Learn about brain health and nootropics to boost brain function
The 1 food you should eat for brain health — and why you can’t replace it with supplements
Leafy greens are packed with chlorophyll, which is a great source of nutrition. A neurologist says there’s a lot you can do for your brain health through small dietary changes.
The first tip he recommends is eating more leafy greens, like spinach and kale.
The nutrients that help plants grow up healthy and green are also good for our brains.
Dean Sherzai, a neurologist and dementia researcher, has a favorite study.
Published in 2018 , and funded by the National Institute on Aging, the blockbuster study — which examined the eating patterns of over 900 older adults living around Chicago — showed that those who ate about one or two cupfuls of salad greens a day, including spinach, kale, collards, and lettuce, had brains that performed about 11 years younger than their lettuce-less peers of the same age.
“Just add green,” Sherzai, half of the husband-and-wife team who call themselves ” The Brain Docs ,” told me when I asked what single change I could make today to stave off neurodegenerative diseases. Doctors Dean and Ayesha Sherzai call themselves “The Brain Docs”Courtesy of The Brain Docs “If you have to start one place, because there’s only so much space in your stomach, add two servings of greens to your diet,” he told Business Insider. With that, “you’ve significantly reduced inflammation, oxidation, glucose dysregulation, and lipid dysregulation,” which are all hallmarks of many age-related diseases.
Sherzai knows it’s tempting to reach for a novel, quick-fix potion that promises to boost brain health , like a fancy supplement, an expensive gummy, or a new smoothie powder. But what he’s discovered, after decades of research, is that some of the “most profound” ways we can influence our own cognitive health are the most old-school.
Our thirst for novelty may be steering us in the wrong direction, away from seeing the truly phenomenal chemical properties of greens. If there is anything like a silver bullet ingredient for your brain, it’s more likely to be the cocktail of nutrients quietly sitting inside bright green leaves, helping them grow. Why chlorophyll from plants is more powerful than green juices and supplements
Lots of chlorophyll on the table here.fcafotodigital/Getty Images When we eat green plants, we are consuming a green pigment molecule called chlorophyll, which helps plants photosynthesize — capturing solar rays and converting them into energy to grow.
Chlorophyll is green because red and blue light from the sun gets taken in and absorbed by the plant for energy. Green light is what’s left over, and what gets reflected back to us visually. And it turns out that those green chlorophyll molecules are packed with a rich bounty of nutrients including iron, magnesium, and nitrogen — ingredients that are fundamental for life, whether it’s a plant’s or a person’s.
Wellness brands have tried to harness this natural dream team combo by putting it in supplements and things like chlorophyll water. But because chlorophyll is so unstable, they often have to take out the magnesium and add in other elements like copper or zinc instead. Experts say it’s unclear whether those industrial versions of chlorophyll could have much of a health benefit at all. What we do know is that you can get the health benefits if you consume chlorophyll in its original packaging. In other words: eat more leaves.
“The chlorophyll itself is maybe not that useful,” Troy Magney, an associate professor focused on plant optics at the University of California, Davis, told Business Insider, reflecting the fact that there is no solid research to support chlorophyll supplementation.
Rather, it’s the chemical “building blocks” of chlorophyll molecules in the leaves we eat that likely help us humans thrive, Magney said. Crack open that dusty chemistry textbook, and you’ll discover many of the various atomic components of the chlorophyll molecule, as well as other ingredients necessary for proper plant metabolism and growth, are great human health boosters.
“Things like iron and magnesium and nitrogen and these nutrients that all are necessary for chlorophyll,” Magney explained.
Magnesium is an essential element for our muscles, nerves, bones, and blood sugar — and roughly half of us aren’t getting enough of it. Iron plays a key role in carting fresh oxygen around our body, while nitrogen helps us grow, and keeps our brain and immune system strong.
People who eat more leafy greens also take in decent amounts of other nutrients including vitamin K, folate, lutein, and beta-carotene. Experts think these nutrients — all present thanks to the bright pigments in the leaves — may work together synergistically in ways that can protect our brains. We know already that they’re great for curbing inflammation, improving eyesight, and protecting DNA. Darker leaves have more nutrients in each bite
Kale is a favorite of The Brain Docs.Galina Oleksenko/Getty Images Sherzai recommends incorporating more of the darkest green plants like spinach and kale into your diet when you can.
“The darker the better,” he said.
That’s because darker greens have, by default, more chlorophyll packed inside of them, and thus more nutrition in every bite.
“There’s more nutrients required to produce more chlorophyll,” Magney said. “So there’s a higher density of these compounds in the leaf itself.”
It’s also a good idea to consume your plants as fresh as possible. When leafy greens start to go bad and turn yellow in your fridge, that’s good evidence that they’re losing some of the green chlorophyll they created while they were growing.
“Those yellow pigments are always there, but we can’t actually see them because the chlorophylls are so intense, they kind of overwhelm the yellow pigments,” Amber Flores, a Ph.D. candidate in plant biology at UC Davis, told BI. “Once the chlorophyll starts to degrade as the leaf begins to senesce, or to die, we start to see the yellows come out.”
There may still be some beneficial carotenoid pigments tucked into those yellowing leaves (and they are great for eye health) but in general, a wilting leaf is becoming less and less nutritious than it used to be.
So look for the very freshest lettuce […]
Neuroscientists discover brain circuitry of placebo effect for pain relief
by University of North Carolina Health Care This image shows that the cells in yellow in the pons (left) receive input from the green cells in the cingulate cortex (rACC, right), with subdivisions Cg1 and Cg2. Credit: Scherrer Lab, UNC School of Medicine The placebo effect is very real. This we’ve known for decades, as seen in real-life observations and the best double-blinded randomized clinical trials researchers have devised for many diseases and conditions, especially pain. And yet, how and why the placebo effect occurs has remained a mystery. Now, neuroscientists have discovered a key piece of the placebo effect puzzle.
Publishing in Nature , researchers at the University of North Carolina School of Medicine—with colleagues from Stanford, the Howard Hughes Medical Institute, and the Allen Institute for Brain Science— discovered a pain control pathway that links the cingulate cortex in the front of the brain , through the pons region of the brainstem, to cerebellum in the back of the brain.
The researchers, led by Greg Scherrer, PharmD, Ph.D., associate professor in the UNC Department of Cell Biology and Physiology, the UNC Neuroscience Center, and the UNC Department of Pharmacology, then showed that certain neurons and synapses along this pathway are highly activated when mice expect pain relief and experience pain relief, even when there is no medication involved.
“That neurons in our cerebral cortex communicate with the pons and cerebellum to adjust pain thresholds based on our expectations is both completely unexpected, given our previous understanding of the pain circuitry, and incredibly exciting,” said Scherrer. “Our results do open the possibility of activating this pathway through other therapeutic means, such as drugs or neurostimulation methods to treat pain.”
Scherrer and colleagues said research provides a new framework for investigating the brain pathways underlying other mind-body interactions and placebo effects beyond the ones involved in pain. The placebo paradox
It is the human experience, in the face of pain, to want to feel better. As a result—and in conjunction with millennia of evolution—our brains can search for ways to help us feel better.
It releases chemicals, which can be measured. Positive thinking and even prayer have been shown to benefit some patients. And the placebo effect —feeling better even though there was no “real” treatment—has been documented as a very real phenomenon for decades.
In clinical research , the placebo effect is often seen in what we call the “sham” treatment group. That is, individuals in this group receive a fake pill or intervention that is supposed to be inert; no one in the control group is supposed to see a benefit. Except that the brain is so powerful and individuals so desire to feel better that some experience a marked improvement in their symptoms.
Some placebo effects are so strong that individuals are convinced they received a real treatment meant to help them.
In fact, it’s thought that some individuals in the “actual” treatment group also derive benefit from the placebo effect. This is one of the reasons why clinical research of therapeutics is so difficult and demands as many volunteers as possible so scientists can parse the treatment benefit from the sham.
One way to help scientists do this is to first understand what precisely is happening in the brain of someone experiencing the placebo effect. Enter the Scherrer lab
The authors of the Nature paper knew that the scientific community’s understanding of the biological underpinnings of pain relief through placebo analgesia—when the positive expectation of pain relief is sufficient for patients to feel better—came from human brain imaging studies, which showed activity in certain brain regions.
Those imaging studies did not have enough precision to show what was actually happening in those brain regions. So Scherrer’s team designed a set of meticulous, complementary, and time-consuming experiments to learn in more detail, with single nerve cell precision, what was happening in those regions.
First, the researchers created an assay that generates in mice the expectation of pain relief and then a very real placebo effect of pain relief. Then the researchers used a series of experimental methods to study the intricacies of the anterior cingulate cortex (ACC), which had been previously associated with the pain placebo effect.
While mice were experiencing the effect, the scientists used genetic tagging of neurons in the ACC, imaging of calcium in neurons of freely behaving mice, single-cell RNA sequencing techniques, electrophysiological recordings, and optogenetics—the use of light and fluorescent-tagged genes to manipulate cells.
These experiments helped them see and study the intricate neurobiology of the placebo effect down to the brain circuits, neurons, and synapses throughout the brain.
The scientists found that when mice expected pain relief, the rostral anterior cingulate cortex neurons projected their signals to the pontine nucleus, which had no previously established function in pain or pain relief. And they found that expectation of pain relief boosted signals along this pathway.
“There is an extraordinary abundance of opioid receptors here, supporting a role in pain modulation,” Scherrer said. “When we inhibited activity in this pathway, we realized we were disrupting placebo analgesia and decreasing pain thresholds. And then, in the absence of placebo conditioning, when we activated this pathway, we caused pain relief.”
Lastly, the scientists found that Purkinje cells—a distinct class of large branch-like cells of the cerebellum—showed activity patterns similar to those of the ACC neurons during pain relief expectation. Scherrer and first author Chong Chen, MD, Ph.D., a postdoctoral research associate in the Scherrer lab, said that this is cellular-level evidence for the cerebellum’s role in cognitive pain modulation.
“We all know we need better ways to treat chronic pain, particularly treatments without harmful side effects and addictive properties,” Scherrer said. “We think our findings open the door to targeting this novel neural pain pathway to treat people in a different but potentially more effective way.”
More information: Grégory Scherrer, Neural circuit basis of placebo pain relief, Nature (2024). DOI: 10.1038/s41586-024-07816-z . www.nature.com/articles/s41586-024-07816-z
Provided by University of North Carolina Health Care
One-dose nasal spray clears toxic Alzheimer’s proteins to improve memory
A nasal spray clears away toxic tau tangles and improves memory One dose of a new treatment, delivered by nasal spray, clears away build-ups of the toxic tau protein associated with Alzheimer’s disease from inside brain cells, improving memory, according to new research. It paves the way for new treatments for the debilitating disease.
A few years ago, abnormal clumps of tau proteins in the brain were found to be associated with Alzheimer’s disease . Since then, researchers have been working on a way of eradicating these toxic tangles, which have become a hallmark of the degenerative disease.
Now, researchers from the University of Texas Medical Branch (UTMB) have developed a breakthrough nasal spray containing antibodies that selectively target and clear away tau tangles, helping to restore cognitive function.
“This nasal spray approach opens new avenues for non-invasive delivery of tau therapeutic antibodies directly to the brain, and it holds promise for many neurogenerative diseases,” said Dr. Rakez Kayed, professor at the Department of Neurology at UTMB and the study’s corresponding author. “Our research highlights the potential of nasal tau immunotherapy to effectively target intracellular tau aggregates – a primary driver of neurodegeneration and cognitive decline in diseases like Alzheimer’s and other tauopathies.”
In healthy brains, tau proteins stabilize microtubules, which provide the scaffolding for cells and help transport nutrients. But when these proteins misfold, they can clump together into neurofibrillary tangles that disrupt the function of neurons and contribute to cognitive decline. Previous research found that disease progression occurs through a ‘seeding’ mechanism, where toxic tau seeds are released from the cell into the extracellular environment, where they propagate.
