By Nicholas Bakalar If you are a morning person, you may be at reduced risk for major depression, a new study suggests. Several studies of the body’s circadian sleep-wake cycle have shown that being an early bird is associated with a lower risk for depression. But those studies were observational so could not prove cause and effect. For example, people who are early birds may have other health or lifestyle behaviors that reduce their risk for depression — they may have a healthier diet, for example, exercise more, or have fewer health conditions, such as chronic pain, that are associated with depression. All these factors, and many others, could explain the decreased risk for depression, and not the fact of being an early bird. Moreover, depression itself causes sleep disturbances, so it could be that depression is a cause of being a night owl, rather than the other way around. The new study, however, offers more compelling evidence that going to bed early and waking early may, in itself, provide protection against depression, independent of other factors. The study, published in JAMA Psychiatry, uses a research method called Mendelian randomization that helps pinpoint the cause of what may be a cause-and-effect relationship. With Mendelian randomization, researchers can compare large groups of people based on genetic variants that are independent of other health or behavioral characteristics — in this case, the tendency to being a night owl or a morning person, inherited traits that are randomly allocated during our development in the womb. More than 340 genetic variants associated with circadian sleep rhythm have been identified, and the researchers can compare large groups of people with the genetic variants for being a morning person with groups that lack them. Nature has, in essence, set up the randomized experiment for them. © 2021 The New York Times Company

Keyword: Biological Rhythms; Depression
Link ID: 27868 - Posted: 06.23.2021

By Katie Free, Joel Goldberg When it comes to our senses, we frequently focus on the external—the crack of thunder, the glare of sunlight, the fragrance of flowers—that captured our attention in the first place. But our bodies also have a whole host of internal senses that tell our brains whether our hearts are beating at the right speed, for example, or whether our blood pressure is too high. These signals travel constantly via hormones and nerves, including a mysterious 100,000-fiber network called the vagus nerve. Now, new techniques are helping scientists map the thin, twisting branches of the vagus nerve—which connects the brain to the heart, intestines, and other internal organs—and make surprising discoveries about its role in memory and emotion. These findings have spawned investigations into treatments for everything from Alzheimer’s disease to post-traumatic stress disorder and have led to the approval of medical implants to help treat epilepsy and depression. When it comes to understanding the brain-mind connection, a gut check might not hurt. © 2021 American Association for the Advancement of Science.

Keyword: Epilepsy; Depression
Link ID: 27867 - Posted: 06.23.2021

An analysis of survey data from more than 280,000 young adults ages 18-35 showed that cannabis (marijuana) use was associated with increased risks of thoughts of suicide (suicidal ideation), suicide plan, and suicide attempt. These associations remained regardless of whether someone was also experiencing depression, and the risks were greater for women than for men. The study published online today in JAMA Network Open and was conducted by researchers at the National Institute on Drug Abuse (NIDA), part of the National Institutes of Health. “While we cannot establish that cannabis use caused the increased suicidality we observed in this study, these associations warrant further research, especially given the great burden of suicide on young adults,” said NIDA Director Nora Volkow, M.D., senior author of this study. “As we better understand the relationship between cannabis use, depression, and suicidality, clinicians will be able to provide better guidance and care to patients.” The number of adults in the United States who use cannabis more than doubled from 22.6 million in 2008 to 45.0 million in 2019, and the number of daily or near-daily users almost tripled from 3.6 million to 9.8 million in 2019. Over the same time span, the number of adults with depression also increased, as did the number of people who reported suicidal ideation or plan or who died by suicide. To date, however, the relationship between trends in cannabis use and suicidality is not well understood. The current study sought to fill this gap.

