Links for Keyword: Depression

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Brain implant that could boost mood by using ultrasound to go under NHS trial

Hannah Devlin Science correspondent A groundbreaking NHS trial will attempt to boost patients’ mood using a brain-computer-interface that directly alters brain activity using ultrasound. The device, which is designed to be implanted beneath the skull but outside the brain, maps activity and delivers targeted pulses of ultrasound to “switch on” clusters of neurons. Its safety and tolerability will be tested on about 30 patient in the £6.5m trial, funded by the UK’s Advanced Research and Invention Agency (Aria). In future, doctors hope the technology could revolutionise the treatment of conditions such as depression, addiction, OCD and epilepsy by rebalancing disrupted patterns of brain activity. Jacques Carolan, Aria’s programme director, said: “Neurotechnologies can help a much broader range of people than we thought. Helping with treatment resistant depression, epilepsy, addiction, eating disorders, that is the huge opportunity here. We are at a turning point in both the conditions we hope we can treat and the new types of technologies emerging to do that.” The trial follows rapid advances in brain-computer-interface (BCI) technology, with Elon Musk’s company Neuralink launching a clinical trial in paralysis patients last year and another study restoring communication to stroke patients by translating their thoughts directly into speech. However, the technologies raise significant ethical issues around the ownership and privacy of data, the possibility of enhancement and the risk of neuro-discrimination, whereby brain data might be used to judge a person’s suitability for employment or medical insurance. © 2025 Guardian News & Media Limited

Tiny fish on ketamine may show how drug eases depression

Jon Hamilton A single dose of the anesthetic ketamine can provide weeks of relief from severe depression. One reason may be that the drug causes long-term changes to a brain circuit involved in "giving up," a team reports in the journal Neuron. The team found that in zebrafish, ketamine alters this circuit in a way that causes the fish to persevere in the face of adversity rather than becoming passive. This resilience appears linked to brain cells called astrocytes, which play a central role in the "giving up" circuit. "Something happens within those cells that changes their response" to adversity, says Misha Ahrens, an author of the study and a senior group leader at HHMI's Janelia Research Campus. "We don't know what that is yet." But if scientists can figure it out, they might be able to develop more effective versions of ketamine and other psychiatric drugs, Ahrens says. The research involved the larval zebrafish, which is smaller than a grain of rice and looks like a tadpole. "It's transparent, so you can basically see what's going on in the entire brain all at once," says Alex Chen of Harvard University, another member of the team. For the experiment, the fish had to be kept stationary so scientists could monitor its brain. "But we still want it to feel like it's swimming through a virtual world," Chen says. The team did this by projecting images indicating forward movement when the animal swished its tail. Then they switched to images showing no progress, no matter what the fish did. © 2025 npr

Related chapters from BN: Chapter 16: Psychopathology: Biological Basis of Behavior Disorders; Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Related chapters from MM:Chapter 12: Psychopathology: The Biology of Behavioral Disorders; Chapter 4: Development of the Brain
Link ID: 29617 - Posted: 01.08.2025

Here’s how Antidepressants can affect weight, mood, libido and other functions.

7 Things Everyone Should Know About Antidepressants By Christina Caron Even if you’ve never taken an antidepressant, you’re probably familiar with the criticism and controversy that surrounds these drugs. It’s not uncommon to hear things like: “Those pills are just a placebo.” “You’ll definitely gain weight.” “Once you start, you’ll become dependent on them.” Is any of this true? Some of these statements have “a kernel of truth,” said Dr. Gerard Sanacora, a professor of psychiatry at the Yale School of Medicine. And it’s important to set the record straight because the expectations people have about their treatment — whether good or bad — “really do play a large role in how the treatment actually unfolds,” he added. Dr. Sanacora and other experts addressed some common questions and misconceptions about antidepressants. Will antidepressants change who I am? When an antidepressant starts to work, you may feel like a different person in some ways, said Naomi Torres-Mackie, a clinical psychologist in New York City. “Picture this giant, dark cloud weighing you down — as that lifts, the world is going to look different,” she said, adding: “But as you get used to it, you may see that it actually allows you to have more joy in your life.” On the other hand, up to half of people who take antidepressants may experience some degree of emotional blunting or numbed emotions, and research suggests that the blunting is more likely to happen with a higher medication dosage. When antidepressants are working correctly, patients should still feel a range of emotions, even if the sadness they used to feel every day is gone, said Dr. Laine Young-Walker, chair of the department of psychiatry at the University of Missouri School of Medicine. © 2024 The New York Times Compan

