Graduate student Emre Caglayan (left) and lead scientist Genevieve Konopka stand in their lab at the Pickens Biomedical Building on the campus of UT Southwestern, Tuesday, Oct. 17, 2023, in Dallas. (ElÃas Valverde II/The Dallas Morning News/TNS) ElÃas Valverde II
The human brain is three times bigger than a chimp’s and more spherical than a Neanderthal’s. Within a maze of bumps and grooves, neurons converse in distinct patterns that give humans unique cognitive abilities.
Scientists haven’t fully deciphered those patterns. But researchers at UT Southwestern Medical Center are determined to solve the molecular mystery of what makes us human.
In a study published in the journal Nature, they compared brain cell types and activities among humans, chimpanzees and rhesus monkeys. Human brains had more of a kind of cell that may help them adapt based on new experience and heal from injury. Certain human neurons also had more of a gene that affects language development.
Genevieve Konopka, whose lab ran the study, has long investigated the molecular mechanisms that lead to brain disease. Understanding the human brain’s inner workings, she said, may help researchers develop therapies to treat conditions like Alzheimer’s and schizophrenia.
The brain’s support crew
Our brains set us apart from other primates. Humans communicate in languages that chimps can’t speak and devise systems of government and religion that don’t exist in the animal kingdom.
Though scientists have compared the cell types and genes in the brains of humans and other primates, they still lack a complete knowledge of how the human brain came to be over millions of years of evolution.
Konopka’s inquiry into brain evolution stemmed from her study of brain disease. In 2019, she compared brain tissue in people with and without schizophrenia and found differences in cells called oligodendrocytes. These cells act like the brain’s support crew, producing insulation that wraps around neurons and helps them send signals faster.
Konopka also saw a difference in oligodendrocytes between human and chimp brains. She realized this support crew could play an important role in both brain disease and human brain evolution.
Konopka wasn’t able to pursue her research further because of technological limits. But in recent years brain studies got a boost from single-cell technology, which allows scientists to capture each cell in a piece of brain tissue and examine the activity of different genes.
Using this technology, Konopka focused on a part of the brain located in what’s called the posterior cingulate cortex. This part is implicated in schizophrenia and is associated with the way we think about ourselves. Konopka said her lab is the first to apply single-cell technology to this region of the brain.
Her lab compared oligodendrocyte amounts and gene activity in human, chimp and rhesus monkey brain tissue. In another experiment, they compared human DNA with genetic information from two ancient human populations: Neanderthals and Denisovans.
Waiting in the wings
Konopka thought her lab would find more oligodendrocytes in human brain tissue compared to that of chimps and rhesus monkeys.
Instead, she found a human-specific increase and gene activity changes in pre-oligodendrocytes: brain cells that haven’t yet evolved to perform their mature functions.
At first, Konopka thought it was a mistake. But after confirming the result, she said, it began to make sense. More pre-oligodendrocytes may help the human brain adapt in response to change or injury, she explained. Having more of these cells may allow us to continue learning into adulthood.
Her lab also found that a gene called FOXP2, which is associated with language development in humans, had higher expression in two types of human neurons. Konopka said the human-specific increase could contribute to the language of human thoughts.
The lab also identified hundreds of genes that may function differently in humans, Neanderthals and Denisovans. These differences shed light on how the human brain evolved over the last 300,000 to 500,000 years, Konopka said.
Konopka’s research adds to the field by not only investigating which genes exist in different brain cells, but also how active they are, according to Doug Broadfield, an associate professor of cell biology at the University of Miami Miller School of Medicine.
“What’s new about this study is that it’s … created a new field of brain evolution,” said Broadfield, who was not involved with the research, “where instead of focusing on the structure of the brain, now we can look at the genetic activity of the brain.”
Konopka hopes to next use single-cell technology to examine brain tissue from people with brain disorders, including schizophrenia.
“We just wanted to set the table, if you will, for future studies looking at brain disease,” she said.
Adithi Ramakrishnan is a science reporting fellow at The Dallas Morning News. Her fellowship is supported by the University of Texas at Dallas. The News makes all editorial decisions.
Manager, Science Communications, University of Utah Health
A collection of cognitive symptoms referred to as “brain fog” occur in up to 10-30% of people who have been infected with the virus that causes COVID-19. But currently there are no treatments for the confusion, fuzzy thinking, and forgetfulness that can last for weeks or months, sometimes interfering with daily life.
Researchers at University of Utah Health are testing whether a non-invasive “brain training” tool that resembles a video game can alleviate these symptoms. They are recruiting up to 200 participants aged 18 and older who feel their cognitive function has worsened after having COVID-19. Clinical trial participants will try a potential treatment in the convenience of their own home for a 10-week study period with a follow-up visit after 90 days. Study coaches will provide support through virtual visits.
The trial, called RECOVER-NEURO, is part of the National Institutes of Health Researching COVID to Enhance Recovery (RECOVER) Initiative . Call 801-230-2285 to learn more or enroll.
Study participants will be offered an online intervention called BrainHQ. Although it may look like a game, it is more like a mental workout, according to Sarah Shizuko Morimoto, PsyD , the principal investigator of RECOVER-NEURO and an associate professor of population health sciences at U of U Health. BrainHQ is a suite of computerized games/exercises that train different cognitive functions such as attention, memory, processing speed, and navigation. The games provide rewards for correct answers, and participants can track their learning curves. As the participant practices, the games adapt to their individual abilities. And as they improve, the games get harder, maximizing the brain’s learning potential.
Cognitive computerized remediation technologies like BrainHQ have already shown promise. Preliminary research led by Morimoto, who develops digital interventions for mental health, revealed that similar activities enhance cognitive function and alleviate symptoms in older adults with treatment-resistant depression. Sarah Shizuko Morimoto, PsyD, is the principal investigator of the RECOVER-NEURO study. Some study participants will test if adding a second non-invasive method increases effectiveness of BrainHQ. The interventions include: BrainHQ: Participants will complete online BrainHQ activities designed to improve memory, attention, and brain processing speed—the time it takes to understand and respond to information.
BrainHQ and PASC Cognitive Recovery (PASC CoRe): Participants in this intervention group will meet virtually with trained study staff to plan and manage personal goals, learn mindfulness skills to focus attention on goal-oriented tasks, and develop strategies to manage mental tiredness.
BrainHQ and Transcranial Direct Current Stimulation (tDCS): tDCS is a safe, non-invasive form of brain stimulation that may “boost” cognitive training outcomes and brain health. Participants in this intervention group will wear a headset connected to the tDCS device while they complete the cognitive activities. The tDCS device will be programmed to deliver a mild electrical current to specific parts of the brain to increase activity during BrainHQ activities.
Non-invasive methods such as these are attractive because they avoid risks associated with medication-based symptom management, Morimoto says. “Over the last year, experts across the country have been meeting to evaluate every suggested treatment for long COVID,” she says. The study’s design was developed with input from experts in neurology, immunology, rehabilitation, psychology, and neuroscience, in collaboration with long COVID patient advocates.
“These experts have decided that the best interventions to test are the ones that are both safe and have data to support their use,” Morimoto says. “We are excited to be able to offer this cutting-edge treatment to patients suffering from long COVID at no cost.”
She adds that the clinical trial may reveal a treatment and provide insights into underlying causes of brain fog. Data captured from the clinical trial could pinpoint which cognitive functions become impaired, identify neural circuits responsible for these deficits, and assess the potential to reshape these circuits for improving cognitive capabilities. That knowledge can be used as the basis for further research, ultimately leading to better treatments and preventive measures.
Find additional RECOVER clinical trials for long COVID at trials.recovercovid.org .
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About RECOVER : The National Institutes of Health Researching COVID to Enhance Recovery (NIH RECOVER) Initiative is a $1.15 billion effort, including support through the American Rescue Plan Act of 2021, that seeks to identify how people recuperate from COVID-19 who are at risk for developing post-acute sequelae of SARS-CoV-2 (PASC). Researchers are also working with patients, clinicians, and communities across the United States to identify strategies to prevent and treat the long-term effects of COVID-19, including long COVID. For more information, please visit recovercovid.org . About University of Utah Health
University of Utah Health is the state’s only academic health care system, providing leading-edge and compassionate care for a referral area that encompasses 10 percent of the US, including Idaho, Wyoming, Montana, and much of Nevada. A hub for health sciences research and education in the region, U of U Health has a $522 million research enterprise and trains the majority of Utah’s physicians, and more than 1,670 scientists and 1,460 health care providers each year at its Colleges of Health, Nursing, and Pharmacy and Schools of Dentistry and Medicine. With more than 20,000 employees, the system includes 12 community clinics and five hospitals: University Hospital, Huntsman Mental Health Institute, Huntsman Cancer Hospital, University Orthopaedic Center, and the Craig H. Neilsen Rehabilitation Hospital. For 14 straight years, U of U Health has ranked among the top 10 US academic medical centers in the rigorous Vizient Quality and Accountability Study.
PhD student used BrainHQ program in thesis work on computerized training Share this article:
Share article via email A person is shown talking with a doctor who’s sitting at a desk and entering information into a computer. The use of a computer-based program called BrainHQ led to significantly improved scores on cognitive tests among people with multiple sclerosis (MS), according to data from a small clinical trial in Nebraska.
The study was led by Samantha Jack, PhD, as part of work she did as a graduate student at the University of Nebraska. Jack published the findings in a PhD thesis titled “ Effect of Computerized Cognitive Training in Persons with Multiple Sclerosis .”
“With the continued development of computerized cognitive testing and computerized cognitive training, clinicians hopefully will start incorporating cognitive performance into their regular discussions with patients,” Jack wrote.
“As the field of MS continues to evolve, my hope is that these convenient options will help make cognition a priority,” she added.
Recommended Reading Benefits seen for patients using online brain training games
Cognitive difficulties, such as trouble with memory and attention, are a common symptom of MS . The mechanisms leading to cognitive impairment in MS patients are not fully understood, but such problems are believed to arise primarily due to lesions and shrinkage of specific brain areas.