Keyword: Depression; Drug Abuse
Link ID: 27866 - Posted: 06.23.2021

By Diana Kwon Long before the earliest animals swam through the water-covered surface of Earth’s ancient past, one of the most important encounters in the history of life took place. A primitive bacterium was engulfed by our oldest ancestor — a solo, free-floating cell. The two fused to form a mutually beneficial relationship that has lasted more than a billion years, with the latter providing a safe, comfortable home and the former becoming a powerhouse, fueling the processes necessary to maintain life. That’s the best hypothesis to date for how the cellular components, or organelles, known as mitochondria came to be. Today, trillions of these bacterial descendants live within our bodies, churning out ATP, the molecular energy source that sustains our cells. Despite being inextricably integrated into the machinery of the human body, mitochondria also carry remnants of their bacterial past, such as their own set of DNA. The DNA that constitutes the human genome is contained within the nucleus of our cells. But mitochondria possess their own set of circular DNA, which is likely a remnant of their ancient bacterial past. These features make mitochondria both a critical element of our cells and a potential source of problems. Like the DNA inside the nuclei of our cells that makes up the human genome, mitochondrial DNA can harbor mutations. Age, stress and other factors may disrupt mitochondria’s many functions. On top of that, mitochondrial injury can release molecules that, due to their similarities to those made by bacteria, can be mistaken by our immune system as foreign invaders, triggering a harmful inflammatory response against our own cells. © 2021 Annual Reviews, Inc

Keyword: Schizophrenia; Alzheimers
Link ID: 27863 - Posted: 06.19.2021

By Bill Hathaway A massive genome-wide association study (GWAS) of genetic and health records of 1.2 million people from four separate data banks has identified 178 gene variants linked to major depression, a disorder that will affect one of every five people during their lifetimes. The results of the study, led by the U.S. Department of Veterans Affairs (V.A.) researchers at Yale University School of Medicine and University of California-San Diego (UCSD), may one day help identify people most at risk of depression and related psychiatric disorders and help doctors prescribe drugs best suited to treat the disorder. The study was published May 27 in the journal Nature Neuroscience. For the study, the research team analyzed medical records and genomes collected from more than 300,000 participants in the V.A.’s Million Veteran Program (MVP), one of the largest and most diverse databanks of genetic and medical information in the world. These new data were combined in a meta-analysis with genetic and health records from the UK Biobank, FinnGen (a Finland-based biobank), and results from the consumer genetics company 23andMe. This part of the study included 1.2 million participants. The researchers crosschecked their findings from that analysis with an entirely separate sample of 1.3 million volunteers from 23andMe customers. When the two sets of data from the different sources were compared, genetic variants linked to depression replicated with statistical significance for most of the markers tested. Copyright © 2021 Yale University

Keyword: Depression; Genes & Behavior
Link ID: 27833 - Posted: 05.29.2021

By Laura Sanders The key ingredient in the illicit drug known as Ecstasy or Molly may offer profound relief from post-traumatic stress disorder. When paired with intense talk therapy, MDMA drastically eased symptoms in people who had struggled with severe PTSD for years, a new study reports. “This is a big deal,” says Steven Gold, a clinical psychologist in Fort Lauderdale and professor emeritus at Nova Southeastern University in Plantation, Fla. “All other things being equal, the use of psychedelic medication can significantly improve the outcome.” The results, published May 10 in Nature Medicine, are preliminary. But the findings offer hope to the millions of people worldwide who have PTSD, for whom new treatments are desperately needed. Antidepressants such as Zoloft and Paxil are often prescribed, but the drugs don’t work for an estimated 40 to 60 percent of people with PTSD. Ninety people participated in the new study, which took place at 15 clinical sites in the United States, Canada and Israel. All the participants received 15 therapy sessions with therapists trained to guide people as they experienced the drug. Half of the participants received MDMA in three eight-hour therapy sessions; the other half received placebos during three eight-hour therapy sessions. True to its nickname Ecstasy, MDMA evokes feelings of bliss and social connectedness. The participants took the drug (or the placebo) while wearing eye covers and listening to music, and occasionally talking with their therapist about their experience. © Society for Science & the Public 2000–2021.