More than an hour of exercise a week may help with ‘baby blues'

Andrew Gregory Health editor Doing more than an hour of moderate intensity exercise each week may reduce the severity of “baby blues” and almost halve the risk of new mothers developing major clinical depression, the largest analysis of evidence suggests. However, researchers behind the study acknowledged that finding the time amid so many new responsibilities and challenges would not be easy, and recovery from childbirth should be prioritised. New mothers could restart exercise with “gentle” walks, which they could do with their babies, and then increase to “moderate” activity when they were ready, they added. This moderate physical activity could include brisk walking, water aerobics, stationary cycling or resistance training, according to the team of academics in Canada. Maternal depression and anxiety are relatively common after giving birth and associated with reduced self-care and compromised infant caregiving and bonding, which could in turn affect the child’s cognitive, emotional and social development, the researchers said. Conventional treatments for depression and anxiety in the first weeks and months after giving birth mostly involve drugs and counselling, which are often associated with, respectively, side-effects and poor adherence, and lack of timely access and expense. Research has previously shown that physical activity is an effective treatment for depression and anxiety in general. But until now it has not been known whether it could reduce the severity of the baby blues in the first few weeks after giving birth or lower the risk of major postpartum depression several months later. © 2024 Guardian News & Media Limited

Related chapters from BN: Chapter 16: Psychopathology: Biological Basis of Behavior Disorders; Chapter 12: Sex: Evolutionary, Hormonal, and Neural Bases
Related chapters from MM:Chapter 12: Psychopathology: The Biology of Behavioral Disorders; Chapter 8: Hormones and Sex
Link ID: 29548 - Posted: 11.09.2024

Is Depression Contagious? The Science Is Uncertain.

By Joshua Cohen The contagious nature of bacterial or viral infections like strep throat or influenza is well understood. You’re at risk of catching the flu, for example, if someone near you has it, as the virus can be spread by way of droplets in the air, among other modes of transmission. But what about a person’s mental health? Can depression be contagious? A JAMA Psychiatry paper published earlier this year seemed to suggest so. Researchers reported finding “an association between having peers diagnosed with a mental disorder during adolescence and an increased risk of receiving a mental disorder diagnosis later in life.” They suggested that, among adolescents, mental health disorders could be “socially transmitted,” though their observational study could not establish any direct cause. It makes some intuitive sense. Psychologists have studied how moods and emotions can spread from person to person. Someone howling with laughter might be contagious in the sense that it makes you laugh, too. Similarly, seeing a friend in emotional pain can evoke feelings of despair — a phenomenon termed emotional contagion. For more than three decades, researchers have investigated whether mental health disorders, too, may be induced by our social environment. Studies have found mixed results on the extent to which friends’, peers’, and families’ mental health can impact an individual’s mental health in turn. The JAMA Psychiatry study — conducted by researchers at the University of Helsinki and other institutions — analyzed nationwide registry data on 713,809 Finnish citizens born between 1985 to 1997. The research team identified individuals from schools across Finland who had been diagnosed with a mental disorder by the time they were in ninth grade. They followed the rest of the cohort to record later diagnoses, up until the end of 2019.