A number of strategies have been shown to help ease or reverse cognitive decline in MS patients. These include cognitive rehabilitation programs, exercise, and medications.
BrainHQ is a computer-based system of games that are designed to exercise cognitive faculties. A free version is available to try online, or consumers can subscribe for greater access. An annual subscription is $96 per person, or a monthly subscription is available for $14.
To fulfill some of her degree requirements, Jack, along with colleagues, conducted a small clinical trial to test whether the games in BrainHQ could help with cognitive issues in people with MS.
The study included 52 adults with relapsing-remitting MS , who were mostly white and female individuals, had mild to moderate disability, and had been living with MS for a mean of 8.3 years.
The participants were divided into two groups. One group had training with the BrainHQ system for 30 minutes three times weekly for six weeks, using games designed to improve attention, processing speed, and memory. The other patients played casual online games through the BrainHQ portal at the same time schedule.
Before and after the intervention, the participants underwent an assessment of cognitive function called the Brief International Cognitive Assessment for MS, or BICAMS.
This test includes three measures of cognition. The Symbol Digit Modalities Test (SDMT) assesses attention and processing speed, while the Brief Visuospatial Memory Test – Revised (BVMT-R) tests memory. The California Verbal Learning Test 2nd Edition (CVLT-II) evaluates both verbal learning and memory.
The results showed that BICAMS scores improved significantly more for patients who underwent the BrainHQ training, compared with the control group that played casual games. This study provides evidence that computerized cognitive training with BrainHQ is a valuable option for [people with] MS suffering from cognitive decline. A statistically significant improvement with BrainHQ was seen for all three subscores on the BICAMS. A particularly strong effect was seen for the CVLT-II, with an average improvement of more than nine points in the BrainHQ group, compared with less than one point in the control group.
“This study provides evidence that computerized cognitive training with BrainHQ is a valuable option for [people with] MS suffering from cognitive decline,” Jack concluded.
She added that this type of computer-based intervention “is convenient for the patient because they can do it at home when they have time and not at a specific time with a neuropsychologist.”
Jack noted, as a study limitation, that there were “very few males and very few non-Caucasian subjects.”
“While MS is more common in Caucasians and females, future studies should try to enroll a more diverse population. Furthermore, future studies should include subjects over age 60 to determine if the BrainHQ program can improve their cognitive functioning,” the researcher wrote.
The BrainHQ system is sold by Posit Science, which was not involved in this study. Henry Mahncke, PhD, the company’s CEO, said “these are very exciting results from independent researchers,” in a Posit Science press release .
“We hope this spurs not just further research, but targeted chronic care improvement programs at leading medical centers and health plans to help patients in need,” Mahncke said.
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Credit: Unsplash/CC0 Public Domain In recent years, the scientific community has seen a push for more findable, accessible, interoperable, and reusable (FAIR) neurophysiology data sharing. While certain measures have been put in place by institutions such as the National Institute of Health (NIH) to promote more FAIR data sharing, some researchers remain hesitant and unwilling to share their data beyond minimum requirements due to multiple disincentives.
In a new Neuron article , a team of researchers, led by co-authors Dr. Vasiliki Rahimzadeh, assistant professor at the Center for Medical Ethics and Health Policy at Baylor College of Medicine, and Dr. Kathryn Maxson Jones, assistant professor of history of technology at Purdue University and formerly a Senior Research Assistant in the Center for Medical Ethics and Health Policy at Baylor during the time of the study, profile three successful instances of data sharing from the NIH BRAIN Initiative Research Opportunities in Humans (ROH) Consortium to highlight the benefits of FAIR data sharing.
“This group is focused on how to maximize the scientific utility of human neuronal data through broad and secure data sharing,” explains Rahimzadeh. “While there has been a lot of attention paid to scientific benefits of data sharing, such as researchers being able to learn from others and expand their own work, far less has been paid to the professional and other social benefits . These value propositions are important for incentivizing researchers to share data more often beyond what is required as a condition of their funding.”
The paper showcases examples of successful data sharing from research groups at the University of Pennsylvania, Cedars-Sinai Medical Center, and Harvard Medical School and Massachusetts General Hospital involving intracranial electrophysiology data from patients. When shared, the data in question was de-identified to protect patient privacy, reformatted into standardized file types and uploaded to institutional or NIH archival databases, where it has been and is being reused for new research, education, training and tool development opportunities.
Rahimzadeh said that by sharing data, the research groups discussed in the paper were able to not only open new doors for collaboration with other groups, but to also support replicability studies that overall enhance scientific rigor.
“The benefits to users include expanding both the diversity and volume of datasets available for research and being able to combine multiple datasets together to find new associations or conduct subgroup analyses that previously might have been infeasible,” she said. “For producers of data, there are benefits of supporting new scientific collaborations and contributing to professional development of trainees who will continue a culture of data sharing.”
Rahimzadeh added that by sharing their data, investigators increase the visibility of their labs, reduce redundancies in similar research studies and benefit from others identifying errors in code or analysis that might otherwise have remained undetected.
“Many pressing research questions about the brain and nervous systems today require analyses of data that are more voluminous and multi-faceted than any single laboratory can reasonably be expected to produce. This makes sharing data all the more important. Additionally, sharing data has had tangible benefits in other fields of life science, such as genomics,” said Dr. Maxson Jones, the co-lead author on the paper, who is now at Purdue University. “Our paper shows that investing in the labor of sharing data in standardized formats comes with its own payoffs.”
Other authors contributing to the paper include Mary A. Majumder, Michael J. Kahana, Ueli Rutishauser, Jie Zheng, Angelique C. Paulk, Sydney S. Cash, Ziv M. Williams, Michael S. Beauchamp, Jennifer L. Collinger, Nader Pouratian, Amy L. McGuire and Sameer A. Sheth. The authors are affiliated with Baylor College of Medicine, Purdue University, the University of Pennsylvania, Cedars-Sinai Medical Center, Boston Children’s Hospital, Massachusetts General Hospital, the University of Pittsburgh and U.T. Southwestern Medical Center.
Provided by Baylor College of Medicine
A speech prosthetic developed by a collaborative team of Duke neuroscientists, neurosurgeons, and engineers can translate a person’s brain signals into what they’re trying to say.
Appearing Nov. 6 in the journal Nature Communications , the new technology might one day help people unable to talk due to neurological disorders regain the ability to communicate through a brain-computer interface.
“There are many patients who suffer from debilitating motor disorders, like ALS (amyotrophic lateral sclerosis) or locked-in syndrome, that can impair their ability to speak,” said Gregory Cogan, Ph.D., a professor of neurology at Duke University’s School of Medicine and one of the lead researchers involved in the project. “But the current tools available to allow them to communicate are generally very slow and cumbersome.”
Imagine listening to an audiobook at half-speed. That’s the best speech decoding rate currently available, which clocks in at about 78 words per minute. People, however, speak around 150 words per minute.
The lag between spoken and decoded speech rates is partially due the relatively few brain activity sensors that can be fused onto a paper-thin piece of material that lays atop the surface of the brain. Fewer sensors provide less decipherable information to decode.
To improve on past limitations, Cogan teamed up with fellow Duke Institute for Brain Sciences faculty member Jonathan Viventi, Ph.D., whose biomedical engineering lab specializes in making high-density, ultra-thin, and flexible brain sensors.
For this project, Viventi and his team packed an impressive 256 microscopic brain sensors onto a postage stamp-sized piece of flexible, medical-grade plastic. Neurons just a grain of sand apart can have wildly different activity patterns when coordinating speech, so it’s necessary to distinguish signals from neighboring brain cells to help make accurate predictions about intended speech.
After fabricating the new implant, Cogan and Viventi teamed up with several Duke University Hospital neurosurgeons, including Derek Southwell, M.D., Ph.D., Nandan Lad, M.D., Ph.D., and Allan Friedman, M.D., who helped recruit four patients to test the implants. The experiment required the researchers to place the device temporarily in patients who were undergoing brain surgery for some other condition, such as treating Parkinson’s disease or having a tumor removed. Time was limited for Cogan and his team to test drive their device in the OR.
“I like to compare it to a NASCAR pit crew,” Cogan said. “We don’t want to add any extra time to the operating procedure, so we had to be in and out within 15 minutes. As soon as the surgeon and the medical team said ‘Go!’ we rushed into action and the patient performed the task.”
The task was a simple listen-and-repeat activity. Participants heard a series of nonsense words, like “ava,” “kug,” or “vip,” and then spoke each one aloud. The device recorded activity from each patient’s speech motor cortex as it coordinated nearly 100 muscles that move the lips, tongue, jaw, and larynx.
Afterwards, Suseendrakumar Duraivel, the first author of the new report and a biomedical engineering graduate student at Duke, took the neural and speech data from the surgery suite and fed it into a machine learning algorithm to see how accurately it could predict what sound was being made, based only on the brain activity recordings.
For some sounds and participants, like /g/ in the word “gak,” the decoder got it right 84% of the time when it was the first sound in a string of three that made up a given nonsense word.
Accuracy dropped, though, as the decoder parsed out sounds in the middle or at the end of a nonsense word. It also struggled if two sounds were similar, like /p/ and /b/.
Overall, the decoder was accurate 40% of the time. That may seem like a humble test score, but it was quite impressive given that similar brain-to-speech technical feats require hours or days-worth of data to draw from. The speech decoding algorithm Duraivel used, however, was working with only 90 seconds of spoken data from the 15-minute test.
Duraivel and his mentors are excited about making a cordless version of the device with a recent $2.4M grant from the National Institutes of Health.
“We’re now developing the same kind of recording devices, but without any wires,” Cogan said. “You’d be able to move around, and you wouldn’t have to be tied to an electrical outlet, which is really exciting.”
While their work is encouraging, there’s still a long way to go for Viventi and Cogan’s speech prosthetic to hit the shelves anytime soon.
“We’re at the point where it’s still much slower than natural speech,” Viventi said in a recent Duke Magazine piece about the technology, “but you can see the trajectory where you might be able to get there.”
This work was supported by grants from the National Institutes for Health (R01DC019498, UL1TR002553), Department of Defense (W81XWH-21-0538), Klingenstein-Simons Foundation, and an Incubator Award from the Duke Institute for Brain Sciences.