Keyword: Stress; Drug Abuse
Link ID: 27826 - Posted: 05.19.2021

By Andrew Jacobs It’s been a long, strange trip in the four decades since Rick Doblin, a pioneering psychedelics researcher, dropped his first hit of acid in college and decided to dedicate his life to the healing powers of mind-altering compounds. Even as antidrug campaigns led to the criminalization of Ecstasy, LSD and magic mushrooms, and drove most researchers from the field, Dr. Doblin continued his quixotic crusade with financial help from his parents. Dr. Doblin’s quest to win mainstream acceptance of psychedelics took a significant leap forward on Monday when the journal Nature Medicine published the results of his lab’s study on MDMA, the club drug popularly known as Ecstasy and Molly. The study, the first Phase 3 clinical trial conducted with psychedelic-assisted therapy, found that MDMA paired with counseling brought marked relief to patients with severe post-traumatic stress disorder. The results, coming weeks after a New England Journal of Medicine study that highlighted the benefits of treating depression with psilocybin, the psychoactive ingredient in magic mushrooms, have excited scientists, psychotherapists and entrepreneurs in the rapidly expanding field of psychedelic medicine. They say it is only a matter of time before the Food and Drug Administration grants approval for psychoactive compounds to be used therapeutically — for MDMA as soon as 2023, followed by psilocybin a year or two later. After decades of demonization and criminalization, psychedelic drugs are on the cusp of entering mainstream psychiatry, with profound implications for a field that in recent decades has seen few pharmacological advancements for the treatment of mental disorders and addiction. The need for new therapeutics has gained greater urgency amid a national epidemic of opioid abuse and suicides. © 2021 The New York Times Company

Keyword: Depression; Drug Abuse
Link ID: 27817 - Posted: 05.12.2021

by Laura Dattaro Many genes linked to autism, schizophrenia and developmental delay share the same functions: They regulate the expression of other genes and support communication between neurons, according to an unpublished study. Researchers presented the findings virtually today at the 2021 International Society for Autism Research annual meeting. (Links to abstracts may work only for registered conference attendees.) Hundreds of genes with diverse functions are linked to autism, but how each contributes to the condition is unclear. In the new work, researchers analyzed the functions of 102 autism-linked genes that previous studies identified by comparing the genetic sequences of thousands of people with autism and those with other conditions, along with their family members and controls. “The genes identified give us an unprecedented opportunity to follow the biology, follow the genetics, to ask the question, where does this converge on function?” said lead investigator Stephan Sanders while presenting the work. Sanders is associate professor of psychiatry at the University of California, San Francisco. Other researchers are studying convergence in 3D brain models called organoids and looking for neuroanatomical similarities and differences across different animal models of autism, including mice and frogs. “Distinguishing causal functions from non-causal functions of these genes is a massive challenge,” Sanders says, and finding points of convergence could help. “The ultimate goal is to identify why disrupting these genes leads to autism.” © 2021 Simons Foundation

Keyword: Autism; Genes & Behavior
Link ID: 27808 - Posted: 05.08.2021

By Paul E. Greenberg Since the early 1990s, I, together with my colleagues, have been studying the economic burden of adults with major depressive disorders (MDD). Over that time, we have tracked shifts in the prevalence of this disease; in the makeup of those suffering from it; and in the nature of treatment both for the disease itself and for the host of comorbidities, such as pain and anxiety disorders, that accompany it. We have then used these data as the basis for calculating the incremental economic burden of adults with MDD—that is, the additional costs traceable to those suffering from the disease in terms of both medical treatment and workplace productivity impacts. Our most recent study was just published in a special issue of PharmacoEconomics (which I also co-edited) that presents new research on the economics of MDD. By focusing on one year during the Great Recession (2010) and another after a long macroeconomic expansion (2018), our analysis provides a helpful profile of the changing economic effects of this widespread and pernicious illness. We report our latest estimates showing that the incremental economic burden of adults with MDD was $326 billion in 2018, 38 percent higher than in 2010. But our work goes deeper than simply providing an economic calculator. This research offers a multifaceted lens through which we can gain a better understanding of how the myriad effects of the illness manifest themselves. Importantly, we find that only 11 percent of the overall burden of illness was attributable to the direct medical costs of treating MDD itself, while the costs of treating comorbid medical conditions made up 24 percent. Another 4 percent was due to suicide-related costs, while fully 61 percent of the total burden in 2018 resulted from a combination of elevated workplace absenteeism and presenteeism (that is, reduced productivity as a result of working while sick). This striking imbalance between medical expenditures to treat either MDD or its comorbidities on the one hand and workplace-related costs on the other is one aspect of the story that has changed dramatically since 2010, when medical costs were equivalent to workplace costs. © 2021 Scientific American,