Related chapters from BN: Chapter 16: Psychopathology: Biological Basis of Behavior Disorders
Related chapters from MM:Chapter 12: Psychopathology: The Biology of Behavioral Disorders
Link ID: 29520 - Posted: 10.16.2024

Former Columbia University psychiatrist committed research misconduct

By Brendan Borrell, Ellie Kincaid A psychiatry researcher who received a warning letter from the U.S. Food and Drug Administration earlier this year committed research misconduct, another federal watchdog found. Bret Rutherford, formerly a research psychiatrist at the New York State Psychiatric Institute and Columbia University, “engaged in research misconduct by recklessly falsely reporting that all human research subjects met the inclusion/exclusion criteria for late-life depression studies,” according to a case summary from the U.S. Office of Research Integrity (ORI) published today. As The Transmitter previously reported, a suicide that occurred during one of Rutherford’s trials in 2021 was followed by a suspension of his research a few months later. The U.S. Office of Human Research Protections subsequently halted all federally funded research involving human participants at the institute in June 2023 and launched a review of its research practices. The ORI’s findings detail how in five published papers, Rutherford reported that 45 research participants were eligible for clinical studies, when in fact they were taking antidepressants or other medications that should have excluded them from participation. Rutherford also included 15 participants who took medications during a 28-day washout period before the trial when they were not supposed to be taking the medications, and he reported full washout periods for 8 participants who underwent shorter periods. The false reporting affected “the reported clinical research methods and results” of the five articles, the ORI’s finding stated. Three of the articles have been retracted, and the other two have been corrected. The Transmitter previously reported on the corrections and two of the retractions, which reference protocol violations in a clinical trial of whether levodopa, a drug for Parkinson’s disease, could help older adults with depression. © 2024 Simons Foundation

Why Depression Symptoms Come on at Night

By Christina Caron It’s not uncommon for our minds to unleash a torrent of difficult feelings under the cover of darkness: sadness and negative thoughts may surface at night, making sleep hard to come by. On social media and elsewhere people often refer to this as “nighttime depression.” But is that really a thing? And if so, why do some people get blue at night? Feeling down after dusk doesn’t necessarily mean that you have a mental health condition, experts said. Understanding why it happens can help you take steps to feel better. What is nighttime depression? Nighttime depression is a colloquial term for depressive symptoms that either appear or worsen late at night. It is not itself a diagnosis. While anxiety can also ramp up at night, and tends to make people feel agitated, tense and restless, nighttime depression is best characterized as a low mood. “It’s a sense of sadness,” said Dr. Theresa Miskimen Rivera, a clinical professor of psychiatry at Rutgers University and president-elect of the American Psychiatric Association. “It’s that feeling of: There’s no joy. My life is so blah.” Nighttime depression can also feel uncomfortable — “not only in your mind, but in your body,” Dr. Rivera added, especially if these feelings interfere with getting enough sleep. © 2024 The New York Times Company

Related chapters from BN: Chapter 16: Psychopathology: Biological Basis of Behavior Disorders; Chapter 14: Biological Rhythms, Sleep, and Dreaming
Related chapters from MM:Chapter 12: Psychopathology: The Biology of Behavioral Disorders; Chapter 10: Biological Rhythms and Sleep
Link ID: 29506 - Posted: 10.05.2024

Brain scan study identifies potential targets to treat youths with severe depression

Natasha May Young people with severe depression experience disruptions in the way regions of their brain communicate with each other which are distinct from those observed in adults, a study has found. The research published on Tuesday in Nature Mental Health could be used to identify potential targets for brain stimulation therapies, extending their existing application from adults to youth. The study analysed the brain scans of 810 young people aged 12-25, of which 440 had major depressive disorder (MDD) and 370 were healthy comparison individuals. The study led by the University of Melbourne found that in those with MDD, some densely connected regions of the brain (known as hubs) showed stronger connectivity and others showed weaker connectivity compared with youth without depression. Young woman running at sunset on Australian beach Nutrition and exercise as good as therapy for mild and moderate depression, study says Prof Andrew Zalesky, the supervising researcher, said they found the connectivity was particularly strong in the part of the brain associated with someone’s internalised thoughts and rumination. “We see that in youth with depression, the default mode is more strongly connected, it’s more activated, which suggests that there is a greater focus on self-thought and self-reflection,” Zalesky said. The study, whose first author was third-year PhD student at the University of Melbourne, Nga (Connie) Yan Tse, also found the extent of these differences could reliably predict how severe a person’s depressive symptoms were. © 2024 Guardian News & Media Limited

