it. Illustration by Anna Vignet/KQED After M graduated from high school in California, she got a job at a fast food restaurant making burgers. Her coworkers were chatting over the fryer one day when M got a weird feeling, like somehow they knew what she was thinking. It was like her coworkers could read her mind and were discussing her thoughts with each other. "I was like, are they talking about burgers or are they talking about me?" says M, now 21. NPR has agreed to identify M by her middle initial because she fears the stigma around her mental illness could disrupt her career path. There was one coworker in particular, a guy she had a crush on, and she was pretty sure he was watching her. She suspected he hacked into her phone so he could listen to her conversations, find out where she was and follow her around. If she was walking down the street, or hanging out in the park, she saw him. Her mom remembers M wanted to sleep with the lights on, repeatedly asking her through the night, "Mom, is someone here?" One day, her mom said M got so paranoid, so scared, she locked herself in the bathroom and just screamed and screamed and screamed. Her mom wanted to call for help. But she didn't have a job at the time. This was about a year into the pandemic, and the hotel where M's mom worked had been closed since the first lockdown. When she lost her job, she lost her family's health benefits, too. "My husband was like, 'What is that going to cost?'" her mom remembers. © 2024 npr

Keyword: Schizophrenia
Link ID: 29076 - Posted: 01.03.2024

By Elizabeth Svoboda Esther Oladejo knew she'd crossed an invisible boundary when she started forgetting to eat for entire days at a time. A gifted rugby player, Oladejo had once thrived on her jam-packed school schedule. But after she entered her teenage years, her teachers started piling on assignments and quizzes to prepare students for high-stakes testing that would help them to qualify for university. As she devoted hours on hours to cram sessions, Oladejo's resolve began to fray. Every time she got a low grade, her mood tanked—and with it, her resolve to study hard for the next test. “Teachers [were] saying, ‘Oh, you can do much better than this,’” says Oladejo, now 18, who lives in Merseyside, England. “But you're thinking, ‘Can I? I tried my best on that. Can I do any more than what I've done before?’” One morning, as Oladejo steeled herself for another endless day, her homeroom teacher passed out a questionnaire to the students, explaining that it would help assess their moods and well-being. Oladejo filled it out, her mind ticking forward to her upcoming classes. Soon after that, someone called to tell her she'd been slotted into a new school course called the Blues Program. Developed by Oregon Research Institute psychologist Paul Rohde and his colleagues at Stanford University, the program—a six-week series of hour-long group sessions—teaches students skills for managing their emotions and stress. The goal is to head off depression in vulnerable teens. Although Oladejo didn't know it at the time, her course was one in an expanding series of depression prevention programs for young people, including Vanderbilt University's Teens Achieving Mastery Over Stress (TEAMS); the University of Pennsylvania's Penn Resiliency Program; Happy Lessons, developed by Dutch social scientists; and Spain's Smile Program. The growing global interest in depression prevention is helping to establish the efficacy of a range of programs in diverse settings. © 2023 SCIENTIFIC AMERICAN,

Keyword: Depression; Development of the Brain
Link ID: 29066 - Posted: 12.27.2023

Ian Sample Science editor Human tears carry a substance that dampens down aggression, according to researchers, who believe the drops may have evolved over time to protect wailing babies from harm. Sniffing emotional tears from women reduced male aggression by more than 40% in computerised tests, and prompted corresponding changes in the brain, though the scientists behind the study think all human tears would have a similar effect. “The reduction in aggression was impressive to us, it seems real,” said Noam Sobel, a professor of neurobiology at the Weizmann Institute of Science in Israel. “Whatever is in tears actually lowers aggression.” Charles Darwin puzzled over the point of weeping. Writing in The Expression of Emotions in Man and Animals in 1872, the great naturalist declared sobbing as “purposeless as the secretion of tears from a blow outside the eye”. But in the 150 years since, researchers have proposed all manner of roles, from signalling vulnerability and helplessness to clearing bacteria from the eyes. Previous work at Sobel’s lab found that sniffing women’s tears reduced male testosterone but it was unclear whether this affected behaviour. In animals, the picture is clearer: subordinate mole rats, for example, cover themselves in tears to protect themselves from aggressors. For the latest study, Dr Shani Agron and others in Sobel’s lab collected tears rolling down women’s faces as they watched sad movies. The researchers did not specifically advertise for female tear donors but nearly all who came forward were women, of whom six were selected because they produced tears in such quantities. The experiments involved 31 men who sniffed either saline or women’s tears before having swabs dabbed with the droplets stuck to their upper lip. The men then took part in a computerised game used in psychology to provoke aggressive behaviour by unfairly deducting players’ points. © 2023 Guardian News & Media Limited

