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Prioritizing the unexpected: New brain mechanism uncovered
by Sainsbury Wellcome Centre Neurons in the mouse visual cortex with VIP neurons in magenta. Credit: Sainsbury Wellcome Centre Researchers have discovered how two brain areas, the neocortex and the thalamus, work together to detect discrepancies between what animals expect from their environment and actual events. These prediction errors are implemented by selective boosting of unexpected sensory information. These findings enhance our understanding of predictive processing in the brain and could offer insights into how brain circuits are altered in autism spectrum disorders (ASDs) and schizophrenia spectrum disorders (SSDs).
The research, published in Nature, outlines how scientists at the Sainsbury Wellcome Centre at UCL studied mice in a virtual reality environment to take us a step closer to understanding both the nature of prediction error signals in the brain as well as the mechanisms by which they arise.
“Our brains constantly predict what to expect in the world around us and the consequences of our actions. When these predictions turn out wrong, this causes strong activation of different brain areas, and such prediction error signals are important for helping us learn from our mistakes and update our predictions. But despite their importance, surprisingly little is known about the neural circuit mechanisms responsible for their implementation in the brain,” explained Professor Sonja Hofer, Group Leader at SWC and corresponding author on the paper.
To study how the brain processes expected and unexpected events, the researchers placed mice in a virtual reality environment where they could navigate along a familiar corridor to get to a reward. The virtual environment enabled the team to precisely control visual input and introduce unexpected images on the walls. By using a technique called two-photon calcium imaging, the researchers were able to record the neural activity of many individual neurons in the primary visual cortex , the first area in our neocortex to receive visual information from the eyes.
“Previous theories proposed that prediction error signals encode how the actual visual input is different from expectations, but surprisingly we found no experimental evidence for this. Instead, we discovered that the brain boosts the responses of neurons that have the strongest preference for the unexpected visual input,” explained Dr. Shohei Furutachi, Senior Research Fellow in the Hofer and Mrsic-Flogel labs at SWC and first author on the study.
“The error signal we observe is a consequence of this selective amplification of visual information. This implies that our brain detects discrepancies between predictions and actual inputs to make unexpected events more salient.” VIP and pulvinar interactions. Credit: Sainsbury Wellcome Centre To understand how the brain generates this amplification of the unexpected sensory input in the visual cortex, the team used a technique called optogenetics to inactivate or activate different groups of neurons. They found two groups of neurons that were important for causing the prediction error signal in the visual cortex: vasoactive intestinal polypeptide (VIP)-expressing inhibitory interneurons in V1 and a thalamic brain region called the pulvinar, which integrates information from many neocortical and subcortical areas and is strongly connected to V1.
But the researchers found that these two groups of neurons interact in a surprising way.
“Often in neuroscience, we focus on studying one brain region or pathway at a time. But coming from a molecular biology background, I was fascinated by how different molecular pathways synergistically interact to enable flexible and contextual regulation. I decided to test the possibility that cooperation could be occurring at the level of neural circuits, between VIP neurons and the pulvinar,” explained Dr. Furutachi.
And indeed, Dr. Furutachi’s work revealed that VIP neurons and pulvinar act synergistically together. VIP neurons act like a switchboard: When they are off, the pulvinar suppresses activity in the neocortex, but when VIP neurons are on, the pulvinar can strongly and selectively boost sensory responses in the neocortex. The cooperative interaction of these two pathways thus mediates the sensory prediction error signals in the visual cortex.
The next steps for the team are to explore how and where in the brain the animals’ predictions are compared with the actual sensory input to compute sensory prediction errors and how prediction error signals drive learning. They are also exploring how their findings could help contribute to understanding ASDs and SSDs.
“It has been proposed that ASDs and SSDs can both be explained by an imbalance in the prediction error system. We are now trying to apply our discovery to ASDs and SSDs model animals to study the mechanistic neural circuit underpinnings of these disorders,” explained Dr. Furutachi.
More information: Sonja Hofer, Cooperative thalamocortical circuit mechanism for sensory prediction errors, Nature (2024). DOI: 10.1038/s41586-024-07851-w . www.nature.com/articles/s41586-024-07851-w
Provided by Sainsbury Wellcome Centre
Power Naps: Surprising Health Benefits and How to Take Them
Power naps are short naps that last 30 minutes or less. Napping has many benefits, such as improved performance at work, better brain function, and mood benefits.1 However, not all naps are created equally.
A power nap differs from a regular nap in that you do not complete an entire sleep cycle with a power nap vs. a longer nap. With a power nap, you are less likely to experience sleep issues at night. Guido Mieth / Getty Images How Long Is a Power Nap?
Power naps are short—between 10 and 30 minutes. Research shows that the ideal length for a power nap is 26 minutes. This duration decreases the risk of drawbacks such as post-nap drowsiness and increases benefits such as alertness and productivity.2
Short naps give you enough rest to increase energy and brain function but not enough time to complete a full sleep cycle . While a 30-minute power nap won’t make up for a lot of sleep debt (the amount of sleep lost from poor sleep), it is less likely to interfere with your ability to fall asleep and get quality sleep at night. Health Benefits of Power Naps
There are many reasons to try power napping, as it’s associated with various benefits , including:3 Better memory function
Decreased fatigue
Decreased reaction time
Fewer accidents
Improved attention
Improved heart health
Improved mood
Increased alertness
Increased safety
Lower stress and anxiety levels
Optimized performance
Are Power Naps Right for You?