Related chapters from BN: Chapter 16: Psychopathology: Biological Basis of Behavior Disorders; Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 12: Psychopathology: The Biology of Behavioral Disorders; Chapter 13: Memory and Learning
Link ID: 29491 - Posted: 09.25.2024

Ketamine targets lateral habenula, setting off cascade of antidepressant effects

By Olivia Gieger Unlike traditional antidepressants, ketamine acts quickly to relieve depression symptoms, and its effects last long after the drug has cleared the system. Researchers have puzzled over what ketamine is doing in the brain to achieve these results. For one thing, the drug acts on N-methyl-D-aspartate (NMDA) glutamate receptors, which appear on neurons all over the brain. “Then the question is: Does the drug hit on all these brain regions simultaneously?” says Hailan Hu, professor of brain science at Zhejiang University. Or does it affect one region first, which sets off a series of downstream antidepressant effects? The answer is the latter, Hu and her colleagues report in a new study. Ketamine acts first on neurons in the lateral habenula, they found, in mice with depression-like symptoms. The structure—known as the “anti-reward” center—is hyperactive in people with depression and in mice modeling the condition, previous work has shown. That activity makes it highly susceptible to the drug’s effects, Hu and her colleagues discovered. Ketamine binds the NMDA receptors of cells in the lateral habenula and renders them inactive, which in turn interrupts downstream mechanisms of depression. The findings, published in Science in August, help explain how the known targets of ketamine are involved in such a rapid antidepressant response, explains Christophe Proulx, associate professor of psychiatry and neuroscience at Laval University. Proulx was not involved in the work but co-authored a Perspective article on it. Spotlighting the lateral habenula’s role also represents a new way of thinking about ketamine’s effects on depression—involving a shift away from a focus on weakened circuits and impaired plasticity, says Todd Gould, professor of psychiatry and neurobiology at the University of Maryland School of Medicine, who was not affiliated with the study. “[The work provides] additional strong evidence supporting a different view about how ketamine may be working.” Although ketamine inactivated NMDA receptors in the lateral habenula of the depressive-like mice, it had less impact in the CA1 region of the hippocampus, Hu and her colleagues observed using in-vitro slice electrophysiology and electrode recordings in awake animals. © 2024 Simons Foundation

Part of brain network much bigger in people with depression

Nicola Davis Science correspondent Researchers have gained new insight into how and why some people experience depression after finding a particular brain network is far bigger in people living with the condition. The surface of the brain is a communication junction box at which different areas talk to each other to carry out particular processes. But there is a finite amount of space for these networks to share. Now researchers say that in people with depression, a larger part of the brain is involved in the network that controls attention to rewards and threats than in those without depression. “It’s taking up more real estate on the brain surface than we see is typical in healthy controls,” said Dr Charles Lynch, a co-author of the research, from Weill Cornell Medicine in New York. He added that expansion meant the size of other – often neighbouring – brain networks were smaller. Writing in the journal Nature, Lynch and colleagues report how they used precision functional mapping, a new approach to brain imaging that analyses a host of fMRI (functional MRI) scans from each individual. The team applied this method to 141 people with depression and 37 people without it, enabling them to measure accurately the size of each participant’s brain networks. They then took the average size for each group. They found that a part of the brain called the frontostriatal salience network was expanded by 73% on average in participants with depression compared with healthy controls. © 2024 Guardian News & Media Limited

