Posts Tagged ‘depression’

By Elizabeth Chuck and Lauren Dunn

The intrusive thoughts started weeks after Stephanie Hathaway gave birth: an overwhelming feeling that her daughter deserved a better mother; that her husband deserved a better wife; that her future was hopeless.

“They just played on repeat in my head,” Hathaway, 33, of South Glastonbury, Connecticut, said. “I was holding my baby one night, and my husband was at a meeting, and I just thought, ‘Oh, my goodness. If I put the baby down, I might hurt myself.’”

Hathaway was diagnosed with postpartum depression — the intense sadness, anxiety or despair that occurs within the first year after giving birth, according to the Centers for Disease Control and Prevention. It affects about one in nine women, although the rate may be as high as one in every five women, the CDC finds.

Hathaway’s doctor put her on antidepressants, which helped some, but it took two weeks for the medication to kick in, and even longer until her doctor found the appropriate dosage for her. As she waited for relief, Hathaway found herself struggling to bond with her newborn, Hadley, who is now 4.

“It’s heartbreaking,” Hathaway, who had never suffered from depression before and is now a mother to two girls, said. “That’s not what I expected to feel.”

Up until this point, new mothers experiencing postpartum depression have been prescribed the same antidepressants used for treating depression in the general population, such as selective serotonin reuptake inhibitors. The drugs can take weeks to take effect, and do not address the hormonal changes that women go through during and after pregnancy.

But on Tuesday, the Food and Drug Administration approved the first drug specifically developed for postpartum depression, called brexanolone, or Zulresso.

Brexanolone is novel because it has a synthetic form of the hormone allopregnanolone, a progesterone derivative, in it. The hormone increases throughout a woman’s pregnancy and then plummets after she gives birth, a possible contributor to postpartum depression.

“This can potentially transform women’s lives and that of their families,” said Dr. Steve Kanes, chief medical officer of Sage Therapeutics, the Cambridge, Mass., biopharmaceutical company that developed brexanolone. “It’s not just the mother who suffers when there’s postpartum depression. It’s the newborn. It’s the other people in their family.”

Brexanolone is not a pill. The drug is delivered intravenously over the course of a 60-hour infusion, meaning it must be administered in a medically supervised setting, such as a skilled facility or a hospital, rather than at patients’ homes.

IMPROVEMENT IN JUST 24 HOURS

Clinical trials for the drug were promising — not just in the number of women it helped, but in the near-instantaneous relief that is provided.

In double-blind, placebo-controlled trials, many women with moderate to severe postpartum depression saw a marked improvement of their symptoms within just 24 hours of receiving the drug. That improvement was still present 30 days after the infusion, the length of the trial.

“This is for postpartum depression, but it is a step in understanding how we treat depression more broadly,” said Dr. Samantha Meltzer-Brody, director of the perinatal psychiatry program at the University of North Carolina at Chapel Hill and the academic principal investigator in the brexanolone trials. “We have had the same treatments for depression for 30 years. There’s an enormous need for new, novel ways to treat depression, and to treat it quickly.”

The drug’s approval comes just weeks after the FDA signed off on esketamine, a fast-acting nasal spray that uses the active ingredients in the club drug ketamine, as a treatment for severe depression.

For patients who are depressed, rapid relief is a priority. Hathaway, the Connecticut mother, was again diagnosed with postpartum depression after she gave birth to her second, a girl named Brenley who is now 2. This time, the antidepressants did not help at all, and Hathaway felt herself slipping deeper and deeper into a state of hopelessness.

She participated in a brexanolone trial, and her response was striking. Between hours 12 and 18 of the 60-hour infusion, she noticed her despair had waned.

“I woke up from a nap, and the thoughts were gone. And they never came back,” Hathaway said. “And then hour after hour, I got my energy back. I got my appetite back. I was eating because I was actually hungry, not because people were making me eat.”