One of the major hurdles that tau-targeting treatments must overcome is targeting intracellular tau – the tau that remains inside cells and is responsible for seeding – which is something that existing immunotherapies don’t do overall. Another is crossing the blood-brain barrier (BBB), a protective barrier between the brain’s blood vessels and the cells and other components that make up the brain tissue.
The researchers’ novel therapy achieves both. Their toxic tau conformation-specific monoclonal antibody 2 (TTCM2) specifically detects and targets disease-relevant tau aggregates. Loaded into micelles, aggregates of molecules that are both water-loving (hydrophilic) and fat-loving (lipophilic), that are delivered intranasally means the treatment quickly arrives in the brain via the nose-to-brain anatomical pathway, bypassing the BBB completely. Nose-to-brain pathway for inhaled drugs A single dose of TTCM2 was administered intranasally to aged mice that had been genetically altered to express human tau. After three hours, TTCM2 was distributed to various brain regions, including the regions’ intracellular compartments, where it cleared “seed-competent” intracellular tau aggregates and tau on the synaptic connections between neurons in the brain.
When they were subjected to behavioral testing, TTCM2-treated mice performed “markedly better” than other cohorts, suggesting that the treatment alleviated short-term memory loss in mice with advanced tau aggregates. The researchers also noticed an increase in biomarkers in the hippocampus, the region of the brain associated with memory formation and cognitive functioning. Crucial to the therapy, the researchers found, was TTCM2’s engagement with TRIM21, an intracellular (inside the cell) antibody receptor, which facilitated the clearance of antibody-bound tau aggregates.
“This method not only improves the delivery of therapeutic antibodies but also enhances their efficacy in clearing tau aggregates and improving cognitive functions,” Kayed said.
The discovery has great potential as a treatment for Alzheimer’s disease and other neurodegenerative diseases caused by a pathological buildup of tau protein.
“This advancement could significantly impact the treatment strategies for Alzheimer’s and related tauopathies, offering new hope for millions of patients suffering from these debilitating conditions,” said Sagar Gaikwad, the study’s first author and a postdoctoral fellow at UTMB.
The researchers plan to continue with preclinical trials of TTCM2 with a view to moving to human trials. Their goal is to translate these promising results into viable treatment options.
The study was published in the journal Science Translational Medicine .
Source: UTMB
Cognitive benefits from high intensity interval training may last for years
Vigorous exercise may have lasting brain benefits, a study suggests. Catherine Ivill/Getty Images The brain is a delicate organ that experiences specific changes with age. Older individuals tend to be at a higher risk for developing dementia.
Researchers are interested in finding what interventions can delay dementia or even improve cognitive function.
A recent study found that high-intensity interval training, or HIIT, in older adults may help improve hippocampal function and help retain this improvement years after the intervention.
Exercise offers multiple health benefits, and researchers are particularly interested in discovering how it affects the brain function of older adults.
A recent study published in Aging and Disease examined three levels of exercise among healthy older adults and how these interventions affected the functioning of the hippocampus , an area of the brain critical to memory consolidation. Researchers found that participants who engaged in high intensity interval training (HIIT) saw improvement in hippocampal function. They also found that they still saw the improvement up to five years after the start of the intervention. How does aging affect dementia risk and the hippocampus?
As people age, some changes occur in the brain, and older adults may find certain activities, like paying attention, slightly harder. They may also take longer to learn new skills.
Older adults are also at a higher risk for dementia , making preventive measures and interventions all the more critical in this age demographic. Researchers of the current study note that age can affect the hippocampus. The hippocampus is a critical part of the brain that assists with memory processing, decision making, and conversion of short-term memories into long-term memories. Alzheimer’s disease, a common dementia type, also affects the hippocampus.
Thus, examining how interventions affect this area of the brain could be highly beneficial in addressing cognitive decline in older adults and possibly preventing dementia . “A key feature of aging dementia is the decline in specific domains of cognitive function, especially those related to spatial learning and memory. The hippocampus is a critical region of the brain that is responsible for the consolidation of spatial information into memories and is particularly susceptible to age, with reports of age-dependent decreased hippocampal volume and connectivity.”
– Study authors Non-study author Dr. Michele Longo, MD , a neurologist at University Medical Center New Orleans, offered the following insight to Medical News Today : “Exercised-mediated responses of biomarkers as predictors for improved hippocampal functional outcomes offers a quantifiable metric to provide an effective exercise regimen. The improvement and long-term retention of hippocampal learning ability following HIIT exercise provides a new insight into how the elderly could be insulated from cognitive decline even though their exercise capabilities may decline with advanced age. This approach could greatly enhance the capacity of clinicians to tailor personalized exercise paradigms, including those at risk of cognitive decline.” Can exercise help improve brain function?
This study was a multidomain, randomized control study. Researchers recruited 194 participants between 65 and 85 years old. They excluded participants who had experienced a stroke, brain trauma , or brain or heart surgery and anyone who was at high risk for experiencing a cardiac event like a heart attack during exercise. Participants did not have diagnosed mental illnesses or cognitive decline at baseline.
Participants were divided into three groups to undergo different levels of exercise intensity:
> Low-intensity training, which included activities like stretching, range of motion, and balance exercises
Medium-intensity training, which was continuous treadmill walking
High-intensity training, which included intervals of treadmill work with a more significant increase in heart rate than the medium-intensity training group
The high-intensity training group further combined aerobic and anaerobic exercise.
Participants underwent exercise programs, exercising three days a week for six months under supervision from exercise physiologists. Researchers had participants undergo a number of tests to examine cognitive and hippocampal function, such as the hippocampal-dependent paired associated learning (PAL) test. They also collected monthly blood samples from participants to gain valuable biomarker information.
Researchers conducted cognitive tests monthly during the intervention and followed up with participants every six months afterward for up to five years. How does exercise intensity affect cognitive improvement?
The study’s results found that the high-intensity interval training group experienced an improvement in hippocampal-dependent spatial learning. The other two groups remained stable rather than showing improvement. This improvement was maintained in the high-intensity interval training group during the five-year follow-up. It appeared to be unrelated to lifestyle and physical activity differences during the follow-up.
Researchers also found that participants who initially performed poorly on PAL assessment initially showed the most improvement if they were part of the high-intensity interval training group. Poor performance participants in the medium-intensity training group also experienced some improvement in these assessments, but less than the high-intensity interval training group. They also found that the high-intensity interval training group had a stable right-hand side hippocampal volume, while the other groups experienced a decrease in this brain area.
With additional brain regions, researchers found the structures to be in better condition in the high and medium-intensity groups than in the low-intensity group. They also observed “improved functional connectivity between multiple neural networks” in the high-intensity interval training group. However, at the 12-month mark, researchers did not observe functional connectivity improvement between network pairs compared to the baseline in any of the groups.
They also observed that changes in certain biomarkers in the high-intensity interval training group correlated with improved associated learning. Researchers did not find that exercise interventions helped improve working memory or emotional recognition.
The results point to the potential brain benefits of exercise, particularly for those engaging in high-intensity interval training.
Non-study author Ryan Glatt, CPT, NBC-HWC , senior brain health coach and director of the FitBrain Program at Pacific Neuroscience Institute in Santa Monica, CA, noted the following clinical implications of the data to Medical News Today : “The study suggests that high-intensity interval training (HIIT) can significantly improve hippocampal-dependent learning in healthy older adults. While promising, the results should be interpreted cautiously due to potential variability in individual responses […]
Trump has long been a skeptic of childhood vaccines, leaked video with RFK Jr. reveals
Tags: 2024 elections , badhealth , badmedicine , badscience , big government , Big Pharma , childhood vaccinations , Dangerous Medicine , Donald Trump , pharmaceutical fraud , presidential elections , rational , Robert F. Kennedy Jr. , skeptics , truth , vaccine damage , vaccine injury , vaccine wars , vaccines , Vote Republican , White House A leaked video of independent presidential candidate Robert F. Kennedy Jr. talking on the phone with former President Donald Trump about the latter’s skepticism of the efficacy and safety of childhood vaccines recently went viral.
The footage is a little over one minute and 40 seconds long, where Kennedy is seen standing close to an American flag in a dimly lit room, holding a phone and listening to Trump on speaker. In the since-deleted footage, Trump can be heard saying, “I agree with you, man. Something’s wrong with that whole system and it’s the doctors you find. Remember I said, ‘I want to do small doses.'”
“When you feed a baby, Bobby, a vaccination that is like 38 different vaccines, and it looks like it’s meant for a horse, not a, you know, 10-pound or 20-pound baby… and then you see the baby all of a sudden starting to change radically. I’ve seen it so many times,” Trump continued. “And then you hear that it doesn’t have an impact, right? But you and I talked about that a long time ago.”
Trump and Kennedy are political rivals who have occasionally criticized each other during the campaign. But the clip is said to have been recorded on July 14, a day before the two saw each other in Milwaukee, Wisconsin. This stoked speculations that Kennedy might be about to exit the race and endorse Trump.
“I would love you to do something,” Trump can be heard saying. “And I think it’ll be so good for you and so big for you. And we’re going to win.” Kennedy then answered: “Yeah.”
A lot of people received the news with optimism, citing a possibility that Kennedy would be a member of Trump’s cabinet as soon as he assumed office. However, Kennedy spokeswoman Stefanie Spear said that he was not dropping out. (Related: RFK Jr. confirms meeting with Trump but firmly denies any plans to withdraw and endorse former POTUS .)
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The leaked footage shows that Trump holds to a stance of skepticism about childhood vaccination that he was publicly known for before the Wuhan coronavirus (COVID-19) jabs rollout under his administration’s Operation Warp Speed. Politico revealed that the said project was the brainchild of Health and Human Services Secretary Alex Azar, “who was often at odds with the White House.”
His advisory board included National Institutes of Health Director Francis Collins and National Institute of Allergy and Infectious Diseases Director Anthony Fauci and his plan won the support of White House senior adviser Jared Kushner as well as White House Chief of Staff Mark Meadows.
Trump was criticized in 2017 for a statement he made in 2015 linking vaccines to autism: “People that work for me, just the other day, two years old, a beautiful child went to have the vaccine and came back and a week later, got a tremendous fever, got very, very sick, now is autistic.”
In 2014, Trump tweeted, “Healthy young child goes to the doctor, gets pumped with massive shot of many vaccines, doesn’t feel good and changes – AUTISM. Many such cases!”
Meanwhile, Kennedy is known for vehemently opposing vaccines, a stance he adopted after the mothers of vaccine-injured children implored him to look into the research linking thimerosal to neurological injuries, including autism. He founded Children’s Health Defense, an organization with the stated mission of “ending childhood health epidemics by eliminating toxic exposure,” largely through vaccines. Kennedy apologizes to Trump for video leak
Kennedy’s son, Bobby Kennedy III, was the one who posted the said video. The independent presidential candidate has already apologized to Trump that the private phone call had been exposed. The younger Kennedy said he just wanted to expose Trump’s “real opinion” on immunizations, but he immediately deleted the clip.
“When President Trump called me, I was taping with an in-house videographer . I should have ordered the videographer to stop recording immediately. I am mortified that this was posted. I apologize to the president,” Kennedy tweeted on X.
In posting the recording, Bobby suggested Fauci should be in prison and appeared to suggest his father should have been Trump’s running mate on a “unity ticket” rather than “JD ‘fire all the unvaccinated nurses’ Vance.” He also implied Republicans and Democrats were subordinate to Pfizer, a multinational vaccine producer. Kennedy III added: “This is not a cheapfake or somebody doing a Trump voice. This is the real deal.”
Spear claimed that the meeting in Milwaukee was to discuss national unity and that Kennedy hopes to meet with leaders of the Democratic Party as well.
Head over to Kennedy.news to read more stories involving independent presidential candidate Robert F. Kennedy Jr.
Watch the video below of the Kennedy-Trump phone call that was leaked where the two discussed the efficacy and safety of childhood vaccines.