The Deeper Issue With Expanding Assisted Dying to Mental Illness

By Elyse Weingarten In 2016, Canada enacted the Medical Assistance in Dying, or MAID, law, allowing individuals with a terminal illness to receive help from a medical professional to end their life. Following a superior court ruling, the legislation was expanded in 2021 to include nearly anyone with a “grievous and irremediable medical condition” causing “enduring physical or psychological suffering that is intolerable to them.” Whether mental illnesses such as depression, schizophrenia, and addiction should be considered “grievous and irremediable” quickly emerged as the subject of intense debate. Initially slated to go into effect in March 2023, a new mental health provision of the law was postponed a year due to public outcry both in Canada and abroad. Then, in February, Health Minister Mark Holland announced it had been delayed again — this time until 2027 — to allow more time for the country’s health care system to prepare. I was horrified by the news of the law’s latest expansion — a reaction that surprised me. Having grown up with a seriously mentally ill family member, I know first-hand how destructive mental illness can be, and I have no illusion that it is always treatable. Additionally, I support assisted suicide in cases of grave and terminal physical illness, so why do I find it so unacceptable to offer it to people who are intractably mentally ill? For nearly half a century, the Western understanding of mental illness has been shaped to adhere to the larger biomedical concepts of disease and wellness. Biological psychiatry, or the biomedical model, views mental illnesses as organically based disorders of the brain, physiologically indistinguishable from other diseases. The Canadian MAID law’s inclusion of mental illness is the culmination of this framework. Yet the widespread condemnation that the amendment received (that the bill’s previous iterations did not) demonstrates that mental and physical illness — though worthy of the same respect — are in no way equivalent, and that we can recognize this intuitively.

Related chapters from BN: Chapter 16: Psychopathology: Biological Basis of Behavior Disorders; Chapter 15: Emotions, Aggression, and Stress
Related chapters from MM:Chapter 12: Psychopathology: The Biology of Behavioral Disorders; Chapter 11: Emotions, Aggression, and Stress
Link ID: 29449 - Posted: 08.22.2024

Moving in Childhood Contributes to Depression

By Ellen Barry In recent decades, mental health providers began screening for “adverse childhood experiences” — generally defined as abuse, neglect, violence, family dissolution and poverty — as risk factors for later disorders. But what if other things are just as damaging? Researchers who conducted a large study of adults in Denmark, published on Wednesday in the journal JAMA Psychiatry, found something they had not expected: Adults who moved frequently in childhood have significantly more risk of suffering from depression than their counterparts who stayed put in a community. In fact, the risk of moving frequently in childhood was significantly greater than the risk of living in a poor neighborhood, said Clive Sabel, a professor at the University of Plymouth and the paper’s lead author. “Even if you came from the most income-deprived communities, not moving — being a ‘stayer’ — was protective for your health,” said Dr. Sabel, a geographer who studies the effect of environment on disease. “I’ll flip it around by saying, even if you come from a rich neighborhood, but you moved more than once, that your chances of depression were higher than if you hadn’t moved and come from the poorest quantile neighborhoods,” he added. The study, a collaboration by Aarhus University, the University of Manchester and the University of Plymouth, included all Danes born between 1982 and 2003, more than a million people. Of those, 35,098, or around 2.3 percent, received diagnoses of depression from a psychiatric hospital. Are you concerned for your teen? If you worry that your teen might be experiencing depression or suicidal thoughts, there are a few things you can do to help. Dr. Christine Moutier, the chief medical officer of the American Foundation for Suicide © 2024 The New York Times Company

Depression, schizophrenia and bipolar disorder linked with ancient viral DNA in our genome

Rodrigo Duarte Around 8% of human DNA is made up of genetic sequences acquired from ancient viruses. These sequences, known as human endogenous retroviruses (or Hervs), date back hundreds of thousands to millions of years – with some even predating the emergence of Homo sapiens. Our latest research suggests that some ancient viral DNA sequences in the human genome play a role in susceptibility to psychiatric disorders such as schizophrenia, bipolar disorder and major depressive disorder. Hervs represent the remnants of these infections with ancient retroviruses. Retroviruses are viruses that insert a copy of their genetic material into the DNA of the cells they infect. Retroviruses probably infected us on multiple occasions during our evolutionary past. When these infections occurred in sperm or egg cells that generated offspring, the genetic material from these retroviruses was passed on to subsequent generations, becoming a permanent part of our lineage. Initially, scientists considered Hervs to be “junk DNA” – parts of our genome with no discernible function. But as our understanding of the human genome has advanced, it’s become evident that this so-called junk DNA is responsible for more functions than originally hypothesised. First, researchers found that Hervs can regulate the expression of other human genes. A genetic feature is said to be “expressed” if its DNA segment is used to produce RNA (ribonucleic acid) molecules. These RNA molecules can then serve as intermediaries leading to the production of specific proteins, or help to regulate other parts of the genome. Initial research suggested that Hervs regulate the expression of neighbouring genes with important biological functions. One example of this is a Herv that regulates the expression of a gene involved in modifying connections between brain cells. © 2010–2024, The Conversation US, Inc.