Keyword: Depression
Link ID: 27806 - Posted: 05.08.2021

By Christina Caron Finding a therapist can be a tough and time-consuming process involving multiple phone calls, waiting lists and insurance hurdles. But what if you were able to walk into your corner drugstore for a bottle of shampoo and also had the option of scheduling a walk-in session for mental health treatment? That’s the future that CVS, the largest retail pharmacy in the United States, is envisioning. Since January the company has added licensed clinical social workers trained in cognitive behavioral therapy to 13 locations in the Houston, Philadelphia and Tampa metro areas. The providers will offer mental health assessments, referrals and counseling either in person or via telehealth, a CVS spokeswoman said, and this spring the company plans to expand to 34 locations in those same regions. The social workers are available during the day, and also on evenings and weekends in the company’s MinuteClinics, which provide a variety of nonemergency health care services either via walk-in or by appointment. The hours are more flexible than what therapists might normally offer, and the social workers partner with the clinic’s nurse practitioners and pharmacists to give prescriptions when needed, said Dr. Daniel Knecht, the vice president of clinical product at CVS Health. CVS is just one of a growing number of retailers who are recognizing the unmet need for mental health providers and hoping to fill the gap. On Thursday, Walmart announced it is acquiring MeMD, which offers online medical and mental health care. Walmart currently provides counseling via Walmart Health, a health center located in a separate building alongside Walmart Supercenters. In Georgia, Walmart Health offers in-person mental health counseling and in Arkansas customers can receive online counseling. Later this year, counseling services will become available at Walmart Health locations in Illinois and Florida, a spokeswoman said. © 2021 The New York Times Company

Keyword: Depression
Link ID: 27805 - Posted: 05.08.2021

By Rachel Nuwer In an important step toward medical approval, MDMA, the illegal drug popularly known as Ecstasy or Molly, was shown to bring relief to those suffering from severe post-traumatic stress disorder when paired with talk therapy. Of the 90 people who took part in the new study, which is expected to be published later this month in Nature Medicine, those who received MDMA during therapy experienced a significantly greater reduction in the severity of their symptoms compared with those who received therapy and an inactive placebo. Two months after treatment, 67 percent of participants in the MDMA group no longer qualified for a diagnosis of PTSD, compared with 32 percent in the placebo group. MDMA produced no serious adverse side effects. Some participants temporarily experienced mild symptoms like nausea and loss of appetite. “This is about as excited as I can get about a clinical trial,” said Gul Dolen, a neuroscientist at Johns Hopkins University School of Medicine, who was not involved in the research. “There is nothing like this in clinical trial results for a neuropsychiatric disease.” Before MDMA-assisted therapy can be approved for therapeutic use, the Food and Drug Administration needs a second positive Phase 3 trial, which is currently underway with 100 participants. Approval could come as early as 2023. Mental health experts say that this research — the first Phase 3 trial conducted on psychedelic-assisted therapy — could pave the way for further studies on MDMA’s potential to help address other difficult-to-treat mental health conditions, including substance abuse, obsessive compulsive disorder, phobias, eating disorders, depression, end-of-life anxiety and social anxiety in autistic adults. © 2021 The New York Times Company