This video is from Dustin Nemo’s channel on Brighteon.com . More related stories:
Elizabeth Nickson: How “mind-numbingly privileged from birth” Robert F. Kennedy Jr.’s “green” agenda destroyed British Columbia .
RFK Jr. supports ABORTION “even if it’s full term”: Decision should be left to the mother rather than the state, he says .
RFK Jr. slams GUILTY verdict on Trump, calls it a blow to democracy and the Democratic Party .
Trump calls RFK Jr. after assassination attempt, talks about vaccine injuries: WATCH . Sources include:
LifeSiteNews.com
BBC.com
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See How the Brain Responds to Psychedelic ‘Magic Mushrooms’
A heat map of brain activity shows stable patterns before and after taking psilocybin in blue and green, while temporary changes are shown in red, orange and yellow. Sara Moser via Washington University School of Medicine in St. Louis The psychedelic drug psilocybin—the active agent in so-called magic mushrooms—causes profound, temporary changes in a network of brain areas involved in introspective thinking, according to a new study published last week in Nature that imaged the brains of people given the drug.
The findings could provide insight into the potential therapeutic effects of psychedelics, a field that’s been gaining notoriety in recent years.
“Psilocybin, in contrast to any other drug we’ve tested, has this massive effect on the whole brain that was pretty unexpected,” Nico Dosenbach , a co-author of the study and neurologist at Washington University, tells the New York Times ’ Andrew Jacobs. “It was quite shocking when we saw the effect size.”
Prior studies have also found that psilocybin disrupts brain networks, but the new research “provides a deeper resolution and insight into the nature of that disruption,” Brian Mathur , a neuroscientist at the University of Maryland who did not contribute to the findings, says to Nature News ’ Max Kozlov.
Using psilocybin can create a disorienting effect , stimulate intense emotions and cause people to temporarily lose their sense of time and space. Researchers are looking into how psilocybin could be used to treat substance use disorders and other mental illnesses. A leading idea suggests the psychedelic compound can improve the brain’s ability to form new neural connections, known as neuroplasticity—which may encourage new perspectives or disrupt harmful patterns of thought.
In previous clinical trials, a single dose of psilocybin has led to rapid and sustained improvement in symptoms of depression , addiction and end-of-life anxiety . Research has also found the drug can change the brains of animals, such as mice and cats . But it’s unclear how the experiences induced by the drug are connected to changes in the human brain, the study authors write.
For the new research, scientists tracked changes in the brains of people who had taken psilocybin using functional magnetic resonance imaging (fMRI). Seven healthy adults received a total of around 18 scans each before, during and for three weeks after receiving a high dose of psilocybin. And, one to two weeks apart from the psilocybin dose, participants received a dose of methylphenidate, the generic form of Ritalin, which served as a control. The researchers also brought four participants back for another dose of psilocybin 6 to 12 months later. Psilocybin’s powerful short- and long-term effects on your brain are revealed by this intrepid precision imaging drug trial published in @Nature . As one of the scientists I was also a study volunteer. Spending hours in an MRI scanner, while tripping on 25 mg was the experience… https://t.co/H0PCxi7Q65 pic.twitter.com/kFL8sP1Nx0 — Nico Dosenbach (@ndosenbach) July 18, 2024 The psilocybin disrupted a set of brain areas called the default mode network that are active when the brain isn’t focused on a particular thing, according to a statement from Washington University. Scientists have found that these neurons may play a role in developing one’s sense of self. With psilocybin, neurons in that network started firing chaotically.
“I’ve never seen an effect this strong,” Shan Siddiqi , a psychiatric neuroscientist at the Harvard School of Medicine who was not involved in the research, says to Nature News .
“The activity in these networks became much more disorganized, and boundaries between the networks essentially evaporated,” Joshua Siegel , first author of the study and a neuroscientist at Washington University, tells the New York Times .
Compared to the control, psilocybin had a three times greater impact on the disorganization of this network.
Once the acute effects of the drug wore off, neurons in the default mode network settled down and resynchronized. But some small changes in the brain didn’t revert to normal for weeks, per the statement. As such, the study indicates psilocybin produces significant but temporary changes in the brain, especially in these areas involved with introspection.
Bertha Madras , a psychobiologist at Harvard Medical School who did not contribute to the findings, tells Medscape Medical News ’ Patrice Wendling that the paper’s sample size is “excruciatingly small for trying to understand brain changes.”
“We had a small number of people, just seven participants in the whole study, but an enormous amount of data on each one,” Siegel says to Science News ’ Laura Sanders.
Currently, psilocybin is not approved by the Food and Drug Administration as a treatment for any condition, the statement notes. Certain states, however, have legalized the drug for use in a supervised environment.
“The results paint a more complex and nuanced picture for how psychedelics change neural activity dynamics than previously thought,” Alex Kwan , a neuroscientist at Cornell University who wasn’t involved in the study, says to Science News .
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Will Sullivan is a science writer based in Washington, D.C. His work has appeared in Inside Science and NOVA Next .
Filed Under: Brain , Future of Mental Health , Health , Illegal Drugs , mental illness , Neuroscience , New Research
Neuropeptides, Not Neurotransmitters, Drive Brain’s Fear Response
Summary: Researchers have discovered that neuropeptides, not neurotransmitters, are the primary messengers in the brain’s fear circuit. This finding could lead to better painkillers and treatments for fear-related conditions.
Using innovative tools, scientists observed neuropeptide release during fear responses in live mice. The study highlights the potential of targeting multiple neuropeptides for more effective therapies.
Key Facts:
> Neuropeptides are the primary messengers in the brain’s fear circuit.
New tools allow real-time observation of neuropeptide release in live mice.
Targeting multiple neuropeptides could improve treatments for PTSD and pain.
Source: Salk Institute
In the split second as you accidentally touch the hot handle of a cast iron skillet, pain and a sense of danger rush in. Sensory signals travel from the pain receptors in your finger, up through your spinal cord, and into your brainstem. Once there, a special group of neurons relays those pain signals to a higher brain area called the amygdala, where they trigger your emotional fear response and help you remember to avoid hot skillets in the future.
This process of translating pain into a threat memory occurs so quickly that scientists thought it must be mediated by fast-acting molecules called neurotransmitters. But when Salk researchers investigated the role of larger, slower-acting molecules called neuropeptides, they discovered these were the primary messengers in this fear circuit. Future insights into neuropeptide signaling in other areas of the brain, as well as the newfound understanding that targeting multiple neuropeptides at once is necessary, should inspire the development of more effective drugs to treat diverse neurological disorders. Credit: Neuroscience News Neuropeptides are known to play an important role in brain communication, but the details have been unclear because scientists didn’t have the proper tools to study them in behaving animals.
To determine the role of neuropeptides in this circuit, the Salk team created two new tools that finally allow scientists to observe and manipulate neuropeptide release in the brains of live mice.
The new study, published in Cell on July 22, 2024, revealed that the danger circuit relies on neuropeptides, not neurotransmitters, as its primary messengers, and more than one neuropeptide is involved in the process.
Their findings could lead to the development of more effective painkillers or new treatments for fear-related conditions like anxiety and PTSD (post-traumatic stress disorder).
“There is so much we have left to uncover about neuropeptides, but thankfully at Salk, we have the legacy of Nobel Prize winner Roger Guillemin’s work to highlight their importance and encourage our discovery,” says senior author Sung Han, associate professor and Pioneer Fund Development Chair at Salk.
“To do this, we created two genetically encoded tools for monitoring and silencing neuropeptide release from nerve endings. We believe these new tools will significantly advance the field of neuropeptide research, and our discovery of their role in fear processing is really just the beginning.”
To process and react to things in our environment, information must travel throughout our body and brain. These signals are sent and received by neurons, which form organized circuits that guide information where it needs to go. Neurons communicate with each other by sending and receiving molecules like neurotransmitters and neuropeptides.
Neuropeptides are generally accepted as neuromodulators that help and modulate the action of main neurotransmitters. However, early pioneers like Roger Guillemin proposed that neuropeptides can act as main transmitters themselves.
This concept has not been rigorously tested due to the lack of tools for visualizing and manipulating their release in behaving animals. The Salk team set out to explore neuropeptides with the goal of developing new tools to better understand their role in brain circuits.
To specifically target neuropeptides, Han’s team took advantage of one of their unique characteristics—while neurotransmitters are packaged in small spheres called synaptic vesicles , neuropeptides are packaged in large dense core vesicles . By engineering biochemical tools to target these large vesicles, they created neuropeptide sensor and silencer tools .
The sensor tags large dense core vesicles with proteins that glow when they are released from the nerve ending, allowing the researchers to watch neuropeptide release in live time. The silencer specifically degrades neuropeptides within large dense core vesicles, revealing what happens in the brain when neuropeptides are absent.
“We have created a novel way to trace neuropeptide travel and function in the brains of living animals,” says Dong-Il Kim, first author of the study and postdoctoral researcher in Han’s lab.
“These tools will help further our understanding of the brain’s neuropeptide circuits and enable neuroscientists to explore questions that were previously difficult to address.”
Using their newly developed neuropeptide sensor and silencer, together with existing sensor and silencer tools for glutamate (the brain’s most abundant neurotransmitter), the researchers looked at how neuropeptides and glutamate behaved in live mice as they experienced a mild stimulus—just enough to stimulate the fear circuit.
They found that neuropeptides, but not glutamate, were released during the stimulus. What’s more, silencing neuropeptide release reduced fear behaviors in the mice, but silencing glutamate had no effect.
To Han’s surprise and delight, this brainstem fear circuit relied on neuropeptides as its primary messenger molecules rather than glutamate. Furthermore, their findings support their ongoing investigation into PACAP—a neuropeptide that modulates panic disorder.
“These new tools and discoveries are an important step toward better neurological drug development,” says Han. “We found that multiple neuropeptides are packaged together in a single vesicle and released all at once by a painful stimulus to function in this fear circuit, which made us think, ‘ This might be why some drugs that target only one neuropeptide are failing in clinical trials.’
“With this new information, we can provide insights to develop new drugs that target multiple neuropeptide receptors at once, which may serve as better painkillers or help treat fear-related disorders like PTSD.”Equipped with their new neuropeptide toolbox, the team will soon begin to explore other brain circuits and processes. Future insights into neuropeptide signaling in other areas of the brain, as well as the newfound understanding that targeting multiple neuropeptides at once is necessary, should inspire the development of more effective drugs to treat diverse neurological disorders.Other authors […]
Remarkable magnetic brain control tech alters appetite and behavior
Researchers have developed a remote, non-invasive method of selectively controlling neurons in the brain using magnetic fields. The technique opens the door to a greater understanding of brain function and, potentially, new treatments for disorders.
In a recently published study, researchers from the Institute for Basic Science (IBS) and Yonsei University, both in South Korea, tested technology they’d developed that remotely – and precisely – manipulates specific parts of the brain using magnetic fields.
“This is the world’s first technology to freely control specific brain regions using magnetic fields,” said Cheon Jinwoo, from the Center for Nanomedicine at IBS, the Department of Nano Biomedical Engineering at Yonsei University, and the study’s co-corresponding author. “We expect it to be widely used in research to understand brain functions, sophisticated artificial neural networks, two-way BCI [brain-computer interface] technologies, and new treatments for neurological disorders.”
The researchers’ cutting-edge technology is called Nano-MIND (which stands for Magnetogenetic Interface for NeuroDynamics). Whereas optogenetics, which controls neurons with light, and electrical deep brain stimulation, used to treat Parkinson’s disease, both require the implantation of invasive electrodes into the brain, magnetogenetics is a wireless, remotely controlled technique.
The Nano-MIND technology relies on magnetic fields and magnetized nanoparticles . Specific types of neurons are genetically modified to express ‘magnetoreceptors’ that attract injected magnetized nanoparticles to their surface. The neurons are activated when the tiny receptor-attached magnets twist in response to very low-strength, externally applied rotating magnetic fields.