Photo by Tim Samuel: https://www.pexels.com/photo/woman-drinking-fresh-lemonade-at-table-with-junk-food-6697265/ Clear Facts:
Fatty and sugar-rich foods, like potato chips and donuts, rival the addictiveness of nicotine and cocaine.
An alarming 14% of adults and 12% of children are addicted to ultra-processed foods.
Ultra-processed foods trigger dopamine levels akin to addictive substances.
Americans might be hooked on more than just their daily cup of joe. According to recent shocking research, the very foods that grace our pantries and fridges are as addictive as some illicit drugs.
Published in the British Medical Journal, the study’s grim findings underscore that roughly 14% of adults and 12% of children are in the grips of ultra-processed foods. These aren’t just any foods. We’re talking about those saturated with refined sugars, artificial flavors, and unhealthy fats – items such as ice cream, potato chips, sugary cereals, and the like. So, what’s the scientific reasoning? These edibles closely mirror the dopamine spike in our brains triggered by hard-hitting substances like nicotine and even alcohol. Not just comparable, but they also surpass the addictiveness of drugs like heroin.
Florida’s addiction specialist Dr. Daniel Bober provided a stark perspective: “What really makes this dangerous is this addiction we have to ultra-processed foods. And these are foods that contain chemicals, emulsifiers, artificial colors. They also contain refined sugars and just the right amount of salt, sugar, and fat to be highly reinforced, which can lead some people to engage in compulsive eating.”
Considering the obesity epidemic, it’s no wonder experts are drawing parallels between the hazardous nature of these foods and illegal narcotics such as cocaine.
Bober drives the point home: “We want a hit, and we want it fast. Whether it’s from cocaine, food, shopping, it all has one thing in common. And that is using compulsive behavior to deal with uncomfortable feelings like loneliness, depression, isolation. It’s something we need to look at because it’s part of our culture.”
The authors of the study echoed this sentiment, noting: “Ultra-processed foods high in refined carbohydrates and added fats are highly rewarding, appealing, and consumed compulsively and may be addictive. Understanding of these foods as addictive could lead to novel approaches in the realm of social justice, clinical care, and policy approaches.”
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16 Expert Tips on How to Be Happy Alonekate_sept2004 – Getty Images [table-of-contents] stripped
Whether you lead a solitary life or are simply feeling lonely, figuring out how to be happy alone goes a long way toward bolstering mental health. Even though everyone gets lonely sometimes, learning how to appreciate some me-time can take your days from okay to great. But, it’s important to remember that it’s okay to not be okay sometimes.
Meet the Experts: Dana Klisanin, Ph.D. , psychologist and CEO of Evolutionary Guidance Media R&D Patrick Porter, Ph.D., neuroscience expert and founder of BrainTap ; Jeff Temple, Ph.D. , licensed psychologist and founding director of the Center for Violence Prevention at University of Texas Medical Branch; Brad Thomas, Ph.D. , NYC-based therapist and licensed clinical psychologist; Jeff Yoo, L.M.F.T. at Moment of Clarity Mental Health Center .
“Being happy in life and with self begins with our choices as adults and how we perceive our contributions to the world,” says Jeff Yoo, L.M.F.T. at Moment of Clarity Mental Health Center . Ahead, mental health experts explain tips for being happy alone, how to ask for help when you need it, and what it is to be alone versus feeling lonely. Alone vs. lonely
Being alone is a physical state where you are not in the company of others, whereas feeling lonely is an emotional state of feeling isolated, regardless of whether you’re physically alone or with others, says Patrick Porter, Ph.D., neuroscience expert and founder of BrainTap . “One can be alone without feeling lonely, and conversely, one can feel lonely in a crowd,” he says. Understanding this difference is crucial, as it impacts how you approach your own mental and emotional well-being.
Aloneness can be a neutral state, says Brad Thomas, Ph.D. , NYC-based therapist and licensed clinical psychologist. “People can be happy being by themselves, and there are other times when they desire to be emotionally connected to others,” he says. Still, we want to keep our eye on these feelings to determine to what extent we are feeling loneliness and how distressing it can be, he adds.
Aloneness can be an enriching experience—giving us the chance to learn more about ourselves and the world around us, says Dana Klisanin, Ph.D. , psychologist and CEO of Evolutionary Guidance Media R&D. “Loneliness can arise when we feel that we have no one to share our experiences with or no one who understands us,” she says. How to be happy alone short-term
In our society, there is a stigma around being alone or feeling lonely that we can flip on its head, says Thomas. “We can take some of the power away from that stigmatization and look at it healthier,” he says. There are many advantages to being alone, like having the time to focus on yourself. “That is taking the power in your hands and understanding what you desire, independent of other people’s reactions,” Thomas explains.
When it comes to things you can start doing right now to be happy alone, experts suggest: Question the narrative
First of all, ask yourself if you are really “unhappy alone” or have you been taught to think you should be unhappy if you are alone, says Klisanin. “Our narratives define us. If your ‘story’ isn’t working, you have permission to change it,” she says. Take a moment for mindfulness
Spend five to 10 minutes each day meditating to center yourself. Focus on your breathing and the present moment, suggests Porter. Accepting solitude as an opportunity rather than a hindrance can shift one’s perspective, adds Klisanin. Get active
Even a 20-minute walk outside can boost endorphin levels, elevating your mood and well-being, says Porter. “Avoid sitting for prolonged periods; our research shows that just two hours of sitting can reduce oxygen in the brain by 10%. Make it a point to get up and move around,” he adds. Take a tech break
Take a break from being on your computer and technology when you can, says Thomas. “Putting away your devices allows you to check in with yourself to see what you desire.” Engage in creative activities
These can be therapeutic and stimulate your brain, says Porter. Whether it’s painting, journaling , gardening , or learning to play a musical instrument, a new hobby can provide a sense of fulfillment and self-expression, says Klisanin. Get inspired
Watching short motivational videos or reading inspirational quotes can uplift your spirits, says Porter—so time to watch some Ted Talks!
Advertisement Practice self-care and grounding
Pamper yourself, whether it’s taking a warm bath or enjoying your favorite healthy snack, says Porter. “Additionally, spend some time outside grounding yourself to release excess energy. Walk on grass barefoot or with leather shoes to achieve a zero point energy state; our research indicates that the average person has up to three volts of disruptive energy flowing through their body,” he adds. How to be happy alone long-term
The more you practice and get into the habit of being alone, the more you’ll understand your path of self-understanding and discovery, says Thomas. With time, “you’ll be able to tolerate so much more ambiguity because you know yourself well,” he says. Experts explain the best tips for figuring out how to be happy alone long-term. Build a routine
A stable routine helps your brain recognize patterns, making you feel more in control and happier, says Porter. “Incorporate a consistent sleep schedule into this routine. Going to bed and waking up at the same time helps regulate your body’s clock and improves your overall well-being,” he says. Set goals
Whether they are short- or long-term, goals give you a sense of purpose, says Porter. “Challenge yourself to tackle new things; this keeps your mind sharp and invokes the beginner’s mindset, which is fantastic for discovering happiness,” he says. Keep your mind sharp
Learning something new is not just rewarding; it enhances brain function, says Porter. “Continuously challenging yourself with new skills not only boosts your self-esteem […]
New CU Boulder research demonstrates that, with practice, older adults can regain manual dexterity that may have seemed lost
Despite what ads for wrinkle cream would have us believe, there’s no magic reversal for aging. As the years pass, a certain amount of change is inevitable but not, it turns out, inexorable.
Fingers that feel less nimble in doing the normal tasks of life—buttoning a shirt, writing a list—are not doomed to stay that way, new research shows . It also demonstrates that, to some extent, age is just a number.
Researchers in the University of Colorado Boulder Department of Integrative Physiology —first author Sajjad Daneshgar and Taylor Tvrdy , both PhD students, and Professor Roger Enoka —worked with more than two dozen study participants ages 60 to 83 to understand whether manual dexterity can improve with time. Sajjad Daneshgar, a PhD student in the CU Boulder Department of Integrative Physiology, conducted research that found manual dexterity can improve with practice in older age. Over six sessions, participants completed a pegboard exercise multiple times, and after the sixth session, data showed that the average time it took to complete the pegboard had decreased for all participants.
“We saw that in older adults, training can improve hand function to a level it was at in middle age,” Daneshgar says. “In a way, practicing helped them go back a decade or two. Most people believe that aging has many negative challenges in terms of function in the hands, but this study shows that what you achieved in the past can really help you as you get older.”
Simple puzzle, complex process
For the study, Daneshgar and his research colleagues recruited right-handed older adults with no history of neurological disease. After an initial familiarization session and evaluation session, participants completed a grooved pegboard test 25 times in each of six sessions.
The test required participants to fit small, keyhole-shaped metal pegs into 25 holes on a board as quickly as possible. The keyholes had different orientations on the board, so participants not only had to manipulate the pegs with their fingers to get them situated correctly, but then fit them correctly.
“At first glance, this looks like a simple puzzle or game, but it’s actually a very complex process,” Daneshgar says. “Your mind is controlling your physical function—and we’re doing a lot more studies on this physical function and what’s going on in the muscles, in the nervous system—and we’re seeing that cognition of the mind, how you learn things, is connected to the muscles and how dexterous you are.”
For example, one of the study participants was a 67-year-old woman who played the piano in her youth. While the average time to complete the pegboard was between 40 and 50 seconds, she could do it in 36—a time faster than some of the researchers could achieve.
“Even though she wasn’t regularly playing the piano during the study, that tells us that perhaps the memory your brain has of controlling those muscles still exists,” Daneshgar says. “Some activities that people do—playing a musical instrument, rock climbing—can be very beneficial for manual dexterity, and even if they’re done earlier in life, the brain may remember controlling those muscles.” During the research, study participants fit small, keyhole-shaped metal pegs into 25 holes on a board as quickly as possible. Practice leads to improvement
However, those who reach their later years without a longtime history of guitar-playing or bouldering shouldn’t despair. Wherever study participants started at baseline—even if their initial times for completing the pegboard were comparatively slow—each saw improvement in their times by the sixth session.