Keyword: Aggression; Chemical Senses (Smell & Taste)
Link ID: 29063 - Posted: 12.22.2023

Perspective by Michael Varnum and Ian Hohm A growing body of research in psychology and related fields suggests that winter brings some profound changes in how people think, feel and behave. The natural and cultural changes that come with winter often occur simultaneously, making it challenging to tease apart the causes underlying these seasonal swings. Live well every day with tips and guidance on food, fitness and mental health, delivered to your inbox every Thursday. We recently conducted an extensive survey of these findings with research colleagues Alexandra Wormley, a social psychologist at Arizona State University, and Mark Schaller, a psychologist at the University of British Columbia. Wintertime blues and a long winter’s nap Do you find yourself feeling down in the winter months? You’re not alone. As the days grow shorter, the American Psychiatric Association estimates that about 5 percent of Americans will experience a form of depression known as seasonal affective disorder, or SAD. People experiencing SAD tend to have feelings of hopelessness, decreased motivation to take part in activities they generally enjoy, and lethargy. Even those who don’t meet the clinical threshold for this disorder may see increases in anxiety and depressive symptoms. Scientists link SAD and more general increases in depression in the winter to decreased exposure to sunlight, which leads to lower levels of the neurotransmitter serotonin. Consistent with the idea that sunlight plays a key role, SAD tends to be more common in more northern regions of the world, such as Scandinavia and Alaska, where the days are shortest and the winters longest. Humans, special as we may be, are not unique in showing some of these seasonally linked changes. For instance, our primate relative the Rhesus macaque shows seasonal declines in mood.

Keyword: Biological Rhythms; Depression
Link ID: 29043 - Posted: 12.13.2023

By Anil Oza Krista Lisdahl has been studying cannabis use among adolescents for two decades, and what she sees makes her worried for her teenage son. “I see the data coming in, I know that he is going to come across it,” she says. As a clinical neuropsychologist at the University of Wisconsin–Milwaukee, she sees plenty of young people who have come into contact with the drug to varying degrees, from trying it once at a party to using potent preparations of it daily. The encounters have become more frequent as efforts to legalize cannabis for recreational use intensify around the world. In some of her studies, around one-third of adolescents who regularly use cannabis show signs of a cannabis use disorder — that is, they can’t stop using the drug despite negative impacts on their lives. But she wants more conclusive evidence when it comes to talking about the drug and its risks to young people, including her son. Deciding what to say is difficult, however. Anti-drug messaging campaigns have dwindled, and young people are forced to consider sometimes-conflicting messages on risks in a culture that increasingly paints cannabis and other formerly illicit drugs as harmless or potentially therapeutic. “Teenagers are pretty smart, and they see that adults use cannabis,” Lisdahl says. That makes blanket warnings and prohibitions practically useless. It’s now a decade since the drug was officially legalized for recreational use by adults aged 18 and older in Uruguay, and aged 21 and older in the states of Colorado and Washington. Many other states and countries have followed, and researchers are desperately trying to get a handle on how usage patterns are changing as a result; how the drug impacts brain development; and how cannabis use correlates with mental-health conditions such as depression, anxiety and schizophrenia. The data so far don’t tell clear stories: young people don’t seem to be using in greater numbers than before legalization, but there seem to be trends towards more problematic use. © 2023 Springer Nature Limited