A COMMON CONDITION

Postpartum depression afflicts as many as 400,000 women in the United States each year. It can include disturbances in sleep or eating patterns in addition to feelings of sadness or apathy. Affected women are often confused and guilt-ridden about why they are feeling down during what is supposed to be a happy time, said Dr. Christine C. Greves, an obstetrician-gynecologist at Orlando Health Winnie Palmer Hospital for Women and Babies.

“As women, we feel like we were born to have a child, and there’s a white picket fence, and life will be great,” said Greves, who does not have ties to Sage Therapeutics. “Then regular life comes into play. You have a child and then you top that with extensive fatigue, hormones, expectations that just can’t be met. It’s all fantasy until we actually have the baby. And then you do feel guilty, because we all want to be Super Mom.”

In the past decade, experts say, there has been more awareness about postpartum depression and more efforts among obstetricians and pediatricians to screen mothers for it.

But having a drug specifically aimed at treating postpartum depression will be one of the most significant steps toward removing any stigma still associated with the condition, said Dr. Kimberly Yonkers, professor of psychiatry, epidemiology and obstetrics, gynecology and reproductive sciences at the Yale School of Medicine.

“It does women a service because it really brings attention to a major medical problem and provides legitimacy, and hopefully will encourage people, whether they use this medication or not, to seek and obtain treatment,” said Yonkers, who does not have ties to the drug company. “We’re all thrilled about that.”

SOME SIDE EFFECTS, AND A HEFTY PRICE TAG

The most common side effects during the brexanolone trial were drowsiness and dizziness. The drug is not believed to have any long-term safety concerns. Kanes, Sage Therapeutics’ chief medical officer, said he expects it will be deemed safe for all mothers, including breastfeeding mothers, but the company is waiting for an FDA ruling on breastfeeding.

The drug comes with a hefty price tag: Sage says it is expected to cost somewhere between $20,000 to $35,000 for the infusion. That does not include the price of a stay in whatever facility it is administered in. It is not clear yet how much insurance would cover.

Kanes pointed out that while high, the cost is a one-time price.

“That’s such an important piece as to why this is so novel. We’re talking about a single treatment that has durable effects,” he said. “This really is a one-time intervention that gets people on their way. It’s transformative.”

For Hathaway, the brexanolone infusion enabled her to return home and be the mother to her daughters that she had wanted to be before postpartum depression took over.

“It’s given them their mom back,” she said. “This is what it was supposed to be like.”

https://www.nbcnews.com/health/womens-health/fda-approves-first-drug-postpartum-depression-n984521

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Before light reaches these rods and cones in the retina, it passes through some specialized cells that send signals to brain areas that affect whether you feel happy or sad.

by Jon Hamilton

Just in time for the winter solstice, scientists may have figured out how short days can lead to dark moods.

Two recent studies suggest the culprit is a brain circuit that connects special light-sensing cells in the retina with brain areas that affect whether you are happy or sad.

When these cells detect shorter days, they appear to use this pathway to send signals to the brain that can make a person feel glum or even depressed.

“It’s very likely that things like seasonal affective disorder involve this pathway,” says Jerome Sanes, a professor of neuroscience at Brown University.

Sanes was part of a team that found evidence of the brain circuit in people. The scientists presented their research in November at the Society for Neuroscience meeting. The work hasn’t been published in a peer-reviewed journal yet, but the researchers plan to submit it.

A few weeks earlier, a different team published a study suggesting a very similar circuit in mice.

Together, the studies offer a strong argument that seasonal mood changes, which affect about 1 in 5 people, have a biological cause. The research also adds to the evidence that support light therapy as an appropriate treatment.

“Now you have a circuit that you know your eye is influencing your brain to affect mood,” says Samer Hattar, an author of the mouse study and chief of the section on light and circadian rhythms at the National Institute of Mental Health. The finding is the result of a decades-long effort to understand the elusive link between light and mood. “It is the last piece of the puzzle,” Hattar says.