“Manual dexterity can be improved by the brain,” Daneshgar says. “It’s not just at the level of the fingers. Signals from the brain are controlling function and practicing aids learning. This study shows that, as far as function in the limbs and hands, learning in terms of muscle training never ends. Whatever level you’re at, you can go back to this training and practicing to see improvement in function.”
Another important outcome from the research is demonstrating that categorizing people’s performance based on chronological age during their later years may not be the best way to understand manual dexterity.
“Whatever you learned in the past is going to be a main player in performance in older age,” Daneshgar says. “Of course, not all people in older age are going to have the same performance, but people who had better practice in the past can, in older age, practice and get to a place where they perform better than middle-age adults.
“But we also showed that practice helps everybody. It doesn’t matter if you have particular experience earlier in life, practice helps all people to do better with no exception.”
Manual dexterity is one of the National Institutes of Health Toolbox biomarkers of neurological health and motor function across the span of life. Daneshgar notes that the research demonstrates manual dexterity is not something that must inevitably worsen over time. With practice, the brain can remember what the fingers once did.
“Manual dexterity relates to our ability to button a shirt or hold a pen,” Daneshgar says. “These are the activities of daily life that we want to be able to do throughout our lives, and they’re abilities that we don’t need to lose.”
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A new technology that is able to translate our brain signals into speech has been developed by a team of neuroscientists, neurosurgeons and engineers at Duke University in North Carolina.
The device—known as a speech prosthetic—is significantly faster than the best speech-decoding technologies available today. It offers hope to patients who have lost their ability to speak.
“This technology would help patients suffering from debilitating neurological disorders such as ALS [amyotrophic lateral sclerosis] and locked-in-syndrome, who have lost the ability to speak and communicate,” Gregory Cogan told Newsweek. He is a professor of neurology at Duke University and one of the lead researchers on this project. “The current tools available to allow them to communicate are generally very slow and cumbersome.” Brain decoder For this project, Cogan teamed up with fellow Duke researcher Jonathan Viventi. He runs a biomedical engineering lab that specializes in creating high-density, ultra-thin and flexible brain sensors. For this project, the team packed 256 microscopic brain sensors onto a piece of flexible, medical-grade plastic the size of a postage stamp.
“Neural speech prostheses work by directly reading the brain signals that control speech motor movement, and then translate these signals directly into readable outputs that can be used to create speech sounds,” Cogan said. “They read your intentions to speak and translate this intention to sound. “These devices would be fitted through a small craniotomy in the skull and implanted directly onto the motor cortex of the brain. We are currently working on a project that will allow for one of these devices to work wirelessly, so that patients could move around freely while using it,” Cogan added.
To test the implant, the team recruited four patients who were already undergoing brain surgery for other conditions. The experiment was fast-paced and involved the team placing the device temporarily in the patients’ brains and asking them to repeat a series of simple words out loud.
“I like to compare it to a NASCAR pit crew,” Cogan said. “We don’t want to add any extra time to the operating procedure, so we had to be in and out within 15 minutes. As soon as the surgeon and the medical team said ‘Go!’, we rushed into action and the patient performed the task.”
Afterwards, Suseendrakumar Duraivel, a biomedical engineering graduate student at Duke, fed this data into a machine learning algorithm to see how accurately it could predict the sounds that were being made based solely on the patients’ recorded brain activity. The results were published in the journal Nature Communications on November 6.
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“We were surprised at how good the results were,” Cogan said. “[This] technology demonstrates a very large improvement over current technology: we achieved 57 times higher spatial resolution and 48 percent higher neural signal strength compared to standard recordings. This increased signal quality improved our ability to read speech brain signals by 35 percent compared to standard tools.
“We expected results that were better than previous methods, but it is very promising to see the results pan out and it really opens the door for better neural speech prostheses in the near future,” Cogan added.
Overall, the decoder was accurate 40 percent of the time. The team members hope to resolve their technology further, while also developing a wireless version of the device to allow patients to move around without restrictions.
“We’re at the point where it’s still much slower than natural speech,” Viventi told Duke Magazine . “But you can see the trajectory where you might be able to get there.”
“The next steps are to get FDA [Food and Drug Administration] approval for our devices, so that we can put them in patients long-term to enable the restoration of their speech and communicative abilities,” Cogan said.
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Researchers have identified the genetic pathway between the heart and brain responsible for fainting, revealing a two-way communication that could lead to new treatments for syncope-related disorders. Neurobiologists have discovered sensory neurons that regulate fainting, providing a foundation for targeted treatments for related disorders.
Syncope, commonly known as fainting, affects nearly 40 percent of people at least once in their lifetime. These transient losses of consciousness can be precipitated by various triggers such as pain, fear, heat, or hyperventilation, and they are a substantial cause of emergency room visits. Despite their prevalence, the fundamental mechanisms underlying syncope have largely remained enigmatic. Breakthrough in Genetic Pathways
Publishing a new report in Nature , University of California San Diego researchers, along with colleagues at The Scripps Research Institute and other institutions, have for the first time identified the genetic pathway between the heart and brain tied to fainting.
One of their unique approaches was to think of the heart as a sensory organ rather than the longstanding viewpoint that the brain sends out signals and the heart simply follows directions. School of Biological Sciences Assistant Professor Vineet Augustine, the paper’s senior author, applies a variety of approaches to better understand these neural connections between the heart and brain. An image of a heart labeled by vagal sensory neurons. In a new study published in the journal Nature , UC San Diego researchers and their colleagues found that these neurons trigger fainting, laying a foundation for addressing fainting-related disorders. Credit: Augustine Lab, UC San Diego
“What we are finding is that the heart also sends signals back to the brain, which can change brain function,” said Augustine. Information resulting from the study could be relevant to better understanding and treating various psychiatric and neurological disorders linked with brain-heart connections, the researchers note in their paper. “Our study is the first comprehensive demonstration of a genetically defined cardiac reflex, which faithfully recapitulates characteristics of human syncope at physiological, behavioral, and neural network levels.” Study on the Bezold-Jarisch Reflex
Augustine, along with Biological Sciences Staff Research Associate Jonathan Lovelace and Graduate Student Jingrui Ma, the first authors of the paper, and their colleagues studied neural mechanisms related to Bezold-Jarisch reflex (BJR), a cardiac reflex first described in 1867. For decades researchers have hypothesized that the BJR, which features reduced heart rate, blood pressure, and breathing, may be associated with fainting. But information lacked in proving the idea since the neural pathways involved in the reflex were not well known. Researchers at UC San Diego and collaborating institutions have highlighted the immense crosstalk between the heart and the nervous system. The video displays heart activity dramatically slowing down with stimulation of vagal sensory neurons, which were found to trigger fainting. Credit: Augustine Lab, UC San Diego
The researchers focused on the genetics behind a sensory cluster known as the nodose ganglia, which are part of the vagus nerves that carry signals between the brain and visceral organs, including the heart. Specifically, vagal sensory neurons, or VSNs, project signals to the brainstem and are thought to be associated with BJR and fainting. In their search for a novel neural pathway they discovered that VSNs expressing the neuropeptide Y receptor Y2 (known as NPY2R) are tightly linked to the well-known BJR responses. Optogenetic Studies and Findings
Studying this pathway in mice, the researchers were surprised to find that when they proactively triggered NPY2R VSNs using optogenetics, a method of stimulating and controlling neurons, mice that had been freely moving about immediately fainted. During these episodes, they recorded from thousands of neurons in the brains of the mice, as well as heart activity and changes in facial features including pupil diameter and whisking.
They also employed machine learning in several ways to analyze the data and pinpoint features of interest. Once NPY2R neurons were activated, they found, mice exhibited rapid pupil dilation and the classic “eye-roll” seen during human fainting, as well as suppressed heart rate, blood pressure, and breathing rate. They also measured reduced blood flow to the brain, an area of collaboration with Professor David Kleinfeld’s laboratory in the UC San Diego Departments of Neurobiology and Physics.
“We were blown away when we saw how their eyes rolled back around the same time as brain activity rapidly dropped,” the researchers reported in a paper summary. “Then, after a few seconds, brain activity and movement returned. This was our eureka moment.”
Further testing showed that when NPY2R VSNs were removed from mice, the BJR and fainting conditions vanished. Previous studies have shown that fainting is caused by a reduction in brain blood flow, which the new study also found to be true, but the new evidence indicated that brain activity itself could be playing an important role. The findings, therefore, implicate the activation of the newly genetically identified VSNs and their neural pathways not only with BJR, but more centrally in overall animal physiology, certain brain networks, and even behavior. Implications and Future Research
Such findings were difficult to tease out previously because neuroscientists study the brain and cardiologists study the heart, but many do so in isolation of the other. “Neuroscientists traditionally think the body just follows the brain, but now it is becoming very clear that the body sends signals to the brain and then the brain changes function,” said Augustine.
As a result of their findings, the researchers would like to continue tracking the precise conditions under which vagal sensory neurons are triggered into action.
“We also hope to more closely examine cerebral blood flow and neural pathways in the brain during the moment of syncope, to better understand this common but mysterious condition,” they note.
They also hope to use their research as a model to develop targeted treatments for fainting-associated conditions.
The study was funded by UC San Diego, Scripps Research Institute, the Helen Dorris Foundation, the National Institutes of Health, the American Heart Association Early Faculty Independence Award, the Mallinckrodt Foundation, the Dorris Scholarship, the Dorris-Skaggs Fellowship, and the Shurl and Kay Curci Foundation Fellowship.
The Wuhan coronavirus (COVID-19) vaccine and the flu vaccine each come with their own set of potential side effects, but when these two risky jabs are administered together, the risks may be even higher. A growing body of evidence is now pointing to one very dangerous side effect in particular: stroke.
Researchers from Kaiser Permanente have found that there is a heightened risk of stroke for individuals under the age of 65 who receive a flu shot and the Pfizer COVID-19 vaccine on the same day. In the study, scientists identified 373 strokes in patients in the 42 days after receiving bivalent vaccination; after 42 days, 1511 strokes were reported.