Despite their positives, power naps are not suitable for everyone. Research shows that napping can decrease sleep quality at night. If any of the following apply to you, power naps might not be the answer to your fatigue :4 Insomnia : Power naps may increase the severity of insomnia as it can make it more difficult to fall asleep at night or stay asleep in people with this problem.
Sleep apnea : Power naps are not a cure for sleep disorders such as sleep apnea . While they can help increase energy and performance, getting quality sleep and addressing the underlying condition is still important.
Determining an ideal sleep schedule is different for everyone. If you struggle with sleep, consider talking to a healthcare provider. A sleep specialist or psychologist will ask about your lifestyle, day-to-day responsibilities, and overall health to determine if power naps could benefit you or if something more serious is contributing to your sleep challenges. How to Take a Power Nap
Learning to power nap can take practice, especially if you don’t typically nap during the day.
Steps to power napping include:5
> Find a time for a short nap, such as a break at work.
Silence your phone notifications and ask others not to disturb you while you nap.
Lie down in a comfortable place.
Set an alarm for the amount of nap time plus the time it takes to fall asleep (for example, 26 minutes of power nap plus five minutes to fall asleep equals 31 minutes for the alarm).
Use earplugs or a sound machine to limit noise. Turn out the lights, close curtains or shades, and use an eye mask to block light. Do a pre-sleep relaxation exercise to reduce stress and calm your thoughts, and prepare for sleep. Stay consistent and nap at the same time each day. Set an Alarm Experts recommend setting an alarm for 15 or 30 minutes when taking a power nap to prevent long naps and train the body and mind for shorter naps during the day.1Before you set an alarm, consider how long it typically takes you to fall asleep and add that amount of time to your target nap duration. For example, if it typically takes 10 minutes to relax and fall asleep, add 10 extra minutes to your alarm so your nap does not end too soon after you fall asleep. Nap Early Midday naps are best for optimizing benefits such as executive function (e.g., attention, focus, memory, etc.) without interfering with nightly sleep.6Napping too close to bedtime—even taking short power naps—can be refreshing enough to make it more difficult to fall asleep at night. It is OK to take power naps in the morning if you’re tired, but most people are not ready to fall asleep until midday or early afternoon.”Early” naps may mean something different to people with alternate sleep schedules, such as those working the night shift . However, the same idea applies: Taking power naps earlier and not too close to the primary stretch of sleep is important. Create a Calm Sleep Environment Preparing the environment for sleep is crucial, especially when creating a new power napping routine. Having a routine cues your brain that it is time to nap, making it easier to fall asleep quickly.Since power naps typically take place during the day, using products such as earplugs and an eye mask can help eliminate outside distractions, make it easier to fall asleep and prevent being awakened by something other than your alarm.1 Summary Power naps are between 10 and 30 minutes, taken during the day, for a boost of energy. They can help improve performance, mood, and safety, among other things. Since they are too short to complete a full sleep cycle, power naps are less likely than longer naps to interfere with nighttime sleep.It is best to nap midday and not too close to bedtime. Power naps are not for everyone and do not cure sleep disorders. Contact a healthcare provider if you suspect a sleep disorder.
Brain Scientists Finally Discover the Glue that Makes Memories Stick for a Lifetime
6 min read
A long-running research endeavor reveals key chemical players that cement memories in place—and still more have yet to be discovered
By Simon Makin Synapse Sebastian Kaulitzki/Science Photo Library/Getty Images The persistence of memory is crucial to our sense of identity, and without it, there would be no learning, for us or any other animal. It’s little wonder, then, that some researchers have called how the brain stores memories the most fundamental question in neuroscience.
A milestone in the effort to answer this question came in the early 1970s, with the discovery of a phenomenon called long-term potentiation, or LTP. Scientists found that electrically stimulating a synapse that connects two neurons causes a long-lasting increase in how well that connection transmits signals. Scientists say simply that the “synaptic strength” has increased. This is widely believed to be the process underlying memory. Networks of neural connections of varying strengths are thought to be what memories are made of.
In the search for molecules that enable LTP, two main contenders emerged. One, called PKMzeta (protein kinase Mzeta), made a big splash when a 2006 study showed that blocking it erased memories for places in rats. If obstructing a molecule erases memories, researchers reasoned, that event must be essential to the process the brain uses to maintain memories. A flurry of research into the so-called memory molecule followed, and numerous experiments appeared to show that it was necessary and sufficient for maintaining numerous types of memory. On supporting science journalism
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The theory had a couple of holes, though. First, PKMzeta is short-lived. “Those proteins only last in synapses for a couple of hours, and in neurons, probably a couple of days,” says Todd Sacktor, a neurologist at SUNY Downstate Health Sciences University, who was co-senior author of the 2006 study. “Yet our memories can last 90 years, so how do you explain this difference?” Second, PKMzeta is created in cells as needed, but then it has to find the right synapses. Each neuron has around 10,000 synapses, only a few percent of which are strengthened, says neuroscientist Andre Fenton, the other co-senior author of the 2006 study, who is now at New York University. The strengthening of some synapses and not others is how this mechanism stores information, but how PKMzeta molecules accomplish this was unknown.