What Happens in the Brain to Cause Depression?

By Steven Strogatz For decades, the best drug therapies for treating depression, like SSRIs, have been based on the idea that depressed brains don’t have enough of the neurotransmitter serotonin. Yet for almost as long, it’s been clear that simplistic theory is wrong. Recent research into the true causes of depression is finding clues in other neurotransmitters and the realization that the brain is much more adaptable than scientists once imagined. Treatments for depression are being reinvented by drugs like ketamine that can help regrow synapses, which can in turn restore the right brain chemistry and improve whole body health. In this episode, John Krystal, a neuropharmacologist at the Yale School of Medicine, shares the new findings in mental health research that are revolutionizing psychiatric medication. STEVEN STROGATZ: According to the World Health Organization, 280 million people worldwide suffer from depression. For decades, people with chronic depression have been told their problem lies with a chemical imbalance in the brain, specifically a deficit in a neurotransmitter called serotonin. And based on this theory, many have been prescribed antidepressants known as selective serotonin reuptake inhibitors, or SSRIs, to correct this chemical imbalance. This theory has become the common narrative, yet almost from the beginning, researchers have questioned the role of serotonin in depression, even though SSRIs do seem to bring a lot of relief to many people. So, if bad brain chemistry isn’t at the root of chronic depression, what is? If the thinking behind SSRIs is wrong, why do they seem to help? And is it possible that as we get closer to the true cause of depression, we may find better treatments for other conditions as well? © 2024 the Simons Foundation.

What You Really Need to Know About Antidepressants

By Christina Caron Antidepressants are among the most prescribed medications in the United States. This is, in part, because the number of people diagnosed with depression and anxiety has been on the rise, and prescriptions jumped sharply among some age groups during the pandemic. Despite the prevalence of these medications, some patients have “significant misconceptions” about how the drugs work, said Dr. Andrew J. Gerber, a psychiatrist and the president and medical director of Silver Hill Hospital in New Canaan, Conn. About 80 percent of antidepressants are prescribed by primary care doctors who have not had extensive training in managing mental illness. Dr. Paul Nestadt, an associate professor of psychiatry at the Johns Hopkins School of Medicine, said patients tell him, “‘You know, Doc, I’ve tried everything.’” But often, he said, “they never got to a good dose, or they were only on it for a week or two.” Here are some answers to frequently asked questions about antidepressants. How do antidepressants work? There are many types of antidepressants, and they all work a bit differently. In general, they initiate a change in the way brain cells — and different regions of the brain — communicate with one another, said Dr. Gerard Sanacora, a professor of psychiatry at the Yale School of Medicine. Clinical trials have shown that antidepressants are generally more effective with moderate, severe and chronic depression than with mild depression. Even then, it’s a modest effect when compared with placebo. © 2024 The New York Times Company

What, if anything, makes mood fundamentally different from memory?