Meanwhile, researchers from the Food and Drug Administration (FDA) have admitted to identifying an elevated risk of stroke for elderly individuals who receive the Pfizer or Moderna vaccines at the same time as the flu vaccine. The finding came from a self-controlled case series involving Medicare beneficiaries who received both vaccines.
They found that people aged 85 and older who received the Pfizer vaccine with their flu shot had higher risks of non-hemorrhagic stroke and transient ischemic attacks, while the elevated risk for those who received the Moderna jab was seen in those aged 65 to 74. Both types of strokes seen in the study are caused by blood clots that block the flow of blood to the brain.
All recipients aged 65 and older experienced a higher risk of non-hemorrhagic stroke 22 to 42 days after receiving a flu and Pfizer COVID vaccine combo; a higher risk of transient ischemic attack was seen in the first 21 days for those who received the flu vaccine and Moderna COVID-19 vaccine combination.
These results are being blamed largely on the high-dose flu vaccine that the patients who were studied received, which is formulated to rev up their immune system. Known as Fluzone, it contains quadruple the flu protection provided by a normal flu jab.
One high-ranking FDA official, Dr. Peter Marks, told a conference that he believes the flu, COVID-19 and RSV vaccines should be spaced out to reduce the risk of adverse events. He noted: “Oftentimes, we suggest if you want to minimize the chance of interactions and minimize confusing side effects from one with another, you wait about two weeks between the vaccines.”
Researchers in Australia have reached a similar conclusion. They note that more adults have reported experiencing negative side effects after getting a flu vaccine and Pfizer’s COVID-19 vaccine at the same time than those that are reported after receiving either of these vaccines on their own. COVID-19 vaccines can raise blood pressure
Although it is not fully clear how a vaccine raises the risk of stroke, studies have demonstrated an increase in blood pressure after getting a COVID-19 shot, which forces the heart to work harder than usual. This stress can damage the inner lining of blood vessels and cause arteries to narrow, which fosters the development of clots. Another risk of the vaccine is the potential to spur an abnormal immune response that results in severe inflammation that blocks the flow of blood to the brain.
On top of the risk of stroke, another concern is the possibility of one vaccine impacting the response of another. For example, one study showed that vaccines that are co-administered create lower levels of antibodies, which means recipients are not getting the full benefits.
It is worth noting that some studies have found that receiving the flu and COVID-19 vaccines simultaneously does not appear to raise stroke risk . However, researchers have acknowledged that more studies are needed to reach a more definitive conclusion about this connection and what may be causing it.
Sources for this article include:
Credit: Pixabay/CC0 Public Domain Brain health in people over age 50 deteriorated more rapidly during the pandemic, even if they didn’t have COVID-19, according to major new research linking the pandemic to sustained cognitive decline.
Researchers looked at results from computerized brain function tests from more than 3,000 participants of the online PROTECT study, who were aged between 50 and 90 and based in the UK. The remote study, led by teams at the University of Exeter and the Institute of Psychiatry, Psychology & Neuroscience (IoPPN) at King’s College London, tested participants’ short-term memory and ability to complete complex tasks.
Through analyzing the results from this large data set, researchers found that cognitive decline quickened significantly in the first year of the pandemic , when they found a 50% change to the rate of decline across the study group . This figure was higher in those who already had mild cognitive decline before the pandemic, according to the research published in The Lancet Healthy Longevity .
This continued into the second year of the pandemic, suggesting an impact beyond the initial 12-month period of lockdowns. The researchers believe this sustained impact to be particularly relevant to ongoing public health and health policy .
The cognitive decline seems to have been exacerbated by a number of factors during the pandemic, including an increase in loneliness and depression, a decrease in exercise, and higher alcohol consumption. Previous research has found that physical activity , treating existing depression, getting back into the community, and reconnecting with people are all important ways to reduce dementia risk and maintain brain health.
Anne Corbett, Professor of Dementia Research and PROTECT Study Lead at the University of Exeter, said, “Our findings suggest that lockdowns and other restrictions we experienced during the pandemic have had a real lasting impact on brain health in people aged 50 or over, even after the lockdowns ended. This raises the important question of whether people are at a potentially higher risk of cognitive decline which can lead to dementia.
“It is now more important than ever to make sure we are supporting people with early cognitive decline , especially because there are things they can do to reduce their risk of dementia later on. So if you are concerned about your memory, the best thing to do is to make an appointment with your GP and get an assessment. Our findings also highlight the need for policymakers to consider the wider health impacts of restrictions like lockdowns when planning for a future pandemic response.”
Professor Dar Aarsland, Professor of Old Age Psychiatry at King’s IoPPN, added, “This study adds to the knowledge of the long-standing health-consequences of COVID-19, in particular for vulnerable people such as older people with mild memory problems. We know a great deal of the risks for further decline, and now can add COVID-19 to this list. On the positive note, there is evidence that lifestyle changes and improved health management can positively influence mental functioning. The current study underlines the importance of careful monitoring of people at risk during major events such as the pandemic.”
More information: Cognitive decline in older adults in the UK during and after the COVID-19 pandemic: a longitudinal analysis of PROTECT study data, The Lancet Healthy Longevity (2023).
Provided by University of Exeter
Summary: Researchers from Cleveland Clinic and OHSU have unveiled a pioneering technique for charting the intricate conversations occurring within our brains. Such insights are key to decoding behavioral alterations in neurological disease patients.
The innovative tool, CaMPARI, allows scientists to witness brain activity in real-time, marking active neurons red and inactive ones green. This breakthrough could offer pathways to better treatments and understanding of diseases like Alzheimer’s.
> The study, using the CaMPARI system, can map real-time brain activity by highlighting active neurons in red and inactive ones in green.
This research is significant for understanding behavior and personality changes in Alzheimer’s disease and related disorders.
The team’s findings, recently published in Nature Communications, have the potential to shape the future of cognitive neuroscience, with the promise of improved treatment options.
Source: Cleveland Clinic
A research team led by Cleveland Clinic and Oregon Health and Science University (OHSU) has developed a new method for mapping how the parts of the brain “speak” to each other, critical to understanding behavior changes in patients with neurological disease.
Diseases like Alzheimer’s disease change how patients communicate and act, affecting their relationships and well-being. Cleveland Clinic’s Hod Dana, PhD, is collaborating with Jacob Raber, PhD, an OHSU behavioral neuroscientist, on mapping out the electrical paths that connect and coordinate the parts of the brain needed to complete different tasks. Decision-making, forming a memory or completing a task all involve brainwaves, signaling pathways that use cells called neurons. Credit: Neuroscience News “Effects on behavior and personality in Alzheimer’s disease and related disorders are caused by changes in brain function,” Dr. Dana says. “If we can understand exactly how the changes occur, we may figure out how to slow down the process or to stop it. Recording brain activity patterns that underlie behavioral changes is the first step to bridging the gap.”
Decision-making, forming a memory or completing a task all involve brainwaves, signaling pathways that use cells called neurons. To study how brainwaves influence behavior and decision making, researchers observe as neurons turn “on” and “off” across the organ in different situations.
Current technologies are unable to map the whole brain while still identifying the single cells. CaMPARI images can be captured during behavior, highlighting neurons that are active as red and inactive neurons as green.
After the test is completed, the red and green markers remain bright for several days. This allows researchers to capture a series of images to track the brain’s activity by mapping where the red appears within the brain.
The team recently published results in Nature Communications on using a calcium sensor system called CaMPARI (Calcium-modulated photoactivatable ratiometric integrator) to map brain activity in preclinical models while completing cognitive tasks. Drs. Dana and Raber plan to use CaMPARI in preclinical work to see how Alzheimer’s-related genes affect the way our neurons signal through our brains in learning and memory.
Drs. Dana and Raber say they hope to take what they learn from their results to develop tests and interventions that can improve the quality of life for patients, providing better treatment options.
“We now have the capability to study the relationship between brain activation and cognitive performance at an unprecedented level,” says Dr. Raber.
“These are the first steps in developing strategies to reverse those changes and improve cognitive performance in those affected by neurological conditions. The future of behavioral and cognitive neuroscience looks bright.”
Funding: This work was funded by NIH R21AG065914 and U01NS123658. About this neuroscience research news
Author: Alicia Reale
Source: Cleveland Clinic
Contact: Alicia Reale – Cleveland Clinic
Image: The image is credited to Neuroscience News
Original Research: Open access.
“ Large-scale recording of neuronal activity in freely-moving mice at cellular resolution ” by Hod Dana et al. Nature Communications
Large-scale recording of neuronal activity in freely-moving mice at cellular resolution
Current methods for recording large-scale neuronal activity from behaving mice at single-cell resolution require either fixing the mouse head under a microscope or attachment of a recording device to the animal’s skull.
Both of these options significantly affect the animal behavior and hence also the recorded brain activity patterns.
Here, we introduce a different method to acquire snapshots of single-cell cortical activity maps from freely-moving mice using a calcium sensor called CaMPARI. CaMPARI has a unique property of irreversibly changing its color from green to red inside active neurons when illuminated with 400 nm light.We capitalize on this property to demonstrate cortex-wide activity recording without any head fixation, tethering, or attachment of a miniaturized device to the mouse’s head. Multiple cortical regions were recorded while the mouse was performing a battery of behavioral and cognitive tests.We identified task-dependent activity patterns across motor and somatosensory cortices, with significant differences across sub-regions of the motor cortex and correlations across several activity patterns and task parameters.This CaMPARI-based recording method expands the capabilities of recording neuronal activity from freely-moving and behaving mice under minimally-restrictive experimental conditions and provides large-scale volumetric data that are currently not accessible otherwise.Join our Newsletter I agree to have my personal information transferred to AWeber for Neuroscience Newsletter ( more information )Sign up to receive our recent neuroscience headlines and summaries sent to your email once a day, totally free.
For those experiencing anxiety and depression, lacing up their running shoes proves to be a better choice instead of taking drugs, according to a study.
The May 15 study published in the Journal of Affective Disorders found that running as therapy for anxiety and depression outperforms the effects of prescription antidepressants on mental and physical health and overall well-being – without negative side effects.