The research effort began in the early 2000s, when Hattar and David Berson, a professor of neuroscience at Brown University, were studying cells in the retina.

At the time, most scientists thought that when light struck the retina, only two kinds of cells responded: rods and cones. But Hattar and Berson thought there were other light-sensitive cells that hadn’t been identified.

“People used to laugh at us if we say there are other photoreceptors distinct from rods and cones in the retina,” Hattar says.

The skeptics stopped laughing when the team discovered a third kind of photoreceptor that contained a light-sensitive substance called melanopsin not found in rods and cones. (The full name of these cells, if you’re interested, is intrinsically photosensitive retinal ganglion cells, or ipRGCs.) These receptors responded to light but weren’t part of the visual system.

Instead, their most obvious function was keeping the brain’s internal clock in sync with changes in daylight. And many scientists assumed that this circadian function also explained seasonal depression.

“People thought that the only reason you get mood problems is because your clock is misaligned,” Hattar says.

Other potential explanations included speculation that reduced sunlight was triggering depression by changing levels of serotonin, which can affect mood, or melatonin, which plays a role in sleep patterns and mood. But the evidence for either of these possibilities has been weak.

Hattar and Berson were pretty sure there was a better reason. And, after years of searching, they found one.

In September, Hattar’s team published a study about mice suggesting a direct pathway between the third kind of photoreceptor in the retina and brain areas that affect mood.

When these cells were present, an artificially shortened cycle of light and dark caused a version of depression in a mouse. But when the team removed the cells with gene-editing tools, the mouse didn’t become depressed.

Sanes knew about the research, in part because he and Berson are neuroscientists at Brown. And he was so intrigued by the discovery of the new pathway between retina and brain in mice that he decided to see whether something similar was going on in human brains.

Sanes’ team put young adults in an MRI machine and measured their brain activity as they were exposed to different levels of light. This allowed the team to identify brain areas that seemed to be receiving signals from the photoreceptors Hattar and Berson had discovered.

Two of these areas were in the front of the brain. “It’s interesting because these areas seem to be the areas that have been shown in many studies to be involved in depression and other affective disorders,” Sanes says.

The areas also appeared to be part of the same circuit found in mice.

The finding needs to be confirmed. But Hattar is pretty confident that this circuit explains the link between light exposure and mood.

So now he’s trying to answer a new question: Why would evolution produce a brain that works this way?

“You will understand why you would need light to see,” he says, “but why do you need light to make you happy?”

Hattar hopes to find out. In the meantime, he has some advice for people who are feeling low: “Try to take your lunch outside. That will help you adjust your mood.”

https://www.npr.org/sections/health-shots/2018/12/21/678342879/scientists-find-a-brain-circuit-that-could-explain-seasonal-depression

by Carly Cassella

Sticks and stones may break your bones, but name-calling could actually change the structure of your brain.

A new study has found that persistent bullying in high school is not just psychologically traumatising, it could also cause real and lasting damage to the developing brain.

The findings are drawn from a long-term study on teenage brain development and mental health, which collected brain scans and mental health questionnaires from European teenagers between the ages of 14 and 19.

Following 682 young people in England, Ireland, France and Germany, the researchers tallied 36 in total who reported experiencing chronic bullying during these years.

When the researchers compared the bullied participants to those who had experienced less intense bullying, they noticed that their brains looked different.

Across the length of the study, in certain regions, the brains of the bullied participants appeared to have actually shrunk in size.

In particular, the pattern of shrinking was observed in two parts of the brain called the putamen and the caudate, a change oddly reminiscent of adults who have experienced early life stress, such as childhood maltreatment.

Sure enough, the researchers found that they could partly explain these changes using the relationship between extreme bullying and higher levels of general anxiety at age 19. And this was true even when controlling for other types of stress and co-morbid depressive symptoms.