Keyword: Drug Abuse; Schizophrenia
Link ID: 29041 - Posted: 12.13.2023

Sydney E. Smith When most people hear about electroconvulsive therapy, or ECT, it typically conjures terrifying images of cruel, outdated and pseudo-medical procedures. Formerly known as electroshock therapy, this perception of ECT as dangerous and ineffective has been reinforced in pop culture for decades – think the 1962 novel-turned-Oscar-winning film “One Flew Over the Cuckoo’s Nest,” where an unruly patient is subjected to ECT as punishment by a tyrannical nurse. Despite this stigma, ECT is a highly effective treatment for depression – up to 80% of patients experience at least a 50% reduction in symptom severity. For one of the most disabling illnesses around the world, I think it’s surprising that ECT is rarely used to treat depression. Contributing to the stigma around ECT, psychiatrists still don’t know exactly how it heals a depressed person’s brain. ECT involves using highly controlled doses of electricity to induce a brief seizure under anesthesia. Often, the best description you’ll hear from a physician on why that brief seizure can alleviate depression symptoms is that ECT “resets” the brain – an answer that can be fuzzy and unsettling to some. As a data-obsessed neuroscientist, I was also dissatisfied with this explanation. In our newly published research, my colleagues and I in the lab of Bradley Voytek at UC San Diego discovered that ECT might work by resetting the brain’s electrical background noise. To study how ECT treats depression, my team and I used a device called an electroencephalogram, or EEG. It measures the brain’s electrical activity – or brain waves – via electrodes placed on the scalp. You can think of brain waves as music played by an orchestra. Orchestral music is the sum of many instruments together, much like EEG readings are the sum of the electrical activity of millions of brain cells. © 2010–2023, The Conversation US, Inc.

Keyword: Depression
Link ID: 29036 - Posted: 12.09.2023

By Taylor Beck One sunny day this fall, I caught a glimpse of the new psychiatry. At a mental hospital near Yale University, a depressed patient was being injected with ketamine. For 40 minutes, the drug flowed into her arm, bound for cells in her brain. If it acts as expected, ketamine will become the first drug to quickly stop suicidal drive, with the potential to save many lives. Other studies of ketamine are evaluating its effect as a vaccination against depression and post-traumatic stress. Between them, the goal is nothing less than to redefine our understanding of mental illness itself. Depression is the most common mental illness in the United States, affecting 30 percent of Americans at some point in their lives. But despite half a century of research, ubiquitous advertising, and blockbuster sales, antidepressant drugs just don’t work very well. They treat depression as if it were caused by a chemical imbalance: Pump in more of one key ingredient, or sop up another, and you will have fixed the problem. But the correspondence between these chemicals (like serotonin) and depression is relatively weak. An emerging competitive theory, inspired in part by ketamine’s effectiveness, has it that psychiatric disease is less about chemical imbalance than structural changes in the brain—and that a main cause of these changes is psychological stress. “I really do think stress is to mental illness as cigarettes are to heart disease,” says Gerard Sanacora, the psychiatry professor running the ketamine trial at Yale. The theory describes stress grinding down individual neurons gradually, as storms do roof shingles. This, in turn, changes the nature of their connections to one another and the structure of the brain. Ketamine, along with some similar molecules, acts to strengthen the neuron against that damage, affecting not just the chemistry of the brain but also its structure. © 2023 NautilusNext Inc.,

Keyword: Depression; Stress
Link ID: 29027 - Posted: 12.02.2023

By John Krakauer & Tamar Makin The human brain’s ability to adapt and change, known as neuroplasticity, has long captivated both the scientific community and the public imagination. It’s a concept that brings hope and fascination, especially when we hear extraordinary stories of, for example, blind individuals developing heightened senses that enable them to navigate through a cluttered room purely based on echolocation or stroke survivors miraculously regaining motor abilities once thought lost. For years, the notion that neurological challenges such as blindness, deafness, amputation or stroke lead to dramatic and significant changes in brain function has been widely accepted. These narratives paint a picture of a highly malleable brain that is capable of dramatic reorganization to compensate for lost functions. It’s an appealing notion: the brain, in response to injury or deficit, unlocks untapped potentials, rewires itself to achieve new capabilities and self-repurposes its regions to achieve new functions. This idea can also be linked with the widespread, though inherently false, myth that we only use 10 percent of our brain, suggesting that we have extensive neural reserves to lean on in times of need. But how accurate is this portrayal of the brain’s adaptive abilities to reorganize? Are we truly able to tap into reserves of unused brain potential following an injury, or have these captivating stories led to a misunderstanding of the brain’s true plastic nature? In a paper we wrote for the journal eLife, we delved into the heart of these questions, analyzing classical studies and reevaluating long-held beliefs about cortical reorganization and neuroplasticity. What we found offers a compelling new perspective on how the brain adapts to change and challenges some of the popularized notions about its flexible capacity for recovery. The roots of this fascination can be traced back to neuroscientist Michael Merzenich’s pioneering work, and it was popularized through books such as Norman Doidge’s The Brain That Changes Itself. Merzenich’s insights were built on the influential studies of Nobel Prize–winning neuroscientists David Hubel and Torsten Wiesel, who explored ocular dominance in kittens. © 2023 SCIENTIFIC AMERICAN,