Keyword: Drug Abuse; Stress
Link ID: 27804 - Posted: 05.05.2021

Ariana Remmel Scientists in search of psychedelic drug treatments have developed a way to determine whether a molecule is likely to cause hallucinations, without testing it on people or animals. Growing evidence suggests that psychedelic compounds, which are active in the brain, have potential to treat psychiatric illnesses such as post-traumatic stress disorder (PTSD), but researchers are trying to find out whether there is a way to keep the beneficial properties of these drugs without the hallucinogenic side effects, which can complicate treatment. It is currently almost impossible to predict whether a potential drug will cause hallucinations before it is tested on animals or people. “That really slows down drug discovery,” says David Olson, a chemical neuroscientist at the University of California, Davis. To address this, a team led by Olson and neuroscientist Lin Tian, also at Davis, designed a fluorescent sensor to predict whether a molecule is hallucinogenic, based on the structure of a brain receptor targeted by psychedelics. Using their approach, the researchers identified a psychedelic-like molecule without hallucinogenic properties that they later found had antidepressant activity in mice1. The discovery adds “more fuel for the fire” of efforts to make drugs from psychedelic-like molecules without side effects, says Bryan Roth, a molecular pharmacologist at the University of North Carolina School of Medicine in Chapel Hill. © 2021 Springer Nature Limited

Keyword: Drug Abuse; Stress
Link ID: 27798 - Posted: 05.01.2021

By Judith Warner Dr. Benjamin Rush, the 18th-century doctor who is often called the “father” of American psychiatry, held the racist belief that Black skin was the result of a mild form of leprosy. He called the condition “negritude.” His onetime apprentice, Dr. Samuel Cartwright, spread the falsehood throughout the antebellum South that enslaved people who experienced an unyielding desire to be free were in the grip of a mental illness he called “drapetomania,” or “the disease causing Negroes to run away.” In the late 20th century, psychiatry’s rank and file became a receptive audience for drug makers who were willing to tap into racist fears about urban crime and social unrest. (“Assaultive and belligerent?” read an ad that featured a Black man with a raised fist that appeared in the “Archives of General Psychiatry” in 1974. “Cooperation often begins with Haldol.”) Now the American Psychiatric Association, which featured Rush’s image on its logo until 2015, is confronting that painful history and trying to make amends. In January, the 176-year-old group issued its first-ever apology for its racist past. Acknowledging “appalling past actions” on the part of the profession, its governing board committed the association to “identifying, understanding, and rectifying our past injustices,” and pledged to institute “anti-racist practices” aimed at ending the inequities of the past in care, research, education and leadership. This weekend, the A.P.A. is devoting its annual meeting to the theme of equity. Over the course of the three-day virtual gathering of as many as 10,000 participants, the group will present the results of its yearlong effort to educate its 37,000 mostly white members about the psychologically toxic effects of racism, both in their profession and in the lives of their patients. © 2021 The New York Times Company

Keyword: Schizophrenia; Depression
Link ID: 27797 - Posted: 05.01.2021

By Laura Sanders For more than a year now, scientists have been racing to understand how the mysterious new virus that causes COVID-19 damages not only our bodies, but also our brains. Early in the pandemic, some infected people noticed a curious symptom: the loss of smell. Reports of other brain-related symptoms followed: headaches, confusion, hallucinations and delirium. Some infections were accompanied by depression, anxiety and sleep problems. Recent studies suggest that leaky blood vessels and inflammation are somehow involved in these symptoms. But many basic questions remain unanswered about the virus, which has infected more than 145 million people worldwide. Researchers are still trying to figure out how many people experience these psychiatric or neurological problems, who is most at risk, and how long such symptoms might last. And details remain unclear about how the pandemic-causing virus, called SARS-CoV-2, exerts its effects. “We still haven’t established what this virus does in the brain,” says Elyse Singer, a neurologist at the University of California, Los Angeles. There are probably many answers, she says. “It’s going to take us years to tease this apart.” Getting the numbers For now, some scientists are focusing on the basics, including how many people experience these sorts of brain-related problems after COVID-19. © Society for Science & the Public 2000–2021.