The connection is further supported by previous functional MRI studies that found differences in the connectivity and activation of the caudate and putamen activation in those with anxiety.

“Although not classically considered relevant to anxiety, the importance of structural changes in the putamen and caudate to the development of anxiety most likely lies in their contribution to related behaviours such as reward sensitivity, motivation, conditioning, attention, and emotional processing,” explains lead author Erin Burke Quinlan from King’s College London.

In other words, the authors think all of this shrinking could be a mark of mental illness, or at least help explain why these 19-year-olds are experiencing such unusually high anxiety.

But while numerous past studies have already linked childhood and adolescent bullying to mental illness, this is the very first study to show that unrelenting victimisation could impact a teenager’s mental health by actually reshaping their brain.

The results are cause for worry. During adolescence, a young person’s brain is absolutely exploding with growth, expanding at an incredible place.

And even though it’s normal for the brain to prune back some of this overabundance, in the brains of those who experienced chronic bullying, the whole pruning process appears to have spiralled out of control.

The teenage years are an extremely important and formative period in a person’s life, and these sorts of significant changes do not bode well. The authors suspect that as these children age, they might even begin to experience greater shrinkage in the brain.

But an even longer long-term study will need to be done if we want to verify that hunch. In the meantime, the authors are recommending that every effort be made to limit bullying before it can cause damage to a teenager’s brain and their mental health.

This study has been published in Molecular Psychiatry.

https://www.sciencealert.com/chronic-bullying-could-actually-reshape-the-brains-of-teens

largest-ever-study-of-genetic-links-to-depression-and-anxiety-launched-309700

The NIHR and King’s College London are calling for 40,000 people diagnosed with depression or anxiety to enrol online for the Genetic Links to Anxiety and Depression (GLAD) Study and join the NIHR Mental Health Bioresource.

Researchers hope to establish the largest ever database of volunteers who can be called up to take part in research exploring the genetic factors behind the two most common mental health conditions – anxiety and depression.

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The GLAD study will make important strides towards better understanding of these disorders and provide a pool of potential participants for future studies, reducing the time-consuming process of recruiting patients for research.

Research has shown 30-40% of the risk for both depression and anxiety is genetic and 60-70% due to environmental factors. Only by having a large, diverse group of people available for studies will researchers be able to determine how genetic and environmental triggers interact to cause anxiety and depression.

Leader of the GLAD study and the NIHR Mental Health BioResource, Dr Gerome Breen of King’s College London, said: “It’s a really exciting time to become involved in mental health research, particularly genetic research which has made incredible strides in recent years – we have so far identified 46 genetic links for depression and anxiety.

“By recruiting 40,000 volunteers willing to be re-contacted for research, the GLAD Study will take us further than ever before. It will allow researchers to solve the big unanswered questions, address how genes and environment act together and help develop new treatment options.”

The GLAD Study, a collaboration between the NIHR BioResource and King’s College London, has been designed to be particularly accessible, with a view to motivating more people to take part in mental health research.

Research psychologist and study lead Professor Thalia Eley, King’s College London, said: “We want to hear from all different backgrounds, cultures, ethnic groups and genders, and we are especially keen to hear from young adults. By including people from all parts of the population, what we learn will be relevant to everyone. This is a unique opportunity to participate in pioneering medical science.”

https://www.nihr.ac.uk/news/nihr-launches-largest-ever-study-of-genetic-links-to-depression-and-anxiety/9201

Mit-Dopamine-Tracking_0

By Anne Trafton

Dopamine, a signaling molecule used throughout the brain, plays a major role in regulating our mood, as well as controlling movement. Many disorders, including Parkinson’s disease, depression, and schizophrenia, are linked to dopamine deficiencies.

MIT neuroscientists have now devised a way to measure dopamine in the brain for more than a year, which they believe will help them to learn much more about its role in both healthy and diseased brains.