The researchers tested Nano-MIND in freely moving mice to see if they could modulate social behavior and feeding. In one experiment, they selectively activated inhibitory GABA receptors in neurons in the medial preoptic area (mPOA) of the hypothalamus, a region considered to be central to parenting. When the neurons were activated in non-maternal female mice, nurturing behaviors – approaching and retrieving mouse pups – were significantly enhanced, with a more than four-fold increase in care time observed. Control mice showed no interest in the pups.
In another experiment, the researchers targeted circuits in the lateral hypothalamus, a complex brain region involved in regulating many physiological processes, including feeding. Activating inhibitory neurons in this region resulted in a 100% increase in appetite and feeding behaviors; whereas activating excitatory neurons decreased appetite and feeding behaviors by more than 50%.
The researchers say that their experiments showed that the Nano-MIND technology can selectively activate particular neurons and circuits to modulate higher brain functions, paving the way for advancements in neuroscience and the potential for therapeutic applications.
In an article commenting on the study, Felix Leroy, PhD, from the Institute of Neurosciences of Alicante, Spain, said that while the tech “offers advantages such as wireless and long-term stimulation capabilities, which could revolutionize the field by enabling non-invasive and precise manipulation of brain activity, including deep and remote areas,” the study has its limitations. The most pressing one is that the long-term effects of magnetogenetic stimulation exerting repeated mechanical forces on the cell’s surface are unknown and require further study.
The study was published in the journal Nature Nanotechnology .
Source: IBS
9 foods that can boost your brain health — and don’t cost more than $1 per serving
Greens and beans both made the list. What we eat makes a difference to our brain health.
Brain doctors Ayesha and Dean Sherzai list 9 favorite foods for boosting cognition.
Everything on their list is a plant.
Brain doctors Ayesha and Dean Sherzai have spent their careers investigating how to have a healthy brain .
“We learned that yes, there are things you can do,” Mr. Sherzai told Business Insider. “Lifestyle has the most profound effect on brain health, more than anybody could imagine.”
One big study the two doctors often reference, which examined the diets of older adults living in public housing and nursing homes around Chicago, showed that those who adhered to a more brain-friendly diet pattern had a 53% lower risk of developing dementia.
“These are unimaginable numbers,” Sherzai said. “No protocols, no weird stuff, no vitamin concoction.”
It’s findings like this that have convinced the ” Brain Docs ,” as they call themselves on social media, to focus on promoting “simple dietary changes” people can make immediately to promote better cognitive health, instead of waiting for drugs to treat the symptoms of dementia later on in life.
“We think that if you take care of brain health, you’ve taken care of all health,” he said. “Everything you need for heart , for liver, for kidney is included in neuro.” 9 evidence-backed foods for brain health
Greens
Spinach, kale, “the darker the better,” Sherzai said. krblokhin/Getty Images Cost: about $1 for one serving of bagged spinach (2 cups)
Evidence: Getting in at least one serving of leafy greens, like lettuce, spinach, or kale per day is associated with better performance on cognitive tests for competencies like working memory, spatial awareness and perception among older adults. Scientists think there’s probably something neuroprotective about the nutrients in the leaves, which include folate, nitrate, and lutein. Legumes
It could be lentils, black beans, or chickpeas. Brent Hofacker/Shutterstock Cost: $0.50 or less per serving for things like canned chickpeas, black beans, or bagged lentils
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Evidence: Studies consistently suggest plant proteins like legumes are good for the aging brain — and nutrition experts suspect that might be in part because they’re packed with B vitamins that help keep our nervous system humming along. Berries
Cost: probably the priciest item on this list, at roughly $3-7 for a carton of fresh berries like strawberries, raspberries, or blackberries. But since a serving of berries is only half a cup, you can still probably squeeze in a serving for $1 or less. You can always opt for (cheaper) frozen berries, which studies show are just as nutritious as the fresh stuff — and sometimes even a little bit more nutritious — because fruits are typically frozen just as they reach peak ripeness.
Evidence: Berries like blueberries, raspberries, and strawberries are rich in chemical compounds that help keep our cells running well. There’s evidence to suggest they may also prevent some of the oxidative stress that’s associated with cognitive decline, but more research is still needed to better understand the precise link between berry eating and better brain health. Whole grains
Quinoa, oats, and brown rice are all classified as whole grains. Getty Images Cost: similar to legumes, generally less (and sometimes far less) than $1 per serving for things like oats, bulgur, corn, millet, quinoa, or brown rice.
Evidence: Whole grains are consistently linked to slower cognitive decline , and experts think that probably has something to do with all the anti-inflammatory effects they have on the body. Whole grains are also great at staving off other health issues, like diabetes, and heart disease, which can accelerate cognitive decline as they impact our vascular health. Nuts
Walnuts are the fan favorite for longevity-seekers. CFOTO/Future Publishing via Getty Images Cost: varies, but considering a one-pound bag of walnuts or almonds typically costs about $5-6, each serving would be less than $0.50
Evidence: Nuts are thought to be great for your brain in large part because they’re loaded with nutrients , including many that naturally improve vascular health and tamp down inflammation. Walnuts are an especially popular choice among nutrition buffs and longevity-seekers because they offer a decent dose of omega-3, which “is the only fat that your brain needs,” Sherzai said. Herbs and spices
Cost: pennies
Evidence: There are various reasons that seasonings can boost cognitive health. A favorite example of many health experts is turmeric , which has nice anti-inflammatory effects and is consistently linked to better cognitive function, but there are also real benefits to various other spices, including cinnamon (anti-inflammatory) and peppers, including black pepper (increases absorption of other nutrients, and may be directly neuroprotective). In general, being able to spice up your dishes in a way that tastes yummy to you also probably means you’ll be able to cook more at home and enjoy less processed foods , which is also a boon for overall health and well-being and linked to lower dementia risk. Seeds
Cost: about $0.35-0.75 per serving for things like chia seeds and pumpkin seeds
Evidence: Much like nuts, seeds are great for the brain because they’re full of fiber, healthy fats, key vitamins and minerals, including fatty acids like omega-3. Crucifers
Cost: between $0.50 and $1 per serving of broccoli or similar brassica veggies, like chard, kale, cauliflower, and Brussels sprouts.Evidence: These crunchy stalks are well-known health foods because they’re great for blood flow. They are consistently linked to less cognitive decline, are great cancer preventers, and lower the incidence of strokes. Tea Green tea is a favorite of health nuts. KMNPhoto/Getty Images Cost: varies, but generally between $0.10 and $0.60 per cup.Evidence: Tea leaves are chock-full of various plant compounds that can be beneficial for our long-term health, improving inflammation (a hallmark of dementia) and possibly even lubricating neurotransmission . You might’ve noticed that everything on this list is a plant What’s in your garden? ibnjaafar/Getty Iamges Experts say it’s too simplistic to attempt to break down these natural foods into exhaustive laundry lists of […]
Ivermectin found to work against Parkinson’s, depression, chronic pain and more
Tags: alternative medicine , anticancer , antiviral , Anxiety , beat depression , brain health , breakthrough , Censored Science , chronic pain , discoveries , EMP , goodhealth , goodmedicine , goodscience , health science , ivermectin , ivermectin science , mental health , Mind , neuroprotective , Parkinsons , prevention , radiation protection , remedies , research , schizophrenia , stroke There is a whole lot more that ivermectin can do than just prevent and treat the Wuhan coronavirus (COVID-19).
In an article posted to his Repurposed Drugs Substack, physician, writer and human rights advocate Justus R. Hope unpacked the latest science on ivermectin, which in addition to fighting viruses, bacteria and cancer also shows unique neuroprotective benefits.
Citing the work of Dr. William Makis, Hope explains that ivermectin prevents P2X4 receptors from internalizing and overexpressing. P2X4 expression is a driver of many neurological diseases including dementia (i.e., Alzheimer’s disease), Parkinson’s disease, multiple sclerosis (MS), chronic neuropathic pain, depression, bipolar disorder and anxiety.
If you suffer from migraines or abuse alcohol, ivermectin may help you as well due to the same P2X4 stabilization effects that provide neuroprotective benefits. Taking ivermectin could help to reduce cravings for and consumption of alcohol in those with an alcohol abuse disorder.
“If it is neuroprotective, and the evidence is growing that it is, and humanity is being bombarded with various toxins and electromagnetic frequencies each day that compromise our nervous system, perhaps there is reason to consider Ivermectin as a neuro-protective repurposed drug worthy of use during this dangerous time in our history,” Hope contends.
(Related: When taking ivermectin, be sure to also eat high-fat foods for maximum absorption.) Supplementing with ivermectin to protect against EMFs
Scientific research published in the journal Neuroscience Bulletin provides further insights into the technical aspects of how P2X4 expression causes degeneration of the nervous system.
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“In various pathological states, such as trauma, ischemia, chronic pain, neurodegenerative processes, and several neuropsychiatric disorders, de novo expression of P2X4 and / or an increase in cell surface P2X4 density has been reported in microglia and / or neurons, thus suggesting possible key and multiple roles of neuronal and microglial P2X4 receptors in the establishment and/or maintenance of these pathologies,” the paper reveals.
“Changes in the intracellular expression of P2X4 may also have important consequences in the pathophysiological context.”
As for the role of allosteric modulators like ivermectin in limiting the damaging effects of P2X4, this study in Frontiers in Pharmacology explains that limiting the expression of P2X4 receptors, as well as two other related proteins, P2X2 and P2X7, “may be of therapeutic benefit in a number of different conditions …”
There are a whole lot of other toxic things in the environment that ivermectin may also block from causing neurological harm, one of them being electromagnetic frequencies (EMFs) from things like cell phone towers, wireless routers, mobile phones, Bluetooth and more.
Hope believes that a growing body of evidence points to ivermectin helping to protect the nervous system from EMF damage “during this dangerous time in our history.”
“Ivermectin may not just be the anti-parasitic, anti-cancer, anti-viral repurposed drug we recognize but may have multiple other neuroprotective benefits for humanity in an era where we all may be subjected to neurotoxins – some apparent, and others invisible – like EMF,” Hope writes.
Aside from a few minor concerns, ivermectin is among the safest medications to ever hit the market. Unless one’s body is so overloaded with parasites that he or she experiences dramatic die-off symptoms from taking it, ivermectin is generally considered to be safe in most people.
“Decades of studies on the effects of ivermectin in humans show that it is very safe,” one commenter wrote.
Another noted that ivermectin won the 2015 Nobel Prize in Medicine for its effectiveness against certain types of parasites, scabies, lice and cancers.
It is also worth noting that Queen Elizabeth was given ivermectin as a treatment for the Wuhan coronavirus (COVID-19): The latest news about ivermectin can be found at IvermectinScience.com .
Sources for this article include:
JustusRHope.substack.com
NaturalNews.com
Ncbi.nlm.nih.gov
FrontiersIn.org
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Scientists define new type of memory loss in older adults
Researchers at Mayo Clinic have established new criteria for a memory-loss syndrome in older adults that specifically impacts the brain’s limbic system. It can often be mistaken for Alzheimer’s disease. The good news: Limbic-predominant Amnestic Neurodegenerative Syndrome, or LANS, progresses more slowly and has a better prognosis, and is now more clearly defined for doctors working to find answers for memory loss patients.
Prior to the researchers developing clinical criteria published in the journal Brain Communications , the hallmarks of the syndrome could be confirmed only by examining brain tissue after a person’s death. The proposed criteria provide a framework for neurologists and other experts to classify the condition in patients living with symptoms, offering a more precise diagnosis and potential treatments. They consider factors such as age, severity of memory impairment, brain scans, and biomarkers indicating the deposits of specific proteins in the brain.
The criteria were developed and validated using data from more than 200 participants in databases for the Mayo Clinic Alzheimer’s Disease Research Center, the Mayo Clinic Study of Aging and the Alzheimer’s Disease Neuroimaging Initiative.
Understanding the condition will lead to better management of symptoms and more tailored therapies for patients suffering from this type of cognitive decline, distinct from Alzheimer’s disease, says David T. Jones, M.D., a Mayo Clinic neurologist and senior author of the study.