The study authors from the Netherlands gave 141 participants with anxiety and/or depression a real-life choice of treatments for their condition – medication or exercise – for a 16-week period. The medication group took escitalopram (an antidepressant that belongs to a group of medicines known as selective serotonin reuptake inhibitors or SSRIs that work by increasing the activity of “happy hormone” serotonin in the brain) and were told to adhere to their prescribed medication. Meanwhile, the exercise group aimed for two to three closely supervised 45-minute group sessions per week for 16 weeks.
At the end of the trial, researchers reported that around 44 percent of both groups showed an improvement in anxiety and depression. Significant improvements in blood pressure, heart function, weight and waist circumference were also reported in the running group. On the other hand, a tendency toward a slight deterioration in these metabolic markers was observed and reported in the antidepressant group. (Related: Exercise: The Miracle antidepressant drug? )
While the physical benefits of running as exercise have been well-established, there is plenty of scientific evidence suggesting that running can also improve your mental health and well-being. Here are some studies that support this belief. Running is a great stress reliever
Dr. David Linden, a professor of neuroscience at Johns Hopkins University School of Medicine, gives credit to a group of neurotransmitters called “endocannabinoids” – biochemical substances produced naturally by the body. These chemicals travel in and around the brain for the stress-reducing effects of a good run.
Endocannabinoids are produced in higher-than-normal concentrations during your runs and once they get into the brain, they exhibit the ability to reduce feelings of anxiety and encourage calm.
Unlike endorphins – biochemicals or hormones your body releases during pleasurable activities such as eating, exercise, massage and even sex – endocannabinoids can move easily through the cellular barrier separating the bloodstream from the brain, where these mood-improving neuromodulators promote short-term psychoactive effects, such as reduced anxiety and feelings of calm, Linden explained.
By making running a regular part of your healthy lifestyle routine, “you stand to earn more than just physical gains over time,” said Linden.
A study published in the journal Biochemical Pharmacology concluded that present findings point to the “endocannabinoid system as a pivotal neuromodulatory pathway relevant in the pathophysiology of mental disorders.” Running improves mood
A team of scientists at the University of Tsukuba in Japan completed a study published in the journal Scientific Reports , which provided evidence that a 10-minute single-bout of moderate-intensity running evokes a positive mood and increased executive function by enhancing arousal levels with activation in prefrontal subregions involved in mood regulation.
Researchers reported that running increased local blood flow to various parts of the prefrontal cortex – the gray matter of the anterior part of the frontal lobe that is highly developed in humans and plays a major role in the regulation of behavioral, cognitive and emotional functioning. Running promotes better sleep quality
Running also improves sleep quality , which can in turn boost your mental health. A study of 51 adolescents with a mean age of 18.3 years has found that 30 minutes of daily morning moderate-intensity running for three consecutive weeks improved sleep and psychological functioning in healthy adolescents, compared with control subjects. The study was published in the Journal of Adolescent Health . Running helps you better process your emotions
Running has been found as a perfect way to separate yourself from a situation for a little while. The key takeaway of a study involving 1.2 million Americans, published in The Lancet: Psychiatry , is that “if you run regularly, you probably experience better mental health days than not.”
Researchers found people who exercise regularly have 43.2 percent fewer days of “not good” mental health per month – characterized by heightened emotional stress –compared to those who don’t exercise regularly.
According to a study published online by JAMA Psychiatry , physical activity has an important and “potentially causal role” in reducing your risk for depression . Data suggests that if you replaced 15 minutes per day of sitting with 15 minutes of vigorous activity like running, you may be able to “outrun” depression. Running builds self-esteem
Researchers in a study published in the journal Neuropsychiatric Disease and Treatment has found that physical activities like running and jogging are directly related to better self-esteem as runners (or joggers) physically grow stronger and surer of themselves with each and every foot strike.
They added that running could provide a feeling of empowerment and freedom by knowing that your body, legs and mind are strong and capable, which can lead to improved perceptions of fitness and body image.
Visit BeatDepression.news for more similar stories.
Watch this video about how running is linked to improved mental health . This video is from the Daily Videos channel on Brighteon.com . More related stories:
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Adapt to stress with these 5 adaptogenic herbs. Sources include: DailyMail.co.uk ScienceDirect.com 1 HopkinsMedicine.org ScienceDirect.com 2 Nature.com ScienceDirect.com 3 JAHOnline.org BrooksRunning.com TheLancet.com ScienceDaily.com Dovepress.com Brighteon.com
( Nanowerk News ) For the first time, a physical neural network has successfully been shown to learn and remember ‘on the fly’, in a way inspired by and similar to how the brain’s neurons work. The result opens a pathway for developing efficient and low-energy machine intelligence for more complex, real-world learning and memory tasks. Key Takeaways
The nanowire-based system can learn and remember ‘on the fly,’ processing dynamic, streaming data for complex learning and memory tasks.
This advancement overcomes the challenge of heavy memory and energy usage commonly associated with conventional machine learning models.
The technology achieved a 93.4% accuracy rate in image recognition tasks, using real-time data from the MNIST database of handwritten digits.
The findings promise a new direction for creating efficient, low-energy machine intelligence applications, such as real-time sensor data processing.
Electrodes interact with the nanowire neural network at the heart of the chip. (Image: University of Sydney) The Research
Published in Nature Communications ( “Online dynamical learning and sequence memory with neuromorphic nanowire networks” ), the research is a collaboration between scientists at the University of Sydney and University of California at Los Angeles. Lead author Ruomin Zhu, a PhD student from the University of Sydney Nano Institute and School of Physics, said: “The findings demonstrate how brain-inspired learning and memory functions using nanowire networks can be harnessed to process dynamic, streaming data.” Nanowire networks are made up of tiny wires that are just billionths of a metre in diameter. The wires arrange themselves into patterns reminiscent of the children’s game ‘Pick Up Sticks’, mimicking neural networks, like those in our brains. These networks can be used to perform specific information processing tasks. Memory and learning tasks are achieved using simple algorithms that respond to changes in electronic resistance at junctions where the nanowires overlap. Known as ‘resistive memory switching’, this function is created when electrical inputs encounter changes in conductivity, similar to what happens with synapses in our brain. In this study, researchers used the network to recognise and remember sequences of electrical pulses corresponding to images, inspired by the way the human brain processes information. Supervising researcher Professor Zdenka Kuncic said the memory task was similar to remembering a phone number. The network was also used to perform a benchmark image recognition task, accessing images in the MNIST database of handwritten digits, a collection of 70,000 small greyscale images used in machine learning. “Our previous research established the ability of nanowire networks to remember simple tasks. This work has extended these findings by showing tasks can be performed using dynamic data accessed online,” she said. “This is a significant step forward as achieving an online learning capability is challenging when dealing with large amounts of data that can be continuously changing. A standard approach would be to store data in memory and then train a machine learning model using that stored information. But this would chew up too much energy for widespread application. “Our novel approach allows the nanowire neural network to learn and remember ‘on the fly’, sample by sample, extracting data online, thus avoiding heavy memory and energy usage.” Mr Zhu said there were other advantages when processing information online. “If the data is being streamed continuously, such as it would be from a sensor for instance, machine learning that relied on artificial neural networks would need to have the ability to adapt in real-time, which they are currently not optimised for,” he said. In this study, the nanowire neural network displayed a benchmark machine learning capability, scoring 93.4 percent in correctly identifying test images. The memory task involved recalling sequences of up to eight digits. For both tasks, data was streamed into the network to demonstrate its capacity for online learning and to show how memory enhances that learning. Source: Universityy of Sydney (Note: Content may be edited for style and length) Nanowerk Newsletter
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Electron microscope image of the nanowire neural network that arranges itself like ‘Pick Up Sticks’. The junctions where the nanowires overlap act in a way similar to how our brain’s synapses operate, responding to electric current. Credit: The University of Sydney For the first time, a physical neural network has successfully been shown to learn and remember “on the fly,” in a way inspired by and similar to how the brain’s neurons work.
The result opens a pathway for developing efficient and low-energy machine intelligence for more complex, real-world learning and memory tasks .
Published today in Nature Communications , the research is a collaboration between scientists at the University of Sydney and University of California at Los Angeles.
Lead author Ruomin Zhu, a Ph.D. student from the University of Sydney Nano Institute and School of Physics, said, “The findings demonstrate how brain-inspired learning and memory functions using nanowire networks can be harnessed to process dynamic, streaming data.”
Nanowire networks are made up of tiny wires that are just billionths of a meter in diameter. The wires arrange themselves into patterns reminiscent of the children’s game “Pick Up Sticks,” mimicking neural networks, like those in our brains. These networks can be used to perform specific information processing tasks.
Memory and learning tasks are achieved using simple algorithms that respond to changes in electronic resistance at junctions where the nanowires overlap. Known as “resistive memory switching,” this function is created when electrical inputs encounter changes in conductivity, similar to what happens with synapses in our brain. Detail of larger image above: nanowire neural network. Credit: The University of Sydney In this study, researchers used the network to recognize and remember sequences of electrical pulses corresponding to images, inspired by the way the human brain processes information.
Supervising researcher Professor Zdenka Kuncic said the memory task was similar to remembering a phone number. The network was also used to perform a benchmark image recognition task, accessing images in the MNIST database of handwritten digits, a collection of 70,000 small greyscale images used in machine learning .
“Our previous research established the ability of nanowire networks to remember simple tasks. This work has extended these findings by showing tasks can be performed using dynamic data accessed online,” she said.
“This is a significant step forward as achieving an online learning capability is challenging when dealing with large amounts of data that can be continuously changing. A standard approach would be to store data in memory and then train a machine learning model using that stored information. But this would chew up too much energy for widespread application.”
“Our novel approach allows the nanowire neural network to learn and remember ‘on the fly,” sample by sample, extracting data online, thus avoiding heavy memory and energy usage.” Electron microscope image of electrode interaction with the nanowire neural network. Credit: The University of Sydney Mr. Zhu said there were other advantages when processing information online.