“Despite all that is known about dopamine as a crucial signaling molecule in the brain, implicated in neurologic and neuropsychiatric conditions as well as our abilty to learn, it has been impossible to monitor changes in the online release of dopamine over time periods long enough to relate these to clinical conditions,” says Ann Graybiel, an MIT Institute Professor, a member of MIT’s McGovern Institute for Brain Research, and one of the senior authors of the study.

Michael Cima, the David H. Koch Professor of Engineering in the Department of Materials Science and Engineering and a member of MIT’s Koch Institute for Integrative Cancer Research, and Rober Langer, the David H. Koch Institute Professor and a member of the Koch Institute, are also senior authors of the study. MIT postdoc Helen Schwerdt is the lead author of the paper, which appears in the Sept. 12 issue of Communications Biology.

Long-term sensing

Dopamine is one of many neurotransmitters that neurons in the brain use to communicate with each other. Traditional systems for measuring dopamine — carbon electrodes with a shaft diameter of about 100 microns — can only be used reliably for about a day because they produce scar tissue that interferes with the electrodes’ ability to interact with dopamine.

In 2015, the MIT team demonstrated that tiny microfabricated sensors could be used to measure dopamine levels in a part of the brain called the striatum, which contains dopamine-producing cells that are critical for habit formation and reward-reinforced learning.

Because these probes are so small (about 10 microns in diameter), the researchers could implant up to 16 of them to measure dopamine levels in different parts of the striatum. In the new study, the researchers wanted to test whether they could use these sensors for long-term dopamine tracking.

“Our fundamental goal from the very beginning was to make the sensors work over a long period of time and produce accurate readings from day to day,” Schwerdt says. “This is necessary if you want to understand how these signals mediate specific diseases or conditions.”

To develop a sensor that can be accurate over long periods of time, the researchers had to make sure that it would not provoke an immune reaction, to avoid the scar tissue that interferes with the accuracy of the readings.

The MIT team found that their tiny sensors were nearly invisible to the immune system, even over extended periods of time. After the sensors were implanted, populations of microglia (immune cells that respond to short-term damage), and astrocytes, which respond over longer periods, were the same as those in brain tissue that did not have the probes inserted.

In this study, the researchers implanted three to five sensors per animal, about 5 millimeters deep, in the striatum. They took readings every few weeks, after stimulating dopamine release from the brainstem, which travels to the striatum. They found that the measurements remained consistent for up to 393 days.

“This is the first time that anyone’s shown that these sensors work for more than a few months. That gives us a lot of confidence that these kinds of sensors might be feasible for human use someday,” Schwerdt says.

Paul Glimcher, a professor of physiology and neuroscience at New York University, says the new sensors should enable more researchers to perform long-term studies of dopamine, which is essential for studying phenomena such as learning, which occurs over long time periods.

“This is a really solid engineering accomplishment that moves the field forward,” says Glimcher, who was not involved in the research. “This dramatically improves the technology in a way that makes it accessible to a lot of labs.”

Monitoring Parkinson’s

If developed for use in humans, these sensors could be useful for monitoring Parkinson’s patients who receive deep brain stimulation, the researchers say. This treatment involves implanting an electrode that delivers electrical impulses to a structure deep within the brain. Using a sensor to monitor dopamine levels could help doctors deliver the stimulation more selectively, only when it is needed.

The researchers are now looking into adapting the sensors to measure other neurotransmitters in the brain, and to measure electrical signals, which can also be disrupted in Parkinson’s and other diseases.

“Understanding those relationships between chemical and electrical activity will be really important to understanding all of the issues that you see in Parkinson’s,” Schwerdt says.

The research was funded by the National Institute of Biomedical Imaging and Bioengineering, the National Institute of Neurological Disorders and Stroke, the Army Research Office, the Saks Kavanaugh Foundation, the Nancy Lurie Marks Family Foundation, and Dr. Tenley Albright.

https://news.mit.edu/2018/brain-dopamine-tracking-sensors-0912

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A 3-D rendering of the serotonin system in the left hemisphere of the mouse brain reveals two groups of serotonin neurons in the dorsal raphe that project to either cortical regions (blue) or subcortical regions (green) while rarely crossing into the other’s domain.