By Nicole Rust We readily (and reasonably) accept that the causes of memory dysfunction, including Alzheimer’s disease, reside in the brain. The same is true for many problems with seeing, hearing and motor control. We acknowledge that understanding how the brain supports these functions is important for developing treatments for their corresponding dysfunctions, including blindness, deafness and Parkinson’s disease. Applying the analogous assertion to mood—that understanding how the brain supports mood is crucial for developing more effective treatments for mood disorders, such as depression—is more controversial. For brain researchers unfamiliar with the controversy, it can be befuddling. You might hear, “Mental disorders are psychological, not biological,” and wonder, what does that mean, exactly? Experts have diverse opinions on the matter, with paper titles ranging from “Brain disorders? Not really,” to “Brain disorders? Precisely.” Even though a remarkable 21 percent of adults in the United States will experience a mood disorder at some point in their lives, we do not fully understand what causes them, and existing treatments do not work for everyone. How can we best move toward an impactful understanding of mood and mood disorders, with the longer-term goal of helping these people? What, if anything, makes mood fundamentally different from, say, memory? The answer turns out to be complex and nuanced—here, I hope to unpack it. I also ask brain and mind researchers with diverse perspectives to chime in. Among contemporary brain and mind researchers, I have yet to find any whose position is driven by the notion that some force in the universe beyond the brain, like a nonmaterial soul, gives rise to mood. Rather, the researchers generally agree that our brains mediate all mental function. If everyone agrees that both memory and mood disorders follow from things that happen in the brain, why would the former but not the latter qualify as “brain disorders”? © 2024 Simons Foundation

Related chapters from BN: Chapter 16: Psychopathology: Biological Basis of Behavior Disorders; Chapter 17: Learning and Memory
Related chapters from MM:Chapter 12: Psychopathology: The Biology of Behavioral Disorders; Chapter 13: Memory and Learning
Link ID: 29251 - Posted: 04.11.2024

Ketamine is in the spotlight thanks to Elon Musk — but is it the right treatment for depression?

By David Adam The drug ketamine is enjoying a second life. First developed as an anaesthetic that was used widely by US battlefield surgeons during the Vietnam war, it is growing in popularity as a treatment for depression and other mental-health conditions. And this week, the drug got its highest-profile endorsement yet. In an interview with US journalist Don Lemon that was released online on Monday, Elon Musk, founder of SpaceX and head of social-media platform X (formerly Twitter), spoke about his own experiences of using the drug to manage what he called a “negative chemical state” similar to depression. Musk said he has a prescription for the drug from “a real doctor” and uses “a small amount once every other week or something like that”. His comments follow the fatal drowning of Friends actor Matthew Perry last October, an incident that an investigation blamed on the drug’s acute effects. It’s complicated. Approved as an anaesthetic by the US Food and Drug Administration in 1970, the drug was delivered intravenously to people undergoing surgery. Ketamine is often still given that way for depression. That requires supervision — typically people attend a private clinic and are monitored by an anaesthetist as well as the prescribing psychiatrist and members of the support staff. Because it’s long out of patent, there’s little commercial interest in developing new versions of the drug. Some companies are trying to package it into more-convenient oral lozenges, but that’s a challenging formulation. “The problem with ketamine is if you take it orally, by and large it doesn’t get through to the system because it’s got low bioavailability,” says Allan Young, a consultant psychiatrist at King’s College London who studies mood disorders.

Pressure grows to ditch controversial forced swim test in rodent studies of depression

By Sara Reardon For the past few decades, scientists studying candidate antidepressant drugs have had a convenient animal test: how long a rodent dropped in water keeps swimming. Invented in 1977, the forced swim test (FST) hinged on the idea that a depressed animal would give up quickly. It seemed to work: Antidepressants and electroconvulsive therapy often made the animal try harder. The test remains popular, appearing in about 600 papers per year. But researchers have recently begun to question the assumption that the test really gauges depression and is a good predictor of human responses to drugs. Opposition to the test is snowballing, driven in part by concerns it is unnecessarily cruel given its spotty results. This month, following similar moves by the Australian government, the United Kingdom’s Home Office announced it would require U.K. researchers to justify the use of the test and would encourage other U.K. ministries that regulate animal research to “completely eliminate” it. Such changes add urgency to efforts to develop better animal tests of psychiatric drugs’ effects. Neurobiologist Anne Mallien of Heidelberg University, who studies the effects of the FST on rodents’ well-being, says she would love to have other options. “The thing is that alternatives are somewhat missing.” In the FST, researchers put a mouse or rat in a container of water, usually for about 5 minutes, and time how long it exerts itself before giving up and simply floating. Rodents will often swim longer when treated with psychiatric drugs. “But does that mean something for [human medicine]?” says neuroscientist Carole Morel at the Icahn School of Medicine at Mount Sinai. The rodents’ high stress levels could complicate the results, and an intelligent animal quickly learns that researchers will rescue it once it gives up.