“If the data is being streamed continuously, such as it would be from a sensor for instance, machine learning that relied on artificial neural networks would need to have the ability to adapt in real-time , which they are currently not optimized for,” he said.
In this study, the nanowire neural network displayed a benchmark machine learning capability, scoring 93.4 percent in correctly identifying test images. The memory task involved recalling sequences of up to eight digits. For both tasks, data was streamed into the network to demonstrate its capacity for online learning and to show how memory enhances that learning.
More information: Online dynamical learning and sequence memory with neuromorphic nanowire networks, Nature Communications (2023). DOI: 10.1038/s41467-023-42470-5
Some cases of OCD are notoriously difficult to treat. Responsive deep brain stimulation may help. Making sure a stovetop isn’t left on or readjusting an askew picture frame is often a natural response when something feels off. Yet, for over two million Americans living with obsessive-compulsive disorder (OCD), this nagging, unsettling feeling is a constant, debilitating presence marked by obsessions, persistent distressing thoughts, and compulsions, which result in repetitive behaviors people feel driven to perform.
Cognitive behavioral therapy and antidepressants can mellow out the obsessions and compulsions that people with OCD experience, but about one-third of those living with OCD don’t see improvement with either therapeutic treatment or medication. These cases are called treatment-resistant OCD, and for these people, there usually isn’t a whole lot that can be done outside of these standard (and unfortunately ineffective) remedies. But a new emerging treatment may provide some much-needed relief. Known as “deep brain stimulation,” this therapy delivers jolts of electricity to the brain in the hopes of fading those persistent, nagging thoughts into a distant memory.
In a study published earlier this month in the journal Neuron , researchers at the University of Pennsylvania used a type of brain stimulation called “responsive deep brain stimulation” to treat a 34-year-old woman with treatment-resistant OCD. Using a brain implant surgically placed to treat her epilepsy, the researchers taught the device to recognize a unique pattern of abnormal brain activity — a potential neural biomarker of OCD — and stimulate it any time it appeared. Within months, the woman’s severe obsessions and compulsions were significantly reduced. Two years after her first treatment, the researchers say her disorder no longer eats up hours of her day.
“This study is a proof-of-principle that we’re very close to finding a marker of OCD that seems to go up and down with effective deep brain stimulation,” Martijn Figee , director of the Mount Sinai Interventional Psychiatry Program, who was not involved in the study, tells Inverse . Resetting the brain
Since the mid-1980s, deep brain stimulation has been used to treat movement disorders like Parkinson’s disease or severe tremors and, in more recent years, Alzheimer’s disease , severe depression , binge eating , and now treatment-resistant OCD have also seen positive results.
About half of people with treatment-resistant OCD who try deep brain stimulation get much better, but the results aren’t consistent. Much of that has to do with the fact that we don’t fully understand how deep brain stimulation works. What scientists do know is that delivering a continuous electrical current through an electrode implanted in the brain helps reset and normalize communication between different areas involved in OCD. This incomplete understanding leads to challenges in fine-tuning deep brain stimulation in a way that’s effective for people dealing with treatment-resistant OCD. People with compulsive hand washing perform excessive and repetitive washing in an attempt to relieve severe distress associated with their fears of contamination. LittleCityLifestylePhotography/E+/Getty Images “We know that when we deliver a therapy continuously, the brain can sort of develop a tolerance to it, and that needs to be changed over time, complicating the therapy,” Casey Halpern , an associate professor of neurosurgery at the University of Pennsylvania who led the study, tells Inverse .
This is where the “responsive” piece of the deep brain stimulation puzzle fits in. Instead of sending electrical signals continuously, responsive deep brain stimulation only stimulates the brain when it picks up certain brain activity. Think of it like a smart thermostat that turns on the heat only when the temperature drops too low. This method of adjusting to the person’s brain activity has been tried before with certain types of epilepsy and depression , so scientists hoped people with treatment-resistant OCD would benefit as well. A smarter deep brain stimulator
For this new study, Halpern and his team worked with a 34-year-old woman with a history of OCD so severe she couldn’t eat around other people out of fear her own food would get contaminated (seafood was one major trigger). She would wash her hands so much to the point of bleeding, and she couldn’t leave her home or go to bed without checking all the doors and windows. The woman’s OCD took up eight hours of her day, and she was unable to live independently. And like other treatment-resistant OCD cases, therapy and medications didn’t seem to help at all.
In 2019, she had a neurostimulation device called a NeuroPace RNS System implanted on top of her skull with electrodes leading into her brain to manage her seizures. After getting the seizures under control, Halpern and his team set to work finding a particular brain signal they could train the implant to recognize. They recorded brain data as the woman went about her day-to-day tasks and in the lab as she interacted, in real life and in virtual reality, with objects meant to provoke her OCD.
Previous studies with deep brain stimulation and people with OCD found a low-frequency brainwave appearing in the basal ganglia — an area of the brain involved in coordinating movement, cognition, and emotion often targeted by stimulation therapies — whenever someone engaged with their obsessions or compulsions.
Halpern and his colleagues came across the same low-frequency electrical activity with the person they were treating for OCD. Specifically, they identified a brain circuit involving the nucleus accumbens, which is part of the basal ganglia associated with motivation and action, and the ventral pallidum, also located in the basal ganglia and is a central hub in the brain’s reward circuits. The researchers called these two regions the NAc-VeP circuit. The researchers recorded brain data while the woman interacted with objects, including those in virtual reality, meant to provoke her OCD. Casey Halpern / University of Pennsylvania After the first day of treatment targeting this circuit whenever it went haywire, Halpern says her patient saw marked improvement in several OCD tendencies, including her urge to check windows and doors at night.
After 24 weeks, according to the study, her patient with OCD reported a […]
Amber Pearson has had a severe form of obsessive compulsive disorder since she was in high school. She would wash her hands so much they became raw and bled. Her bedtime routine easily took 45 minutes because it involved checking that all the doors and windows were closed and the stove was off. She was so afraid of food contamination that she couldn’t eat next to other people. Even on holidays, she ate on the couch away from her family. Therapy and medication didn’t help.
“Every decision I made was based on my OCD. It was always in the back of my mind,” Pearson says.
In her twenties, she developed epilepsy. After suffering a serious seizure that caused her to lose consciousness, her doctors considered treating her with deep brain stimulation, or DBS. The procedure involves surgically implanting a device that delivers electrical pulses to a specific brain region. Scientists think DBS works by resetting abnormal brain circuits, similar to what a pacemaker does for the heart.
DBS has been used for the past three decades to control tremors in people with Parkinson’s disease, and researchers are currently exploring it to restore upper body movement to stroke survivors and as a treatment for some psychiatric disorders . The US Food and Drug Administration permits its use for OCD as a last resort. Pearson wondered if the implant might help treat both of her conditions, so in 2019, she underwent an experimental brain surgery at Oregon Health & Science University.
In a study published this month in the journal Neuron , Pearson’s medical team reported that a single 32-millimeter-long electrode, tuned to detect her unique neural signals, was able to control both. Unlike traditional DBS, which provides constant stimulation, Pearson’s device is a “responsive” one; it only delivers jolts of electricity when it detects irregular patterns in her brain associated with the start of a seizure or compulsive thoughts.
Responsive DBS is already used for epilepsy, but Pearson’s medical team says it’s the first time it’s been used for OCD, as well as to simultaneously treat two conditions.
“This is pretty remarkable,” says Rachel Davis, an associate professor of psychiatry and neurosurgery at the University of Colorado School of Medicine, who researches DBS but was not involved in the new study.
Pearson’s seizures were occurring in a part of the brain called the insula, so her neurosurgeon, Ahmed Raslan, thought he could target a small region there for her epilepsy, plus the ventral striatum, which sits just above and behind the eyes. This contains the nucleus accumbens—an area associated with motivation and action, including compulsive urges. “It was an area that could be targeted with the same electrode,” Raslan says.
The team used a device made by a company called NeuroPace, based in Mountain View, California. Other electrodes used for deep brain stimulation only emit electrical pulses. This one also collects brain signals and delivers electricity only when it is programmed to detect a certain trigger.
First, the Oregon team used the device to get Pearson’s epilepsy under control. Next, Raslan sought out Casey Halpern, an associate professor of neurosurgery at Penn Medicine who is studying the nucleus accumbens as a DBS target for psychiatric conditions. To program the stimulation for Pearson’s OCD, Halpern and his team first needed to figure out what neural trigger they were looking for.
To do this, they needed to know which neural signatures in Pearson’s brain activity corresponded with her experience of obsessive thoughts. As she went about her ordinary life at home, Pearson would swipe a magnet over her head when she felt obsessive thoughts, and her implanted device would time-stamp the moment of each event.
Halpern and his colleagues also worked with Pearson in the lab, intentionally exposing her to items that triggered her OCD. For example, because one of Pearson’s triggers was seafood contamination, the team gave her seafood to handle while monitoring her brain activity as she became distressed.
By analyzing these brain recordings, Halpern was able to identify a unique neural signature in the ventral striatum that corresponded to times when Pearson felt she had to act on her compulsions. “We found that low-frequency oscillations would elevate in power during those moments,” Halpern says. This low-frequency signal was the same whether Pearson was experiencing a distressing situation in the lab or at home.
The researchers programmed her device to only deliver stimulation when it detects this type of brain activity—and only briefly. After a few seconds to a minute, it shuts off. The goal, Halpern says, is to restore normal function to abnormal neural circuits.
Over the next six to eight months, Pearson’s OCD symptoms decreased significantly, and her brain activity triggered the stimulation less often. She told her doctors that before, she was sometimes spending eight hours a day performing compulsions. Now, she estimates that it’s more like 30 minutes. The effects have persisted over the two years since the stimulation has been turned on. “It wasn’t instantaneous. It took a few months to notice changes,” she says. “I slowly started noticing things disappearing from my routine. Then, more things would disappear.”
Pearson doesn’t wash her hands as often, and now her knuckles don’t bleed. Her bedtime routine takes just 15 minutes. The best part, she says, is that her relationships with her friends and family are a lot better. She can enjoy a meal with them without feeling distressed.