“In our clinical work, we see patients whose memory symptoms appear to mimic Alzheimer’s disease, but when you look at their brain imaging or biomarkers, it’s clear they don’t have Alzheimer’s. Until now, there has not been a specific medical diagnosis to point to, but now we can offer them some answers,” Jones says. “This research creates a precise framework that other medical professionals can use to care for their patients. It has major implications for treatment decisions, including amyloid-lowering drugs and new clinical trials, and counseling on their prognosis, genetics and other factors.”
Decades of work to understand and classify different types of dementia is ongoing, says Nick Corriveau-Lecavalier, Ph.D., the paper’s first author. These findings build upon scientists’ continued efforts to untangle neurological conditions that often have similar symptoms or can occur simultaneously, but can have drastically different treatments and prognoses.
“Historically, you might see someone in their 80s with memory problems and think they may have Alzheimer’s disease, and that is often how it’s being thought of today,” Corriveau-Lecavalier says. “With this paper, we are describing a different syndrome that happens much later in life. Often, the symptoms are restricted to memory and will not progress to impact other cognitive domains, so the prognosis is better than with Alzheimer’s disease.”
Without signs of Alzheimer’s disease, the researchers looked at the involvement of one possible culprit — a buildup of a protein called TDP-43 in the limbic system that scientists have found in the autopsied brain tissue of older adults. Researchers have classified the build-up of these protein deposits as limbic-predominant age-related TDP-43 encephalopathy, or LATE. These protein deposits could be associated with the newly defined memory loss syndrome, but there are also other likely causes and more research is needed, the authors say.
With clinical criteria established by Jones, Corriveau-Lecavalier and co-authors, practitioners could soon diagnose LANS in patients so those living with memory loss might better understand options for treatment and potential progression of the disease, opening doors for research to further illuminate the characteristics of the disease.
The research was funded in part by National Institutes of Health grants P30 AG062677, P50 AG016574, U01 AG006786, R37 AG011378 and R01 AG041851 and by the Robert Wood Johnson Foundation, the Elsie and Marvin Dekelboum Family Foundation, the Liston Family Foundation, the Edson Family, the Gerald A. and Henrietta Rauenhorst Foundation and the Foundation Dr. Corinne Schuler.
Drs. Jones and Corriveau-Lecavalier reported no conflicts of interest. A complete list of co-authors and financial disclosures is available in the manuscript.
Scientist’s MRIs Highlight Psilocybin Boosting Brain Plasticity
NPR reports on fascinating research that shows how taking the psychedelic drug psilocybin changes brain process, producing mind-altering effects and temporary boosts to the brain’s ability to adapt and change. In other research news, CBD may protect skin from the sun.
NPR: This Is Your Brain On Drugs: How Psilocybin Can Trigger Plasticity In the name of science, Dr. Nico Dosenbach had scanned his own brain dozens of times. But this was the first time he’d taken a mind-bending substance before sliding into the MRI tunnel. “I was, like, drifting deeper into weirdness,” he recalls. “I didn’t know where I was at all. Time stopped, and I was everyone.” Dosenbach, an associate professor of neurology at Washington University School of Medicine in St. Louis, had been given a high dose of psilocybin, the active substance in magic mushrooms, by his colleagues. (Hamilton, 7/18)
Axios: CBD May Help Protect Skin From Sun Damage: Study An active ingredient in marijuana could help shield skin from sun damage, according to new research in the Journal of the American Academy of Dermatology. (Goldman, 7/17)
Also —
NPR: The Pros And Cons Of Mammograms Should Be Explained To Women, Study Says New research makes the case for educating women in their 40s — who’ve been caught in the crossfire of a decades-long debate about whether to be screened for breast cancer with mammograms — about the harms as well as the benefits of the exam. After a nationally representative sample of U.S. women between the ages of 39 and 49 learned about the pros and cons of mammography, more than twice as many elected to wait until they turn 50 to get screened, a study released Monday in the Annals of Internal Medicine found. (Cohen, 7/17)
CNN: Women With Endometriosis Face Fourfold Higher Risk Of Ovarian Cancer, Study Suggests The risk of developing ovarian cancer appears to jump about fourfold among women with endometriosis, compared with women who haven’t been diagnosed with the condition, a new study finds. (Howard, 7/17)
Stat: Bone Marrow Donors Needn’t Be Perfect Match In Cancer Care: Study As a hematologist-oncologist in Miami, Mikkael Sekeres always hopes his patients will find a perfect match for the bone marrow transplant they need to save their lives — but he doesn’t expect it. Most of his patients are Latino or African American, and rates of perfect matches are much lower for racial or ethnic minorities. That gloomy picture could soon change. (Chen, 7/17)
The New York Times: Moving In Childhood Contributes To Depression, Study Finds Researchers who conducted a large study of adults in Denmark, published on Wednesday in the journal JAMA Psychiatry, found something they had not expected: Adults who moved frequently in childhood have significantly more risk of suffering from depression than their counterparts who stayed put in a community. In fact, the risk of moving frequently in childhood was significantly greater than the risk of living in a poor neighborhood, said Clive Sabel, a professor at the University of Plymouth and the paper’s lead author. (Barry, 7/17)
Axios: Medical Debt Fuels Mental Health Treatment Gap As many as 1 in 4 U.S. adults with depression and anxiety can’t pay their medical bills — a situation that could be limiting their ability to get timely psychiatric care, Johns Hopkins researchers found. (Bettelheim, 7/18)
Stat: ‘Too Early To Say’ When Novartis Will File Myelofibrosis Drug A Novartis executive on Thursday said “it’s too early to say” whether the company would still submit an experimental myelofibrosis drug for regulatory approval this year, amid questions about the medicine’s data profile and whether it’s sufficient for filing. (Joseph, 7/18)
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The Aging Brain: Is Decline Preventable?
July 17, 2024 – The changes can begin in middle age, but they’re not usually noticeable until decades later. By age 60 and beyond, the changes can pick up speed and may become obvious.
“As we get older, our brain actually starts to shrink and lose mass,” said Marc Milstein, PhD, a Los Angeles brain health researcher. The start of that shrinkage, as well as the path it takes, can vary, said Milstein, who wrote The Age-Proof Brain .
“Starting at 40, our overall brain volume can start shrinking about 5% every 10 years,” he said. “Our brain has connections where our memories are stored, and as we age, we lose some of these connections. That can make it challenging to remember and to learn new information.”
As scary as that may sound, “We can slow down this process,” Milstein said.
Those who have apparently slowed down the process the most are called “super agers” and are the focus of intense research. But plenty of other people, beyond their 70 th birthday, boast that they wow their friends often with their spectacular memories and other mental skills.
‘Typical’ Brain Changes Over Time
With age, the hippocampus – critical for making new memories and accessing old ones – loses volume. When learning new information, Milstein likens the hippocampus to a “waiting room” of the brain . “It’s one of the first places information goes.”
And the brain has to decide: Is this information worth transferring on to longer-term memory? As we get older, our brain’s ability to not be distracted can have a negative impact on our ability to transfer this information, Milstein said. That’s why multitasking when we get older can make it more challenging to learn new information, he said. The prefrontal cortex – important for managing emotions and stress – also shrinks.
These structural changes and shrinkage vary from person to person, said David B. Reuben, MD, a professor of medicine and chief of geriatrics at the UCLA David Geffen School of Medicine. “How much it contributes to decline is variable.”
By your late 70s and into the 80s, the speed of processing information can slow, he said. He likens it to a computer that needs an update. “Before you update your computer, you get the same answers, but they’re slower,” he said.
Deficits in retrieval, or what Reuben calls “tip of the tongue” syndrome, can happen, too, and they’re normal. “You know you know it, but you can’t get the word or words out.” Then, sometime later, it may pop into your head, so you relax and figure your memory is OK.
With age, mixing up a name can happen, just as it can earlier in life, said Joe Verghese, MD, a cognitive neurologist and chief of the Division of Cognitive & Motor Aging at Montefiore Medical Center in the Bronx, NY.
If it’s an isolated incident, it’s not a red flag, he said. It’s more apt to happen in a stressful situation. But it can happen to anyone. “It’s like an older mother calling her first son by her second son’s name,” said Verghese, who admitted he once called his son by his dog’s name.
The reduction in brain volume can lead to noticeable changes in thinking skills, Verghese said. But, he said, it’s important to point out that in normal aging, “the degree of shrinkage doesn’t always correlate to how you perform cognitively, or in day-to-day life.” In other words, your brain could have noticeable shrinkage but you are still getting through the day mostly fine.
If brain imaging such as an MRI is repeated over time, the shrinkage would probably be noticeable as the years go on, comparing one scan to another, Verghese said. But in clinical practice, he said, he doesn’t do serial MRIs to assess shrinkage; rather, he goes by how people are doing clinically, by assessing if they are walking, talking, and thinking normally.
He is an expert in the link between gait and dementia, finding that changes in how you walk can be used to predict mild issues with mental skills as well as dementia.
“How you walk is an important indicator of health, of how well you are doing cognitively as well as physically,” Verghese said.
That’s because walking involves processes from the brain to the nerve endings in the feet. When walking gets stiff, it could signal a number of issues – from arthritis and the need for more movement to possible Parkinson’s or other conditions. A stiff gait isn’t normal, he said. “You should be able to walk freely. If you are not doing so, there is a reason for it,” although it might not be treatable.
Enter the Exceptions
Despite brain shrinkage, some people continue to impress friends with their memory skills later in life.
Sylvia Schmidt, 89, is a longtime member of a book club where most members are at least a decade younger. But she was the only one who realized they had already read a book the leader once selected. Others argued with her at first, said Schmidt, who lives in a retirement community in Fullerton, CA. But the leader looked up the book ( As a Driven Leaf ) and proved her right, and now they all know better. “They all remark I have a phenomenal memory,” Schmidt said proudly.
She recently had a detailed political discussion with another resident who at first insisted her details about an incident, complete with dates, were incorrect. When his girlfriend looked up the details, finding Schmidt’s version accurate, he changed his mind.
Perry Solomon, 79, of Santa Monica, CA, is a consultant to small and medium-size businesses. Recently, he was talking about travel hassles with his wife and could still describe, in detail, an incident that happened more than 40 years ago during a family trip.
“It was about how our passports were stolen as our daughters were sitting on our suitcases but got sidetracked [by a thief] on a sidewalk in Manhattan while we were checking out of the hotel,” Solomon said.
He’s also on the advisory board of several companies and said […]
Meet the Brain Cells that May Help Us Adapt to Changes in Day Length
Study illuminates circadian rhythms, psychiatric disorders with seasonal flare-ups
4 min read Serotonin glows green in a microscope image of cells in the mouse brain stem. Image: Giacomo Maddaloni At a glance: Study in mice reveals a brain circuit — and brain cell behavior — that affects the ability to adapt to changes in day length.
Findings add another piece to the puzzle of how circadian rhythms work.
Work may inform treatments for conditions exacerbated by changes in day length, such as seasonal affective disorder and bipolar disorder.
Harvard Medical School scientists have discovered a brain circuit that influences the ability to adapt to changes in day length, like those that occur from season to season or when traveling across time zones.
The study, based on research in mice and published July 17 in Nature , fills in another piece of the workings of circadian rhythms: the ways in which the brain adjusts behavior and body functions on a 24-hour cycle, based on external signals such as the presence and absence of day light.
The work also reveals a new way brain cells can behave.
Get more HMS news here
If affirmed in humans in further studies, the findings could help researchers understand the basis of mistimed sleep-wake and activity cycles, which can contribute to the development of certain diseases, including neurologic, heart, and metabolic disorders.
Further findings also could inform the design of treatments for people who struggle with sharp changes in day length or timing, such as shift workers and travelers, or people who have health conditions that are exacerbated by changes in day length or timing, including schizophrenia and seasonal affective, major depressive, and bipolar disorders.