As Liqun Luo was writing his introductory textbook on neuroscience in 2012, he found himself in a quandary. He needed to include a section about a vital system in the brain controlled by the chemical messenger serotonin, which has been implicated in everything from mood to movement regulation. But the research was still far from clear on what effect serotonin has on the mammalian brain.

“Scientists were reporting divergent findings,” said Luo, who is the Ann and Bill Swindells Professor in the School of Humanities and Sciences at Stanford University. “Some found that serotonin promotes pleasure. Another group said that it increases anxiety while suppressing locomotion, while others argued the opposite.”

Fast forward six years, and Luo’s team thinks it has reconciled those earlier confounding results. Using neuroanatomical methods that they invented, his group showed that the serotonin system is actually composed of at least two, and likely more, parallel subsystems that work in concert to affect the brain in different, and sometimes opposing, ways. For instance, one subsystem promotes anxiety, whereas the other promotes active coping in the face of challenges.

“The field’s understanding of the serotonin system was like the story of the blind men touching the elephant,” Luo said. “Scientists were discovering distinct functions of serotonin in the brain and attributing them to a monolithic serotonin system, which at least partly accounts for the controversy about what serotonin actually does. This study allows us to see different parts of the elephant at the same time.”

The findings, published online on August 23 in the journal Cell, could have implications for the treatment of depression and anxiety, which involves prescribing drugs such as Prozac that target the serotonin system – so-called SSRIs (selective serotonin reuptake inhibitors). However, these drugs often trigger a host of side effects, some of which are so intolerable that patients stop taking them.

“If we can target the relevant pathways of the serotonin system individually, then we may be able to eliminate the unwanted side effects and treat only the disorder,” said study first author Jing Ren, a postdoctoral fellow in Luo’s lab.

Organized projections of neurons

The Stanford scientists focused on a region of the brainstem known as the dorsal raphe, which contains the largest single concentration in the mammalian brain of neurons that all transmit signals by releasing serotonin (about 9,000).

The nerve fibers, or axons, of these dorsal raphe neurons send out a sprawling network of connections to many critical forebrain areas that carry out a host of functions, including thinking, memory, and the regulation of moods and bodily functions. By injecting viruses that infect serotonin axons in these regions, Ren and her colleagues were able to trace the connections back to their origin neurons in the dorsal raphe.

This allowed them to create a visual map of projections between the dense concentration of serotonin-releasing neurons in the brainstem to the various regions of the forebrain that they influence. The map revealed two distinct groups of serotonin-releasing neurons in the dorsal raphe, which connected to cortical and subcortical regions in the brain.

“Serotonin neurons in the dorsal raphe project to a bunch of places throughout the brain, but those bunches of places are organized,” Luo said. “That wasn’t known before.”

Two parts of the elephant

In a series of behavioral tests, the scientists also showed that serotonin neurons from the two groups can respond differently to stimuli. For example, neurons in both groups fired in response to mice receiving rewards like sips of sugar water but they showed opposite responses to punishments like mild foot shocks.

“We now understand why some scientists thought serotonin neurons are activated by punishment, while others thought it was inhibited by punishment. Both are correct – it just depends on which subtype you’re looking at,” Luo said.

What’s more, the group found that the serotonin neurons themselves were more complex than originally thought. Rather than just transmitting messages with serotonin, the cortical-projecting neurons also released a chemical messenger called glutamate – making them one of the few known examples of neurons in the brain that release two different chemicals.

“It raises the question of whether we should even be calling these serotonin neurons because neurons are named after the neurotransmitters they release,” Ren said.