Keyword: Alzheimers; Depression
Link ID: 27792 - Posted: 04.28.2021

By Joshua Kendall When adults claim to have suddenly recalled painful events from their childhood, are those memories likely to be accurate? This question is the basis of the “memory wars” that have roiled psychology for decades. And the validity of buried trauma turns up as a point of contention in court cases and in television and movie story lines. Warnings about the reliability of a forgotten traumatic event that is later recalled—known formally as a delayed memory—have been endorsed by leading mental health organizations such as the American Psychiatric Association (APA). The skepticism is based on a body of research showing that memory is unreliable and that simple manipulations in the lab can make people believe they had an experience that never happened. Some prominent cases of recovered memory of child abuse have turned out to be false, elicited by overzealous therapists. But psychotherapists who specialize in treating adult survivors of childhood trauma argue that laboratory experiments do not rule out the possibility that some delayed memories recalled by adults are factual. Trauma therapists assert that abuse experienced early in life can overwhelm the central nervous system, causing children to split off a painful memory from conscious awareness. They maintain that this psychological defense mechanism—known as dissociative amnesia—turns up routinely in the patients they encounter. © 2021 Scientific American

Keyword: Stress; Learning & Memory
Link ID: 27761 - Posted: 04.08.2021

By Rachel Schraer People diagnosed with Covid-19 in the previous six months were more likely to develop depression, dementia, psychosis and stroke, researchers have found. A third of those with a previous Covid infection went on to develop or have a relapse of a psychological or neurological condition. But those admitted to hospital or in intensive care had an even higher risk. The study authors pointed to both the effects of stress, and the virus having a direct impact on the brain. UK scientists looked at the electronic medical records of more than half a million patients in the US, and their chances of developing one of 14 common psychological or neurological conditions, including: Anxiety and mood disorders were the most common diagnosis among those with Covid, and these were more likely to be down to the stress of the experience of being very ill or taken to hospital, the researchers explained. Conditions like stroke and dementia were more likely to be down to the biological impacts of the virus itself, or of the body's reaction to infection in general. Covid-19 was not associated with an increased risk of Parkinson's or Guillain-Barré syndrome (a risk from flu). Cause and effect The study, published in the Lancet Psychiatry journal, was observational. So the researchers couldn't say whether Covid had caused any of the diagnoses - and some people would have had a stroke or depression in the next six months regardless. But by comparing a group of people who had had Covid-19 with two groups - with flu and with other respiratory infections respectively - the researchers at the University of Oxford concluded Covid was associated with more subsequent brain conditions than other respiratory illnesses. © 2021 BBC.

Keyword: Depression; Alzheimers
Link ID: 27760 - Posted: 04.08.2021

Jon Hamilton A study of mice that hear imaginary sounds could help explain human disorders like schizophrenia, which produce hallucinations. D-Keine/Getty Images A technique that induces imaginary sounds in both mice and people could help scientists understand the brain circuits involved in schizophrenia and other disorders that cause hallucinations. The technique appears to offer "a way to study psychotic disorders in animals," says Adam Kepecs, a professor of neuroscience and psychiatry at Washington University School of Medicine in St. Louis. It also shows how levels of the brain chemical dopamine determine the likelihood that a mouse or a person will perceive something that isn't really there, Kepecs and a team report in this week's issue of the journal Science. Until now, scientists have had no good way to study precisely how hallucinations occur in the brain. "This study is valuable because it will allow us to use mice and dig into the cellular, molecular, physiological details," says Eleanor Simpson, a researcher at the New York State Psychiatric Institute. That's important, Simpson says, because it could lead to better treatments for disorders like schizophrenia. "We have drugs that treat hallucinations but they're not very good," she says. "They don't work for everybody and they have a lot of terrible side effects which prevent people from using them." The study came about because "a mouse can't tell you when it's hallucinating," Kepecs © 2021 npr