“We know that solar light dictates organismal physiology and behavior, and that we have health issues if our body doesn’t properly anticipate the light-dark cycle, but we tend to think about that on a daily scale, not seasonally,” said Susan Dymecki , the George Fabyan Professor of Genetics in the Field of Comparative Pathology in the Blavatnik Institute at HMS, whose lab conducted the work.
“Finding a neural circuit that contributes significantly to the ability to adapt to changes in the day-night cycle is exciting,” she said. “It would be wonderful if it can help us better understand how our brains work and how we might help people synchronize to those changes.”
Furthermore, the researchers said, the results offer insights into how exposure to forms of artificial light at night, including digital screens, may confuse the brain’s sense of day length and affect human health. Part of a circadian circuit
The team — led by Giacomo Maddaloni , research fellow in genetics in the Dymecki lab — identified a brain circuit with multiple groups of neurons that together recognize, decode, and drive behavioral adaptation to changes in the amount of daylight.
Central to this circuit is a set of neurons dubbed mr En1-Pet1. Maddaloni and colleagues found that these neurons receive signals from a brain region called the preoptic area, which is told directly about whether it’s light or dark by nerve cells in the retina at the back of the eye.
The team determined that mr En1-Pet1 neurons then send signals to three areas of the brain involved in circadian rhythms and sleep-wake patterns, including the body’s master circadian clock, called the superchiasmatic nucleus or SCN.
This discovery placed the mrEn1-Pet1 neurons within a brain circuit that starts with light detection and continues to circadian rhythm regulation. But how were the neurons communicating, the researchers wondered. A tale of two chemicals
Scientists already knew that mrEn1-Pet1 neurons release serotonin, a chemical involved in a myriad of functions from breathing rate to mood to appetite. Maddaloni and colleagues, however, found that mrEn1-Pet1 cells can likely also release the chemical glutamate, which activates neurons that receive it.
A common understanding among scientists has been that neurons that can release one or more chemicals do so to all the brain regions they “talk” to. To their surprise, Dymecki’s team found that the mrEn1-Pet1 neuronsdeploy serotonin and glutamate independently — sometimes together, sometimes separately, sometimes in different amounts — to the three brain regions they connect to.
“It’s really cool, the mechanism these cells use,” said Maddaloni.
The team’s experiments indicated that the mrEn1-Pet1 neuronstake the environmental cue of light or dark duration and change their deployment of serotonin and glutamate accordingly. This appears to provide information to the master circadian clock, which incorporates it with other inputs to decide whether it should adjust the animal’s biological response and ultimately its behavior.
Blocking various parts of the circuit impaired mice’s ability to adjust to changes in day length. When the team made “day” length longer or shorter in the lab, mimicking summer or winter, mice with disruptions in the mrEn1-Pet1 system took much longer to sync their sleep and wake times to the new day length than normal mice and lagged in shifting their wheel-running activity to appropriate times and lengths.
“The results were really striking,” said Maddaloni. “Mice kept waking up according to the previous light cycle. They were ‘blind’ to the changes in season.”
When the mrEn1-Pet1 neurons are disrupted, the SCN doesn’t adjust properly, confirmed Dymecki. “It affects a fundamental mechanism in the master circadian regulator.”
Dymecki and Maddaloni want to find out whether this ability to deploy different neurotransmitters to different brain regions is unique to mrEn1-Pet1 neurons. From mouse to human
How applicable the findings are to human health will depend on whether our brains have mrEn1-Pet1 neurons and a comparable circadian circuit.Although her team hasn’t yet looked for mrEn1-Pet1 cells in human brain tissue, Dymecki is encouraged by the fact that the neurons reside in the mouse brain stem, an evolutionarily ancient area that changes very little across mammals.Another promising sign: Every time the team has looked in the human brain stem for other types of serotonin-releasing cells present in the mouse brain stem, they’ve found them.Also, imaging studies have shown a link between abnormalities in this brain region in humans and conditions such as bipolar disorder, […]
Your Brain Might Try to Stockpile Estrogen During Menopause—And It Could Explain Brain Fog
FG Trade / Getty Images Key Takeaways
A new study shows that the menopause transition is associated with an increase in estrogen receptors in the brain.
This increase in estrogen receptors is also linked to brain fog and mood changes.
More research is needed, but researchers theorize that the increase in estrogen receptors is the brain’s way of compensating for a decline in circulating estrogen.
The research is important because of how symptoms impact quality of life and are a risk factor for dementia.
Shifting hormone levels contribute to dozens of symptoms during the menopause transition.1 Common menopause symptoms include cognitive and mood changes, such as brain fog, depression, and anxiety.2 For the first time, researchers have preliminary evidence showing why.
A first-of-its-kind study suggests these changes are related to an increase in the number of estrogen receptors in the brain, despite estrogen levels decreasing throughout the body.
Researchers from Weill Cornell Medicine used positron emission tomography (PET) imaging to analyze estrogen activity in the brain. They found that over the menopause trajectory, estrogen receptors increase across various brain regions. This increase was associated with worse cognitive performance and an increase in mood symptoms.3
The study lays a foundation for further research on menopause treatments and symptom prevention, which may be important for dementia prevention.
“My interest in this topic stemmed from the observation that hormonal changes during menopause have profound effects on women’s brain structure and function,” Lisa Mosconi, PhD , director of the Women’s Brain Initiative and associate director of the Alzheimer’s Prevention Program at Weill Cornell Medicine, told Verywell. “Yet there’s limited understanding of how these changes occur at a molecular level.” What Happens in the Brain During the Menopause Transition?
A hallmark of the menopause transition is a reduction in estrogen. By the time people reach their final menstrual period, estrogen levels will have decreased by 50%.4 Most symptoms of menopause have links to estrogen decline. But now Mosconi and her colleagues have shown how an increase in the number of sites that estrogen binds to in the brain—called receptors—might be leading to cognitive and mood symptoms.3
Their small proof-of-concept study included 54 healthy women aged 40 to 65. The researchers evenly categorized the participants as premenopausal, perimenopausal, and postmenopausal. The researchers then used PET scans to study their brains, including a tracer that binds to estrogen receptors. The technique offered the opportunity for insights not possible with other imaging tools.3
“This method allowed us to see directly where and how estrogen receptors respond to estrogen changes over the menopausal transition,” Mosconi said.
The scans showed progressively higher estrogen receptor density in participants who were perimenopausal and postmenopausal when compared to the premenopausal control group. A measure of estrogen receptor density in four key brain regions predicted with 100% accuracy whether a participant was premenopausal or postmenopausal.3
The study does have some limitations, including that it is observational, does not prove cause and effect, and has a small sample size. “I wish there could have been a larger study group,” Sonia Durairaj, MD , an internal medicine physician at Harbor Health and a Menopause Practitioner certified by the North American Menopause Society, told Verywell. She was not involved with the research. “But the group of 54 women was an overall well-selected group, and different variables were taken into account.” If Estrogen Levels Drop During Menopause, Why Is the Brain Creating More Estrogen Receptors?
The researchers don’t yet know why estrogen receptor density increases over the course of the menopausal transition. But they have a theory that the brain may be trying to capture any available estrogen.
“For now, it seems plausible that the brain may compensate for lower circulating estrogen levels by increasing estrogen receptors to maintain sensitivity to the hormone’s effects and minimize the impact of menopause on cognitive health and overall brain function,” Mosconi said.
Further analysis showed that higher estrogen receptor concentrations in specific brain regions were also associated with the participants’ self-reports of menopausal cognitive and mood symptoms.
In postmenopausal participants, the higher receptor concentrations in cognitive regions of the brain, such as the hippocampus and frontal cortex, were associated with lower scores on some cognitive tests. In the same participants, higher estrogen receptor density in different brain regions, including the thalamus, was linked to mood changes, such as depression.3
Mosconi said the study is the first, to the best of their knowledge, to show three things. First, it visualizes estrogen activity in the living human brain. Second, it demonstrates an increase in estrogen receptor density in specific areas of the brain at the perimenopausal and postmenopausal stages. And finally, it shows that these effects are associated with brain symptoms of menopause, such as low mood and poorer memory function.3
“Far too long, women’s symptoms have been chopped up to a phase of life with little to no [information] on the science or physiology of why,” Jillian LoPiano, MD , chief health officer at Wisp, told Verywell. LoPiano was not involved with the research. “The more we know about these physiological processes, the better we can provide specific and innovative care for symptomatic peri- and postmenopausal women.”
Is ‘Menopause Brain’ Real? Improving Mood During Menopause Would Enhance Quality of Life
Menopause symptoms can greatly affect quality of life. In an older 2013 survey of more than 8,000 women ages 40 to 64, self-reported menopause symptoms were associated with lower quality-of-life scores, higher work impairment, and higher healthcare utilization than those without symptoms. Mood changes, such as depression and anxiety, had the highest associations.5
More than half of people undergoing the menopause transition experience mood changes.6 Up to 62% experience brain fog, an umbrella term used to describe cognitive issues like difficulty concentrating, communicating, and remembering things.78
“We know that brain fog, cognitive changes, and mood impact many women during the perimenopause and menopausal years and lead to negative impacts on quality of life,” Mindy Goldman, MD , chief clinical officer of Midi Health and a clinical professor emeritus of obstetrics at UC San Francisco, told Verywell. “We know that these symptoms impact both […]
Are These Plant Molecules the Secret to Brain Health?
Key points
Polyphenols, found in fruits, vegetables, tea, and wine, boost brain health and cognitive function.
Flavonoids and phenolic acids are key polyphenol groups with diverse health benefits, including brain support.
Polyphenols have anti-inflammatory, epigenetic and neuroprotective properties that may enhance brain vitality.
Consuming polyphenol-rich foods like berries, dark chocolate, and tea may support long-term brain health.
Source: Austin Perlmutter/DALL-E/OpenAI In recent years, polyphenols have gained significant attention in the health and wellness community. These naturally occurring compounds, found abundantly in fruits, vegetables, tea, coffee, and wine (as well as diets eaten by the longest-lived people on Earth), are typically touted for their antioxidant properties and health benefits. One of the most intriguing and promising areas of research is how polyphenols impact brain health. This blog delves into the fascinating world of polyphenols and their positive effects on the brain and how to leverage this information in your diet today! Understanding Polyphenols
Polyphenols are a diverse group of nutrients found in plants called phytochemicals. There are over 8,000 different polyphenol compounds. They are broadly categorized into groups, including flavonoids, phenolic acids, and others. Each group contains a variety of subtypes, each with its own unique properties and potential health benefits. Flavonoids: Found in fruits, vegetables, tea, and wine, flavonoids are the largest group of polyphenols. Examples include quercetin, kaempferol, and catechins.
Phenolic Acids: Commonly found in coffee, fruits, and vegetables, phenolic acids include compounds such as caffeic acid and ferulic acid.
Polyphenols and Brain Health: The Connection
The connection between polyphenols and brain health is an area of active research, with numerous studies indicating that these compounds can have a protective and enhancing effect on brain function. The mechanisms through which polyphenols exert their positive effects on the brain include antioxidant activity, anti-inflammatory properties, modulation of neuroplasticity-related signaling pathways, and improved cerebral blood flow.
Recently, it’s also been proposed that polyphenols can improve health through effects on epigenetic expression (changing how our genes are used). In this article, we’ll focus on the immune, signaling pathway, and epigenetic potential of these molecules.
1. Polyphenols May Possess Anti-Inflammatory Properties.
Chronic inflammation in the brain is a significant factor in the development of neurodegenerative diseases ranging from Alzheimer’s to depression . Due in part to an ability to modify immune cells directly, as well as their effects on other pathways, including the gut microbiome , it’s believed that polyphenols can help regulate the immune system and keep chronic inflammation in check, properties that can help mitigate this risk.
2. Polyphenols Can Influence Key Signaling Pathways.
In addition to their effects on immune-related pathways, polyphenols also modulate various signaling pathways that are linked to brain health. They influence pathways involved in cell survival, neurogenesis (the formation of new neurons), and synaptic plasticity (the ability of synapses to strengthen or weaken over time). These pathways are essential for learning, memory, and overall cognitive function.