Taken together, these findings indicate that the brain’s serotonin system is not made up of a homogenous population of neurons but rather many subpopulations acting in concert. Luo’s team has identified two groups, but there could be many others.

In fact, Robert Malenka, a professor and associate chair of psychiatry and behavioral sciences at Stanford’s School of Medicine, and his team recently discovered a group of serotonin neurons in the dorsal raphe that project to the nucleus accumbens, the part of the brain that promotes social behaviors.

“The two groups that we found don’t send axons to the nucleus accumbens, so this is clearly a third group,” Luo said. “We identified two parts of the elephant, but there are more parts to discover.”

https://medicalxpress.com/news/2018-08-brain-serotonin.html

BY ARISTOS GEORGIOU

Young people suffering from treatment-resistant depression (TRD) showed a significant reduction of their symptoms after being administered ketamine injections, according to a study published in the Journal of Child and Adolescent Psychopharmacology.

Researchers from the University of Minnesota (UM) and the nonprofit Mayo Clinic found that ketamine caused an average decrease of 42 percent on the Children’s Depression Rating Scale (CDRS)—the most widely used rating scale in research trials for assessing the severity of depression and change in depressive symptoms among adolescents.

Ketamine is perhaps best known for being a popular recreational drug and a useful medical anesthetic, but a growing body of research is indicating that the compound could be an effective treatment for depression. Several recent studies have shown that even a single dose in adults can lead to rapid reductions in depressive symptoms. However, relatively little research has been conducted into ketamine’s antidepressant effects in adolescents.

“Adolescence is a very important time for studying depression, first because depression often starts during these years, and second because it is an important time for brain development,” Kathryn Cullen, from the Department of Psychiatry at UM, told Newsweek.

“When adolescent depression persists without successful treatment, it can interfere with achieving important developmental milestones. Finding the right treatment is critical to allow the restoration of healthy brain development and prevent negative outcomes like chronic depression, disability and suicide.”

Unfortunately, about 40 percent of adolescents do not respond to their first intervention and only half of nonresponders respond to the second treatment, according to the researchers.

“Standard antidepressant treatments do not work for everyone and take weeks to months to take effect, a time period when patients are at risk for continued suffering and suicide attempts,” Cullen said. “The field is in need of new treatment options. Ketamine has a very different mechanism of action than standard treatments.”

The latest study involved 13 young people ages 12 to 18 who had failed two previous trials of antidepressants. During a two-week period, the researchers gave them six ketamine infusions.

They found that the treatment was well tolerated, with the participants showing an average decrease in CDRS scores of 42.5 percent. Five of the participants met the criteria for clinical response and remission. Of these, three were still in remission after six weeks, while the remaining two relapsed within two weeks.

According to the scientists, the results demonstrate the potential role for ketamine in treating adolescents with TRD. However, they note that the study was limited by its small sample size, so future research will be needed to confirm these results.

“The purpose of our study was to investigate the effects of ketamine for TRD in younger patients for whom this indication for ketamine administration is not well studied,” Mark Roback, a professor of pediatrics at the University of Minnesota, told Newsweek.

“I think our results show promise for this population, however this study is just a beginning. The study serves to point out the need for further, rigorous, study designed to answer the many questions that remain about ketamine for TRD, such as optimal dosing and route of administration, dosing interval and treatment length, and long-term effects—just to name a few.”

James Stone, a clinical senior lecturer from the Institute of Psychiatry, Psychology and Neuroscience at King’s College London, who was not involved in the study, told Newsweek that there is “a lot of potential for the use of ketamine as a second or third line antidepressant where other treatments have failed.”

“Although ketamine is potentially a huge breakthrough in the treatment of depression, we still don’t know about the long-term safety, or about how to keep people well from depression without requiring regular ketamine dosing,” Stone added. “Further studies are needed to address these questions.”

https://www.newsweek.com/ketamine-shows-promise-treatment-adolescents-depression-1054021