Keyword: Learning & Memory; Regeneration
Link ID: 29019 - Posted: 11.22.2023

by Grace Huckins In 1961, the late psychiatrist Daniel Freedman made what would become one of the most replicated — and most mysterious — discoveries in the history of autism research. Comparing blood levels of the neurotransmitter serotonin in 4 non-autistic and 23 autistic children, he found significantly higher levels among the latter group. Since then, researchers have repeatedly identified this trait, called hyperserotonemia, in about a third of autistic people tested. It’s not difficult to theorize how hyperserotonemia might be linked to a range of autism traits. Neurons that release serotonin extend into practically every part of the brain, where they modulate signals sent among other neurons. Selective serotonin reuptake inhibitors (SSRIs), drugs that raise levels of serotonin in the brain’s synapses, treat psychiatric conditions, such as anxiety and obsessive-compulsive disorder, that can co-occur with autism. And serotonin prompts the gut to contract and facilitate digestion, which is often impaired in autistic people. So when Edwin Cook, professor of psychiatry at the University of Illinois at Chicago, began to study the biology of autism in the 1980s, hyperserotonemia seemed like an obvious place to start. “We didn’t have much [else],” he says. “There were plenty of mothers of older patients I saw who had been labeled refrigerator mothers,” a term that refers to the discredited idea that unaffectionate mothers cause autism. The serotonin finding offered a tangible, biological clue. Even today, with decades more autism research to look back on, the hyperserotonemia result stands out. “It’s one of the few robust biological clues that we’ve had in autism,” says Jeremy Veenstra-VanderWeele, professor of psychiatry at Columbia University and a former advisee of Cook’s. But so far, it has escaped explanation. Nor have researchers been able to definitively link hyperserotonemia to specific genetic, anatomical or behavioral traits in autistic people. This apparent lack of progress has led some to disregard work on the neurotransmitter, according to serotonin researcher Georgianna Gould, associate professor of physiology at the University of Texas Health Science Center at San Antonio. “I’ve actually seen reviews come back that say that serotonin has nothing to do with autism,” she says. © 2023 Simons Foundation

Keyword: Autism; Obesity
Link ID: 28998 - Posted: 11.11.2023

By Azeen Ghorayshi Doctors and patients have long known that antidepressants can cause sexual problems. No libido. Pleasureless orgasms. Numb genitals. Well over half of people taking the drugs report such side effects. Now, a small but vocal group of patients is speaking out about severe sexual problems that have endured even long after they stopped taking selective serotonin reuptake inhibitors, the most popular type of antidepressants. The drugs’ effects have been devastating, they said, leaving them unable to enjoy sex or sustain romantic relationships. “My clitoris feels like a knuckle,” said Emily Grey, a 27-year-old in Vancouver, British Columbia, who took one such drug, Celexa, for depression from age 17 to 23. “It’s not a normal thing to have to come to terms with.” The safety label on Prozac, one of the most widely prescribed S.S.R.I.s, warns that sexual problems may persist after the drug is discontinued. And health authorities in Europe and Canada recently acknowledged that the medications can lead to lasting sexual issues. But researchers are only just beginning to quantify how many people have these long-term problems, known as post-S.S.R.I. sexual dysfunction. And the chronic condition remains contested among some psychiatrists, who point out that depression itself can curb sexual desire. Clinical trials have not followed people after they stop the drugs to determine whether such sexual problems stem from the medications. “I think it’s depression recurring. Until proven otherwise, that’s what it is,” said Dr. Anita Clayton, the chief of psychiatry at the University of Virginia School of Medicine and a leader of an expert group that will meet in Spain next year to formally define the condition. Dr. Clayton published some of the earliest research showing that S.S.R.I.s come with widespread sexual side effects. © 2023 The New York Times Company