For instance, the consumption of cocoa (which is rich in polyphenols like epicatechin and catechin) has been shown to enhance brain-derived neurotrophic factor (BDNF) levels and is linked to improved cognition . BDNF is a protein that supports the survival and growth of neurons, playing a critical role in long-term memory formation.
3. Polyphenols May Beneficially Impact Epigenetics .
One of the biggest recent breakthroughs in science has been the understanding that our DNA is regulated by small molecules attached to it. This is the study of epigenetics— and it shows us that many of the things we thought were “fixed” about our health may actually be modifiable through lifestyle. New research using polyphenols , including those found in Tartary buckwheat indicates that polyphenols in our diet may regulate epigenetics, which may be immensely important in the context of other research showing that epigenetics may influence everything from brain development to mental health disorders. Practical Tips for Incorporating Polyphenols Into Your Diet
Given the potential brain-boosting benefits of polyphenols, incorporating these compounds into your diet is a smart move. Here are some practical tips to help you get started:
1. Eat a Rainbow of Fruits and Vegetables: Different colors of fruits and vegetables indicate the presence of various polyphenols. Aim to include a wide range of colorful produce in your diet.
2. Enjoy a Cup of Tea: Both green and black tea are rich in polyphenols. Drinking a few cups of tea daily can provide a substantial amount of these beneficial compounds. To maximize the benefits, skip the added sugar!
3. Indulge in Dark Chocolate: Dark chocolate with a high cocoa content is an excellent source of flavonoids. Enjoying a small piece of dark chocolate can be a delightful way to boost your polyphenol intake. Look for brands without much added sugar.
4. Incorporate Nuts and Seeds: Flaxseeds, walnuts, and other nuts are good sources of lignans and other polyphenols. Add them to your meals or snacks for an extra health boost.
5. Use Spices and Herbs: Some of the most concentrated sources of polyphenols are spices like cloves, cinnamon, paprika, ginger, rosemary and black pepper.
6. Try Adding in Unique Foods: Bitter foods like bitter melon, beer (can be non- alcoholic ), and Tartary buckwheat are surprisingly rich in polyphenols. Conclusion
Polyphenols are remarkable compounds with a wide range of health benefits, particularly for the brain. Their antioxidant, anti-inflammatory, and neuroprotective properties make them powerful allies in the quest for optimal brain health. By incorporating a variety of polyphenol-rich foods into your diet, you can support cognitive function, protect against neurodegenerative diseases, and enhance overall brain vitality.As research continues to uncover the myriad ways polyphenols impact brain health, it becomes increasingly clear that these plant compounds are an essential component of a brain-healthy diet. So, the next time you enjoy a cup of tea, a handful of berries, or a piece of dark chocolate, remember that you’re not just indulging in a tasty treat—you’re also nourishing your brain with the power of polyphenols.
Experimental nasal spray boosts cognitive function in mouse models of dementia
Researchers were able to improve memory in mouse models of dementia through an experimental nasal spray treatment. Image credit: YEVHEN HOLOBORODKO/Getty Images. A novel intranasal antibody treatment shows potential in fighting tau protein buildup, which is a key factor in neurodegenerative diseases such as Alzheimer’s.
A single dose of this treatment in aged mice with tau pathology significantly reduced tau accumulation and improved cognitive function.
This approach could pave the way for new therapies targeting tau-related neurodegenerative conditions.
Scientists at the University of Texas Medical Branch have recently announced a novel method of combating neurodegenerative conditions like Alzheimer’s disease and other forms of dementia .
They have revealed a pioneering nasal spray treatment that has demonstrated effectiveness in eliminating harmful tau protein accumulation and enhancing cognitive abilities in aged mouse models suffering from neurodegenerative diseases.
Their study results appear in the journal Science Translational Medicine . What role does tau accumulation play in dementia?
Like other forms of dementia, Alzheimer’s disease results from the death of brain cells, making it a neurodegenerative condition characterized by gradual brain cell loss.
Tau is a protein associated with microtubules in the human brain, aiding in the stabilisation of microtubules, which are important for maintaining the cell’s shape and organisation in neurons.
In a healthy brain, tau proteins ensure proper cellular order.
However, in neurodegenerative diseases, tau proteins can become abnormally twisted, forming tangles that interfere with neuronal function and cause cognitive decline.
In individuals with Alzheimer’s disease, the brain tissue progressively loses nerve cells and connections, while small deposits called plaques and tangles accumulate on the nerve tissue.
Plaques, composed of a protein called beta-amyloid, form between dying brain cells, while tangles, made up of tau, develop within the nerve cells.
The exact cause of these changes remains unclear, though multiple factors may contribute to their occurrence.
Existing tau immunotherapies have faced challenges in effectiveness due to their limited capacity to penetrate the intracellular compartments where these tau accumulations are located. Novel antibody treatment may prevent the spread of tau
In the new study, an intranasal antibody treatment has shown promise in targeting, dismantling, and preventing the spread of tau protein.
The buildup of tau protein inside neurons is linked to Alzheimer’s and other neurodegenerative conditions and engineering antibodies to selectively attack tau may help clear this build up and enhance cognitive function.
However, tau antibody treatments are still in the development stage and have had limited success in clinical trials.
In this study, researchers introduced a monoclonal tau antibody named toxic tau conformation–specific monoclonal antibody-2 (TTCM2), which specifically targeted pathological tau deposits in post mortem brain tissue from patients with Alzheimer’s, dementia with Lewy bodies and progressive supranuclear palsy.
TTCM2 also inhibited the seeding activity of patient-derived tau oligomers in tau biosensor cells, indicating its potential to prevent the spread of tau fibrils among neurons.
Further tests showed that TTCM2 was effective when delivered via lipid molecule compartments, or micelles, through the noses of aged mice with tauopathy.
According to the study, a single one dose of TTCM2 micelles was sufficient to disperse throughout the brains of the mice, reduce tau pathology and improve cognition.
Investigating the mechanisms behind TTCM2’s efficacy, researchers found that the antibody interacts with an intracellular receptor known as tripartite motif-containing 21 (TRIM21).
The researchers note that their findings align with a recent study showing that TRIM21 is essential for effective tau immunotherapy.
First author Sagar Gaikwad, PhD , from the Department of Neurology at The Mitchell Center for Neurodegenerative Diseases, University of Texas Medical Branch, explained the key findings to Medical News Today .
“Our study shows that the nasal tau immunotherapy importantly reverses Alzheimer’s pathology in mice and a single dose is enough to achieve this,” Gaikwad explained. “This also improves memory and behavior in aged mice.” “Importantly, our TTCM2 antibody effectively recognizes and neutralizes pathological tau in the brain tissues from patients with Alzheimer’s disease. This research could lead to new treatments that improve quality of life and potentially reverse or delay the onset of severe symptoms in patients with Alzheimer’s disease and related dementia.”
– Sagar Gaikwad, PhD Experts hail ‘promising’ experimental treatment Jason Krellman, PhD , an associate professor of neuropsychology in the Department of Neurology at Columbia University Irving Medical Center, not involved in this study, told MNT that “we’ve known for many years that dysfunction of tau is a prominent feature of neurodegenerative diseases such as Alzheimer’s.”“Relatedly, the amount of dysfunctional tau in the brain correlates positively with the severity of cognitive impairment in people with Alzheimer’s disease,” he added. “Therefore, treatments to reduce tau have been a major focus of research.”Krellman explained what the recent study achieved: “The researchers used an immunotherapy treatment that reduces the amount of dysfunctional tau in the brains of mice as well as prevents the production of ‘tau seeds,’ which allow the dysfunction to spread through the brain. Getting such treatments into the brain has been challenging because of the blood-brain barrier, the brain’s protective blockade against numerous but not all outside substances. The researchers managed to circumvent this barrier by using a novel method of administration, delivery through the nose to be sure absorption by the brain was rapid and more complete.” The expert found the results of this animal study encouraging. He noted that it is “especially promising was that the mice showed improvement in cognitive function via their behavioral responses in tests that assess recognition memory and spatial awareness.” Kubanych Takyrbashev, MD, health and wellness advisor at NAO, also not involved in the research, agreed, noting that the study “addresses a critical challenge in the field of neurodegenerative diseases.” Why would an antibody nasal spray be a promising treatment? “Developing a conformation-specific antibody for tau that can selectively target toxic tau aggregates is a significant advancement. What makes this study particularly compelling is the innovative delivery method: Using lipophile micelles for intranasal administration. This method effectively bypasses the blood-brain barrier, a major hurdle in treating neurological disorders,” Takyrbashev explained. He pointed out that “the antibody’s ability to specifically target and […]
Scientists find small regions of the brain can take micro-naps while the rest of the brain is awake and vice versa
by University of California – Santa Cruz Hengen’s artistic interpretation of the varied brain wave patterns that produce the fundamental states of sleep and wake. Credit: Keith Hengen Sleep and wake: They’re totally distinct states of being that define the boundaries of our daily lives. For years, scientists have measured the difference between these instinctual brain processes by observing brain waves, with sleep characteristically defined by slow, long-lasting waves measured in tenths of seconds that travel across the whole organ.
For the first time, scientists have found that sleep can be detected by patterns of neuronal activity just milliseconds long, 1,000 times shorter than a second, revealing a new way to study and understand the basic brain wave patterns that govern consciousness. They also show that small regions of the brain can momentarily “flicker” awake while the rest of the brain remains asleep, and vice versa from wake to sleep.
These findings, described in a new study published in the journal Nature Neuroscience , are from a collaboration between the laboratories of Assistant Professor of Biology Keith Hengen at Washington University in St. Louis and Distinguished Professor of Biomolecular Engineering David Haussler at UC Santa Cruz. The research was carried out by Ph.D. students David Parks (UCSC) and Aidan Schneider (WashU).
Over four years of work, Parks and Schneider trained a neural network to study the patterns within massive amounts of brain wave data, uncovering patterns that occur at extremely high frequencies that have never been described before and challenge foundational, long-held conceptions of the neurological basis of sleep and wake.
“With powerful tools and new computational methods, there’s so much to be gained by challenging our most basic assumptions and revisiting the question of ‘what is a state?'” Hengen said. “Sleep or wake is the single greatest determinant of your behavior, and then everything else falls out from there. So if we don’t understand what sleep and wake actually are, it seems like we’ve missed the boat.”
“It was surprising to us as scientists to find that different parts of our brains actually take little naps when the rest of the brain is awake, although many people may have already suspected this in their spouse, so perhaps a lack of male-female bias is what is surprising,” Haussler quipped. Understanding sleep
Neuroscientists study the brain via recordings of the electrical signals of brain activity , known as electrophysiology data, observing voltage waves as they crest and fall at different paces. Mixed into these waves are the spike patterns of individual neurons.
The researchers worked with data from mice at the Hengen Lab in St. Louis. The freely-behaving animals were equipped with a very lightweight headset that recorded brain activity from 10 different brain regions for months at a time, tracking voltage from small groups of neurons with microsecond precision.
This much input created petabytes—which are one million times larger than a gigabyte—of data. David Parks led the effort to feed this raw data into an artificial neural network, which can find highly complex patterns, to differentiate sleep and wake data and find patterns that human observation may have missed. A collaboration with the shared academic computer infrastructure located at UC San Diego enabled the team to work with this much data, which was on the scale of what large companies like Google or Facebook might use.
Knowing that sleep is traditionally defined by slow-moving waves, Parks began to feed smaller and smaller chunks of data into the neural network and asked it to predict whether the brain was asleep or awake.
The team found that the model could differentiate between sleep and wake from just milliseconds of brain activity data. This was shocking to the research team—it showed that the model couldn’t have been relying on the slow-moving waves to learn the difference between sleep and wake. Just as listening to a thousandth of a second of a song couldn’t tell you if it had a slow rhythm, it would be impossible for the model to learn a rhythm that occurs over several seconds by just looking at random isolated milliseconds of information.