Keyword: Schizophrenia; Hearing
Link ID: 27758 - Posted: 04.03.2021

By Benedict Carey When I joined the Science staff in 2004, reporters in the department had a saying, a reassuring mantra of sorts: “People will always come to the science section, if only to read about progress.” I think about that a lot as I say goodbye to my job, covering psychiatry, psychology, brain biology and big-data social science, as if they were all somehow related. The behavior beat, as it’s known, allowed tremendous freedom: I wrote about the mental upsides of binge drinking, playing the lotto and sports fandom. I covered basic lab research, the science of learning and memory, the experience of recurrent anguish, through the people who had to live with it. And much, much more. Like most science reporters, I had wanted to report on something big, to have a present-at-the-creation run that would shake up our understanding of mental health problems. At minimum, I expected research that would help people in distress improve their lives. But during my tenure, the science informing mental health care did not proceed smoothly along any trajectory. On the one hand, the field attracted enormous scientific talent, and there were significant discoveries, particularly in elucidating levels of consciousness in brain injury patients who appear unresponsive; and in formulating the first persuasive hypothesis of a cause for schizophrenia, based in brain biology. On the other hand, the science did little to improve the lives of the millions of people living with persistent mental distress. Almost every measure of our collective mental health — rates of suicide, anxiety, depression, addiction deaths, psychiatric prescription use — went the wrong direction, even as access to services expanded greatly. What happened? After 20 years covering the field, here and at The Los Angeles Times, I have a few theories, and some ideas on what might be required to turn things around. © 2021 The New York Times Company

Keyword: Depression; Stress
Link ID: 27757 - Posted: 04.03.2021

By Perri Klass, M.D. When parents bring their children in for medical care these days, there is no such thing as a casual, “Hey, how’s it going?” We doctors walk into every exam room prepared to hear a story of sadness and stress, or at the very least, of coping and keeping it together in this very hard year, full of isolation, loss, tragedy and hardship, with routines disrupted and comfort hard to come by. Parents have carried heavy burdens of stress and responsibility, worrying about themselves but also watching their children struggle, and there is worldwide concern about depression and suicidality among young people. But it isn’t only the adults and the young adults and teenagers who are suffering and sad; young children can also experience depression, but it can look very different, which makes it challenging for parents — or doctors — to recognize it and provide help. Rachel Busman, a clinical psychologist at the Child Mind Institute in New York City, said that it can be hard to think about depression in younger children because we picture childhood as a time of innocence and joy. But as many as 2 to 3 percent of children ages 6 to 12 can have serious depression, she said. And children with anxiety disorders, which are present in more than 7 percent of children aged 3 to 17, are also at risk for depression. Dr. Helen Egger, until recently the chair of child and adolescent psychiatry at N.Y.U. Langone Health, said that according to her epidemiologic research, between 1 and 2 percent of young children — as young as 3 — are depressed Depression was originally conceived of as an adult problem. Maria Kovacs, professor of psychiatry at the University of Pittsburgh School of Medicine, said that in the 1950s and ’60s, there were child psychiatrists who believed that children did not have sufficient ego development to feel depression, but that research that she and other colleagues did in the ’70s showed that “school age children can suffer from diagnosable depression.” © 2021 The New York Times Company

Keyword: Depression; Development of the Brain
Link ID: 27756 - Posted: 04.03.2021

Researchers at the National Institutes of Health (NIH) have discovered specific regions within the DNA of neurons that accumulate a certain type of damage (called single-strand breaks or SSBs). This accumulation of SSBs appears to be unique to neurons, and it challenges what is generally understood about the cause of DNA damage and its potential implications in neurodegenerative diseases. Because neurons require considerable amounts of oxygen to function properly, they are exposed to high levels of free radicals—toxic compounds that can damage DNA within cells. Normally, this damage occurs randomly. However, in this study, damage within neurons was often found within specific regions of DNA called “enhancers” that control the activity of nearby genes. Fully mature cells like neurons do not need all of their genes to be active at any one time. One way that cells can control gene activity involves the presence or absence of a chemical tag called a methyl group on a specific building block of DNA. Closer inspection of the neurons revealed that a significant number of SSBs occurred when methyl groups were removed, which typically makes that gene available to be activated. An explanation proposed by the researchers is that the removal of the methyl group from DNA itself creates an SSB, and neurons have multiple repair mechanisms at the ready to repair that damage as soon as it occurs. This challenges the common wisdom that DNA damage is inherently a process to be prevented. Instead, at least in neurons, it is part of the normal process of switching genes on and off. Furthermore, it implies that defects in the repair process, not the DNA damage itself, can potentially lead to developmental or neurodegenerative diseases.

Keyword: Epigenetics; Parkinsons
Link ID: 27744 - Posted: 03.27.2021