“What this highlights is that OCD is a disorder of the brain, just like epilepsy and Parkinson’s,” Halpern says. “This isn’t a disorder of will. There’s a pathological signal that we’re seeing in the brain.”
Davis says she was initially skeptical of the idea that OCD could be treated with occasional bursts of stimulation. “Often people with OCD have a baseline level of dread or anxiety,” she says. For that reason, she assumed patients would need constant stimulation to keep their brain circuits regulated. Her center has implanted nine OCD patients with traditional DBS devices that provide steady stimulation. Although the Neuron report is just one case study, she thinks it’s impressive that Pearson’s symptoms […]
Laughter has many proven benefits, especially for your lungs, heart, immune system and mental health. According to a new study by researchers in Brazil, laughter provides substantial benefits to people with heart disease as it could significantly boost their cardiovascular function .
The study’s remarkable findings were presented at the annual meeting of the European Society of Cardiology – the world’s largest heart conference – in Amsterdam last August. What laughter can do for your heart
Having a sense of humor is good for your heart. When you laugh, you don’t just increase your oxygen intake, which is great for your lungs, you also provide exercise for your heart. And people whose hearts are weakened by heart disease can greatly benefit from this cardio exercise. (Related: Walking 8,000 brisk steps once or twice a week found to boost heart health .)
Marco Saffi, a professor from the Hospital de Clínicas de Porto Alegre in Brazil who led the study, told the Guardian : “Our study found that laughter therapy increased the functional capacity of the cardiovascular system. Laughter therapy could be implemented in institutions and health systems like the NHS [National Health System of the UK] for patients at risk of heart problems.”
Saffi and his team conducted their study to find out if laughter therapy, a non-invasive, non-pharmacologic and easily implementable intervention , can improve cardiovascular health and reduce common symptoms of heart disease, which include a reduced ability of the heart to pump oxygen throughout the body and an impaired capacity of the arteries to expand.
The Brazilian researchers recruited 26 adults with an average age of 64 for their 12-week experiment. All the participants have been diagnosed with coronary artery disease (CAD), a condition caused by the accumulation of plague in the arteries that supply blood to the heart.
The researchers divided the participants into two groups, one of which was tasked to watch comedy programs every week for three months while the other watched serious documentaries about Nature or politics.
The study found that the participants who were assigned to watch comedy programs showed improvement in their cardiovascular function, as evidenced by a 10 percent increase in the amount of oxygen their hearts were able to pump into their bodies. Their arteries’ ability to dilate also improved after 12 weeks of laughter therapy.
Before and after the experiment, the researchers took blood samples from the participants to check their levels of inflammatory biomarkers and how much plaque is deposited in their arteries. Comparison of blood analysis results showed that those who received laughter therapy had greatly reduced inflammatory biomarkers at the end of the study, which meant that their risks of heart attack and stroke also went down .
“When patients with coronary artery disease arrive at [a] hospital, they have a lot of inflammatory biomarkers. Inflammation is a huge part of the process of atherosclerosis when plaque builds up in the arteries,” Saffi explained.
“This study found that laughter therapy is a good intervention that could help reduce that inflammation and decrease the risk of heart attack and stroke.” (Related: Do these exercises in the morning to boost your heart function and reduce your risk of heart disease and stroke .)
Saffi and his team believes that the cardiovascular improvements brought about by laughter therapy may have something to do with the increase in endorphins released by the brain. Endorphins are the “feel-good” chemicals released during pleasurable activities , such as exercise, eating and having sex. These happy hormones also help lower blood pressure and decrease the strain on your heart by reducing the levels of stress hormones like cortisol.
Because of their promising findings, Saffi and his team are optimistic about the prospect of laughter therapy becoming a widely implemented intervention for heart disease in the future. Saffi thinks it could also help reduce the dependence of heart disease patients on pharmaceutical medications, which cause unfavorable side effects. But more and larger studies are needed to validate their findings.
Laughter therapy is not just limited to TV programs. You can enjoy the benefits of laughter by hanging out with your friends and doing fun activities with your family and loved ones. Saffi recommends doing things that can make you laugh at least twice a week for best results. Other health benefits of laughter
A good laugh can provide plenty of short-term health benefits . For instance, laughing can stimulate your lungs, heart and muscles, and helps cool down your stress response. It can also increase then decrease your heart rate and blood pressure, leaving you with a pleasant, relaxed feeling afterward.
Laughing also helps relax the muscles of your body and promotes good blood circulation. In fact, a hearty laugh can leave your muscles relaxed for a good 45 minutes after . Thanks to these effects, laughter is the best natural medicine for stress and can help reduce some of its physical symptoms.
Frequent laughter also offers some amazing long-term benefits. According to psychiatrist Dr. William Fry, a professor at Stanford University , “mirthful laughter” markedly enhances your body’s resistance to illness . Research shows that people who laugh often tend to release more T cells from the spleen into the bloodstream. T cells are a type of immune cells whose functions include activating other immune cells, killing infected cells and regulating your immune response.
Laughter also promotes a positive mood via the release of more endorphins, which can help fight stress, anxiety and depression. This has the added benefit of improving your self-esteem and increasing your pain tolerance. (Related: Not all pain should be treated with NSAIDs .)
A study by Swiss researchers found that people who are laughing are able to keep their hands submerged in ice water longer than people who are not. This increased tolerance to pain remained 20 minutes after the participants had stopped laughing. The researchers attributed this effect to the release of endorphins and the reduction in muscular tension. This finding shows that laughter therapy could also help people who are suffering from chronic pain.
Laughter is one of the best […]
The first-line pharmacological treatment for major depressive disorder (MDD) is antidepressant drugs known as selective serotonin reuptake inhibitors (SSRIs). However, a significant proportion of people don’t respond to these drugs.
Given that major depression is a global mental health problem that is on the r ise, it is important to find novel pharmacological treatments for those who do not respond to the current ones. But to do that, we need to understand exactly how the drugs work – which we currently don’t.
MDD is a debilitating and distressing mental health disorder, trapping sufferers in a rigid and negative state of mind. There’s even evidence suggesting that this lack of flexibility is associated with cognitive changes , including negative thoughts and biases and problems with learning and memory.
In our new study, published in Molecular Psychiatry , we show that an SSRI called ecitalopram may actually make brains more “plastic” — meaning more flexible and adaptive, more able to facilitate communication between neurons (brain cells). Brain plasticity is simply the ability of neural circuits to change through growth and reorganization. Learning involves brain plasticity, including changes in neural circuits, and can help people to recover from depression.
One novel treatment option for depression, approved by the US Food and Drug Administration, is intranasal esketamine (an anesthetic made from ketamine), although it has not as yet been approved for use by the NHS. The psychedelic drugs LSD and psilocybin are also being investigated for treatment-resistant depression in research studies but are not yet approved by regulatory bodies. When these studies are conducted, there is careful monitoring by a medical professional to ensure participant safety.
We know that both SSRIs and psychedelics target the same brain receptor (known as the 5HT-2A). By contrast, eskatamine, similar to ketamine, works on a different receptor (N-methyl-D-aspartate or NMDA) and affects the brain’s chemical glutamate.
So, how do SSRIs and psychedelics work to reduce symptoms of depression? At present, we don’t have the full picture. However, the 5HT-2A receptor is linked to the brain chemical serotonin, increasing levels of it in the brain. And a recent study has indeed shown that serotonin appears to be reduced in people with depression.
SSRIs, however, also affect the neurotransmitters GABA and glutamate. The latter has been linked to learning, cognition, and memory – suggesting SSRI may actually help to restore cognitive function . Although the exact mechanisms of psychedelics are not yet fully understood, their antidepressant effects seem to work in a similar way to SSRIs, given their effects on 5HT-2A receptors. However, there are also other reactions to psychedelics, such as hallucinations. Measuring brain plasticity
All these drugs have, therefore, been suggested to affect brain plasticity. However, in humans, it can be difficult to estimate levels of brain plasticity. One common method that scientists have used is to measure a protein called the brain-derived neurotrophic factor (BDNF) in blood samples.
BDNF helps brain plasticity by increasing the number of synapses (locations where neurons can communicate with each other), as well as the branches and growth of developing neurons. Synapses are particularly important in brain functioning as they allow the transmission of chemical and electrical signals from one neuron to another. Similarly, synapses also store brain chemicals for release.
There have been some studies showing that antidepressant drugs increase BDNF. However, better techniques are required to study plasticity in the human brain.
One approach to developing better drugs is to find antidepressant drugs with a faster mechanism of action. According to the NHS website, SSRIs usually need to be taken for two to four weeks before any benefit is felt.
We suspected that one reason for this delayed effect may be that brain plasticity needs to occur with SSRI treatment. As this process involves rewiring, such as the creation of synapses and circuits, it isn’t instant but is thought to take approximately 14-21 days.
In our study, which was a collaboration between the University of Cambridge and the University of Copenhagen, we used a novel technique to measure plasticity in the human brain following SSRI treatment for the first time.
Thirty-two participants underwent positron emission tomography (PET) scanning to detect the amount of a protein called “synaptic vesicle glycoprotein 2A”, or SV2A, in the brain. We know that SV2A is a marker of the presence of synapses. An increased amount would suggest that more synapses are present and, therefore, that brain plasticity is higher.
Our results showed a rise in this protein as a result of taking escitalopram (an SSRI). We found that, in those taking escitalopram, increased SV2A was associated with increased duration of the drug. Our findings suggest that brain plasticity increases over three to five weeks in healthy humans following daily intake of escitalopram.
This is the first real evidence in humans that SSRIs really do boost neuroplasticity – seen in the brain – and that this is one of the reasons it can treat depression. Similar evidence from studies in the human brain is still required for psychedelics.
It makes sense that if antidepressant treatment facilitates brain plasticity, this should make it easier for people taking these treatments to learn new things. We know that the ability to adopt new strategies and change them if they don’t work (supported by what researchers call cognitive flexibility) is key to recovering from depression .
This article was originally published on The Conversation by Barbara Jacquelyn Sahakian and Christelle Langley at the University of Cambridge. Read the original article here .