“We’re seeing information at a level of detail that’s unprecedented,” Haussler said. “The previous feeling was that nothing would be found there, that all the relevant information was in the slower frequency waves. This paper says, if you ignore the conventional measurements, and you just look at the details of the high frequency measurement over just a thousandth of a second, there is enough there to tell if the tissue is asleep or not. This tells us that there is something going on a very fast scale—that’s a new hint to what might be going on in sleep.”
Hengen, for his part, was convinced that Parks and Schneider had missed something, as their results were so contradictory to bedrock concepts drilled into him over many years of neuroscience education. He asked Parks to produce more and more evidence that this phenomenon could be real.
“This challenged me to ask myself, ‘To what extent are my beliefs based on evidence, and what evidence would I need to see to overturn those beliefs?'” Hengen said. “It really did feel like a game of cat and mouse, because I’d ask David [Parks] over and over to produce more evidence and prove things to me, and he’d come back and say, ‘Check this out.’ It was a really interesting process as a scientist to have my students tear down these towers brick by brick, and for me to have to be okay with that.” Local patterns
Because an artificial neural network is fundamentally a black box and does not report back on what it learns from, Parks began stripping away layers of temporal and spatial information to try to understand what patterns the model could be learning from.
Eventually, they got down to the point where they were looking at chunks of brain data just a millisecond long and at the highest frequencies of brain voltage fluctuations.
“We’d taken out all the information that neuroscience has used to understand, define, and analyze sleep for […]
Propofol Disrupts Brain’s Stability/Excitability Balance to Induce Unconsciousness
Genetic Engineering & Biotechnology News There are many drugs that anesthesiologists can use to induce unconsciousness in patients, but exactly how these drugs cause the brain to lose consciousness has been a longstanding question. A study in non-human primates by MIT neuroscientists has now answered that question for one commonly used anesthesia drug, propofol.
Using a novel technique known as DeLASE (delayed linear analysis for stability estimation) to analyze neuronal activity, the researchers’ study in macaques discovered that propofol induces unconsciousness by disrupting the brain’s normal balance between stability and excitability. The findings indicated that the drug causes brain activity to become increasingly unstable, until the brain loses consciousness.
The new findings could help researchers develop better tools for monitoring patients as they undergo general anesthesia. “The brain has to operate on this knife’s edge between excitability and chaos,” said Earl K. Miller, PhD, the Picower Professor of Neuroscience and a member of MIT’s Picower Institute for Learning and Memory. “It’s got to be excitable enough for its neurons to influence one another, but if it gets too excitable, it spins off into chaos. Propofol seems to disrupt the mechanisms that keep the brain in that narrow operating range.”
The team further indicated the potential to apply their method for tracking changes in the stability of neural dynamics as part of monitoring treatment for psychiatric and mood disorders. Miller, and Ila Fiete, PhD, a professor of brain and cognitive sciences, the director of the K. Lisa Yang Integrative Computational Neuroscience Center (ICoN), and a member of MIT’s McGovern Institute for Brain Research, are senior authors of the team’s report on their anesthesia-related study, published in Neuron . In their paper, titled “ Propofol anesthesia destabilizes neural dynamics across cortex ,” the researchers concluded “Overall, our analysis suggests a mechanism for anesthesia that involves destabilizing brain activity to the point where the brain loses the ability to maintain conscious awareness.” Lead authors on the report are MIT graduate student Adam Eisen and MIT postdoc Leo Kozachkov, PhD.
Every day, hundreds of thousands of people undergo general anesthesia, the authors wrote. Propofol binds to GABA receptors in the brain, inhibiting neurons that have those receptors. Other anesthesia drugs act on different types of receptors. But while the pharmacological action and neurophysiological response of propofol, are well recognized, the mechanism by which propofol and other anesthetics render unconsciousness are not well understood. Miller, Fiete, and colleagues hypothesized that propofol, and possibly other anesthesia drugs, interfere with a brain state known as dynamic stability. “One hypothesis is that anesthesia disrupts dynamic stability—the ability of the brain to balance excitability with the need to be stable and controllable,” the team commented.
In this state, neurons have enough excitability to respond to new input, but the brain is able to quickly regain control and prevent them from becoming overly excited. “Brain states should be sufficiently excitable for generation of widespread activity and information integration. But they also need to be controllable and stable, reliably producing the same computations,” the investigators further noted.
Prior studies on how anesthesia drugs affect this balance have reported conflicting results. Some suggested that during anesthesia the brain shifts toward becoming too stable and unresponsive, which leads to loss of consciousness. Others found that the brain becomes too excitable, leading to a chaotic state that results in unconsciousness. “Previous work on cortical stability during anesthesia has produced contradictory results, suggesting that anesthesia either destabilizes or excessively stabilizes neural dynamics,” the authors noted.
Part of the reason for these conflicting results is that it has been difficult to accurately measure dynamic stability in the brain. “This could be due to a paucity of studies using high-density intracortical electrophysiology and the inability to therefore apply sufficiently rich dynamical tools to assess stability,” the team continued.
Measuring dynamic stability as consciousness is lost would help researchers determine if unconsciousness results from too much stability or too little stability. For their newly reported study the researchers analyzed electrical recordings made in the brains of animals that received propofol over an hour-long period, during which they gradually lost consciousness. The recordings were made in four areas of the brain that are involved in vision, sound processing, spatial awareness, and executive function. “… we used a dataset of local field potential (LFP) recordings with hundreds of electrodes from multiple brain regions in two non-human primates (NHPs, specifically adult rhesus macaque monkeys) as they lost and regained consciousness due to propofol anesthesia … “Electrodes were placed in four areas: ventrolateral prefrontal cortex, frontal eye fields, posterior parietal cortex, and auditory cortex.”
These recordings covered only a tiny fraction of the brain’s overall activity, so to overcome that the researchers used a technique called delay embedding. This technique allows researchers to characterize dynamical systems from limited measurements by augmenting each measurement with measurements that were recorded previously. “We introduce a new approach—delayed linear analysis for stability estimation (DeLASE). DeLASE directly quantifies changes in stability in neural data,” they explained.
The researchers were able to validate their method, and applied the technology to quantify how the brain responds to sensory inputs, such as sounds, or to spontaneous perturbations of neural activity. They then used their method to determine the impact of propofol anesthesia on the stability of neural dynamics by analyzing multi-electrode activity recorded in two non-human primates. They found that in the normal, awake state, neural activity spikes after any input, then returns to its baseline activity level. However, once propofol dosing began, the brain started taking longer to return to its baseline after these inputs, remaining in an overly excited state. This effect became more and more pronounced until the animals lost consciousness. The results, the team suggested, indicate that propofol’s inhibition of neuron activity leads to escalating instability, which causes the brain to lose consciousness.
To see if they could replicate this effect in a computational model, the researchers created a simple neural network. When they increased the inhibition of certain nodes in the network, as propofol does in the brain, network activity became destabilized, similar to the […]
5 Science-backed health benefits of garlic
Tags: #nutrition , anticancer , diabetes , disease prevention , food cures , food is medicine , food science , functional food , garlic , goodfood , goodhealth , heart disease , heart health , herbal medicine , Herbs , metabolic syndrome , natural cures , natural health , natural medicine , nutrients , organics , Osteoarthritis , prevent cancer , prevention , stomach cancer , superfoods Many savory dishes feature garlic, a flavorful superfood. According to scientific data, garlic offers many amazing health benefits , such as supporting optimal heart health and protecting against cancer.
Known scientifically as Allium sativum , garlic is a culinary staple and an impressive powerhouse of bioactive compounds with beneficial effects on human health.
Garlic is a great source of potassium, which helps with muscle contraction and heart function.
Garlic also contains selenium that your body uses for reproduction and deoxyribonucleic acid (DNA) production.
Additionally, garlic contains manganese , a mineral that is used by the body for building strong bones and maintaining a healthy immune system.
Here are five science-backed benefits of incorporating garlic into a balanced diet: Supports optimal cardiovascular health
According to a study published in the journal Proceedings From the National Academy of Sciences , consuming garlic boosts the production of hydrogen sulfide.
This bioactive compound acts as a powerful antioxidant and assists with cellular signaling to increase circulation and relax blood vessels. This could explain why garlic has long been known as a natural treatment that can also prevent heart disease , which includes atherosclerosis , coronary artery disease, heart attack and stroke. Helps reverse or treat metabolic syndrome
A study published in the Journal of Dietary Supplements revealed that consuming crushed raw garlic significantly improved fasting blood sugar, waist circumference, cholesterol levels (both by lowering triglyceride levels and raising high-density lipoprotein (HDL) levels) and blood pressure in those with metabolic syndrome.
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Metabolic syndrome is a deadly collection of comorbidities, including high cholesterol, high blood sugar, high blood pressure and excessive abdominal fat. Helps protect against different types of cancer
According to a meta-analysis published in the journal Gastroenterology , consuming vegetables from the Allium family, which includes garlic, onions, leeks and chives, significantly reduces someone’s risk of developing stomach cancer .
Several studies have also suggested that garlic consumption can reduce the risk of cancer in the brain, esophagus, lungs and prostate. (Related: Harness the legendary power of garlic, the everyday superfood, with this simple recipe .) Helps with diabetes management
A meta-analysis published in the journal Food & Nutrition Research evaluated nine randomized controlled trials looking at garlic consumption in patients with Type 2 diabetes.
The results revealed that there were statistically significant improvements in blood sugar and other key diabetic biomarkers when the subjects took garlic supplements, which contained a compound called allicin, with daily amounts ranging from 0.05 to 1.5 grams. Helps protect against osteoarthritis
A cross-sectional study published in the journal BMC Musculoskeletal Disorders revealed that women who regularly consume garlic and other Allium vegetables had a significantly reduced risk of hip osteoarthritis.
The authors suggested that this could be due to diallyl disulfide, a compound in garlic believed to repress enzymes that break down skeletal bone matrixes.
Additionally, diallyl disulfide is well-known due to its antioxidant, anti-inflammatory and antimicrobial properties, contributing to garlic’s ability to support optimal cardiovascular health and protect against various diseases.
Other reported benefits of garlic include a reduced risk of preterm delivery, alcohol-induced liver damage and the common cold. How to incorporate garlic into your daily routine
Now that you know about the health benefits of garlic , how much garlic do you need to eat to reap these benefits?
The exact amount isn’t confirmed yet.
According to a study published in the journal Proceedings From the National Academy of Sciences , a concentration of garlic extract equivalent to about two medium-sized garlic cloves per day should be enough.
That may sound like a lot, but garlic is a versatile ingredient. You can easily add it to almost any meal, such as homemade salad dressings, hummus, chicken, fish, meat, poultry, stir-fry, omelets and more.
Here are more ways to add garlic to your regular diet:
Eat it raw
This isn’t the most palatable way to consume garlic, but research, such as an August 2013 study published in the journal Food and Chemical Toxicology , suggests that garlic loses its powerful anti-inflammatory properties once it has been heated. Know the right way to prepare garlic If you are going to cook garlic, chop, slice, or smash the cloves for at least 10 minutes before putting it on the heat.Preparing garlic this way initiates an enzymatic process that maximizes its health-boosting benefits. Try an aged garlic extract If you can’t stomach the taste of fresh garlic or have trouble with it due to indigestion, try a high-quality aged garlic extract instead. Make garlic bread at home Follow the steps below to make garlic bread : > Chop one clove of garlic. Mix the garlic with a teaspoon of your preferred oil. Toast a piece of whole-wheat bread. Spread the garlic and oil mixture on the toast while it is still warm. Store garlic cloves in the pantry or a cupboard in your kitchen. Room-temperature places that remain cool and dark are the perfect places to store garlic.If you’re worried about having smelly “garlic breath,” chew on raw mint. You can also try eating lettuce, fennel seeds, or apples after a garlicky lunch or dinner.If you have a heart condition and are taking heart medications, […]