Related chapters from BN: Chapter 16: Psychopathology: Biological Basis of Behavior Disorders; Chapter 1: Introduction: Scope and Outlook
Related chapters from MM:Chapter 12: Psychopathology: The Biology of Behavioral Disorders; Chapter 1: Cells and Structures: The Anatomy of the Nervous System
Link ID: 29201 - Posted: 03.21.2024

Brain’s ‘Background Noise’ May Explain Value of Shock Therapy

By Elizabeth Landau Electroconvulsive therapy has a public relations problem. The treatment, which sends electric currents through the brain to induce a brief seizure, has barbaric, inhumane connotations — for example, it was portrayed as a sadistic punishment in the film One Flew Over the Cuckoo’s Nest. But for patients with depression that does not improve with medications, electroconvulsive therapy (ECT) can be highly effective. Studies have found that some 50% to 70% of patients with major depressive disorder see their symptoms improve after a course of ECT. In comparison, medications aimed at altering brain chemistry help only 10% to 40% of depression patients. Still, even after many decades of use, scientists don’t know how ECT alters the brain’s underlying biology. Bradley Voytek, a neuroscientist at the University of California, San Diego, said a psychiatrist once told him that the therapy “reboots the brain” — an explanation he found “really unsatisfying.” Recently, Voytek and his collaborators paired their research into the brain’s electrical patterns with patient data to explore why inducing seizures has antidepressant effects. In two studies published last fall, the researchers observed that ECT and a related seizure therapy increased the unstructured background noise hiding behind well-defined brain waves. Neuroscientists call this background noise “aperiodic activity.” The authors suggested that induced seizures might help restore the brain’s balance of excitation and inhibition, which could have an overall antidepressant effect. “Every time that I talk to someone who’s not in this field about this work they’re like, ‘They still do that? They still use electroshock? I thought that was just in horror movies,’” said Sydney Smith, a graduate student in neuroscience in Voytek’s lab and the first author of the new studies. “Dealing with the stigma around it has become even more of a motivation to figure out how it works.” © 2024 Simons Foundation.

Psychedelic drugs and the law: What’s next?

By Ben Seal When Oregon’s first psilocybin service center opened in June 2023, allowing those over 21 to take mind-altering mushrooms in a state-licensed facility, the psychedelic revival that had been unfolding over the past two decades entered an important new phase. Psilocybin is still illegal on the federal level. But now, as researchers explore the therapeutic potential of psilocybin and other psychedelics, including LSD and MDMA (also known as Molly or ecstasy), legal reform efforts are spreading across the country — raising tensions between state and federal laws. As a class, psychedelic drugs were outlawed in the United States by the Controlled Substances Act of 1970. The act designated psychedelics as Schedule I drugs — the most restrictive classification, indicating a high potential for abuse and no accepted medical use. That status limits research to federally approved scientific studies and restricts federal funding to research with “significant medical evidence of a therapeutic advantage.” Despite these limitations, researchers have demonstrated the potential of psychedelics in the treatment of post-traumatic stress disorder, major depressive disorder, anxiety and addiction. A 2020 systematic review of recent research found that psychedelics can lessen symptoms linked to a variety of mental health conditions. While that review found no serious, long-term adverse physical or psychological effects from ingesting psychedelics, more research is needed on the latter. Today, decades after research on the effects of hallucinogens on the brain was sidelined by the act, academic and cultural interest in psychedelics is on the rise. More than 60 percent of Americans now support regulated therapeutic use of psychedelics, while nearly half support decriminalization, and nearly 45 percent support spiritual and religious use. An estimated 5.5 million US adults use psychedelics each year.

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Links for Keyword: Depression