Keyword: Depression; Sexual Behavior
Link ID: 28996 - Posted: 11.11.2023

Sara Reardon Psychedelic drugs have been undergoing a major makeover in psychiatry, earning mainstream acceptance that has eluded them for decades. In 2019, a variant of ketamine — an animal tranquillizer well known as a club drug — was approved by the US Food and Drug Administration (FDA) for treating post-traumatic stress disorder (PTSD). In May, Oregon opened its first treatment centre for administering psilocybin — the hallucinogenic compound found in magic mushrooms — following the state’s decision to legalize it (psilocybin remains illegal at the federal level). And, after decades of effort, the Multidisciplinary Association for Psychedelic Studies, a non-profit research organization in San Jose, California, formally asked the FDA for approval to market MDMA — also known as molly or ecstasy — as a treatment for PTSD. Most specialists expect the MDMA approval to go through on the weight of clinical evidence and popular support. Two large trials have shown that the drug can reduce the symptoms of PTSD when administered in controlled therapy sessions1,2. And it seems to do so more quickly than other treatments. But how MDMA and other psychedelics work is still largely a mystery, both because the drugs have long been illegal and because psychiatric conditions are difficult to study in animals. Psychedelic drug MDMA moves closer to US approval following success in PTSD trial With the regulatory landscape shifting, legal psychedelic research is becoming easier — and potentially more profitable. Neuroscientists, psychiatrists, pharmacologists, biochemists and others are entering the field, bringing fresh ideas about what the drugs do at a cellular and molecular level and trying to unravel how these mechanisms might help to relieve symptoms of psychiatric conditions. From a clinical perspective, understanding how the drugs work might not matter. “You don’t need to know the mechanism of the drug to have a very effective therapy,” says David Olson, a biochemist at the University of California, Davis. But, understanding more about psychedelics could lead to the development of proprietary drugs that are safer, less hallucinogenic and ultimately more effective. It could also affect the way psychedelics are administered in the clinic — helping providers to tailor treatments to each person. Several key questions are driving the basic research that progresses in the background as MDMA and others march towards the market. © 2023 Springer Nature Limited

Keyword: Depression; Stress
Link ID: 28986 - Posted: 11.04.2023

By Regina G. Barber What your parents didn't tell you about pulling an all-nighter? It might just ease depression for several days. At least, that's what researchers found happened to mice in a study published in the journal Neuron Thursday. Most people who've stayed up all night know the "tired and wired" feeling they get the next day. The body might be exhausted, but the brain feels jittery, hyperactive or even giddy. Even after these changes wear off, sleep loss can have a strong antidepressant effect in people that lasts several days. But researchers hadn't figured out why sleeplessness might have this effect —until this study from neurobiologists at Northwestern University. To study all of this, the team looked at the effects of sleep loss in mice. They induced sleep loss in some of the mice, while the others got a typical night's rest. They found that after this sleepless night, the mice were more excitable, more aggressive, more sexual and less depressed than mice that got a regular amount of sleep. Of course, researchers can't just ask mice whether they feel "less depressed." Instead, they created a depression-like state in all the mice before either disrupting their sleep or allowing them to rest by repeatedly giving them small shocks. In response to these shocks, the mice entered a depressive-like state and eventually stopped trying to escape their cages. Then, they tested the mice's response to shocks again. The ones that had stayed up all night showed a reversed depressive state, indicated by more attempts to escape the shocks. Dopamine is responsible for the brain's reward response. Changes in the brain's dopamine system have also been implicated in conditions like depression and in sleep regulation. And so, to see how the mice's brains responded to their sleepless night, the researchers measured dopamine neuron activity. They saw that sleep-deprived mice showed higher dopamine activity in three regions: the prefrontal cortex, nucleus accumbens and hypothalamus. © 2023 npr

Keyword: Sleep; Depression
Link ID: 28985 - Posted: 11.04.2023