A new study published in Science Advances by Sacktor, Fenton and their colleagues plugs these holes . The research suggests that PKMzeta works alongside another molecule, called KIBRA (kidney and brain expressed adaptor protein), which attaches to synapses activated during learning, effectively “tagging” them. KIBRA couples with PKMzeta, which then keeps the tagged synapses strengthened.
Experiments show that blocking the interaction between these two molecules abolishes LTP in neurons and disrupts spatial memories in mice. Both molecules are short-lived, but their interaction persists. “It’s not PKMzeta that’s required for maintaining a memory, it’s the continual interaction between PKMzeta and this targeting molecule, called KIBRA,” Sacktor says. “If you block KIBRA from PKMzeta, you’ll erase a memory that’s a month old.” The specific molecules will have been replaced many times during that month, he adds. But, once established, the interaction maintains memories over the long term as individual molecules are continually replenished.
The findings boost a theory that has seen some pushback. In 2013 two studies showed that mice genetically engineered to lack PKMzeta could form long-term memories. Furthermore, the molecule researchers had used to block PKMzeta in the earlier studies — known as ZIP (zeta-inhibitory peptide)—also abolished memories in these mice, showing that it must be interacting with some other molecule. Three years later Sacktor and Fenton proposed an explanation. The researchers published a study suggesting that another, related protein, PKCiota/lambda, stepped in to take over PKMzeta’s job in animals engineered to lack PKMzeta from birth. PKCiota/lambda exists in normal animals’ synapses in small and fleeting quantities, but the researchers found that it was greatly elevated in mice lacking PKMzeta. They also showed that ZIP blocks PKCiota/lambda, which explains why it erased memories in the engineered mice.
This became a serious criticism of PKMzeta studies: ZIP’s effects were not as specific as originally thought. Not only does it block molecules other than PKMzeta, but one study also found that it even suppresses brain activity .
The new study addresses this issue. The researchers used two different molecules to block PKMzeta and KIBRA from interacting. They first showed that both of these blockers only prevent PKMzeta from attaching to KIBRA. Neither stop PKCiota/lambda from doing so. Experiments showed that both blockers reversed LTP and disrupted memories in normal mice but had no effect on memory storage in mice engineered to lack PKMzeta. “Evidence is more trustworthy when you have converging results showing the same thing with different methods,” says Janine Kwapis, a neuroscientist at Pennsylvania State University, who was not involved in the study. “It’s really convincing.”
The results show that blocking PKMzeta—but not PKCiota/lambda—in normal, nonengineered animals erases memories, so under ordinary circumstances, iota/lambda cannot be crucial to long-term memory storage because its presence in the brain does not prevent memories being erased. “We nailed it,” Sacktor says. “There’s no getting away from [the conclusion that] PKMzeta is critical.” Fenton and Sacktor think PKCiota/lambda is an evolutionary relic that was involved in memory eons ago. Once PKMzeta evolved, it replaced iota/lambda, and it does a better job. But when scientists knock out the PKMzeta gene in laboratory animals, the animals compensate by falling back on iota/lambda.
The study also makes sense of a previously puzzling finding. In 2011 Sacktor and colleagues showed that boosting PKMzeta in rats enhanced old memories . “You could enhance a memory that had almost but not quite gone,” Sacktor says. “That had never been seen before.” This was unexpected because indiscriminately strengthening synapses should weaken memories, not strengthen them. “That was a weird finding,” says […]
Widely used sleep supplement can boost memory and combat cognitive decline
Credit: Unsplash+ Recent research from Tokyo Medical and Dental University has uncovered a potential new approach to preserving memory and protecting against cognitive decline, a common issue as we age.
The study, led by scientists including Atsuhiko Hattori, focused on melatonin, a hormone known for regulating sleep, and its metabolites—substances that melatonin breaks down into once inside the body.
The researchers found that these metabolites, particularly one called AMK, may help improve memory and shield against cognitive deterioration.
Memory testing in mice often relies on their natural curiosity. When presented with familiar and unfamiliar objects, mice typically spend more time exploring the new, unfamiliar ones.
This behavior indicates that they remember the familiar objects, showcasing their cognitive function. However, as cognitive decline sets in, mice begin to treat all objects as if they are new, suggesting a deterioration in memory—similar to how memory loss can manifest in humans.
In their study, the researchers explored whether melatonin’s metabolites could enhance memory. After familiarizing mice with certain objects, they administered doses of melatonin and its metabolites, including AMK, about an hour later.
The next day, they tested the mice’s memory of these objects. The results were promising: memory significantly improved after treatment, with AMK showing the strongest effect.
The researchers discovered that all three metabolites of melatonin accumulated in the hippocampus, a key area of the brain involved in converting experiences into long-term memories.
Crucially, they also found that if melatonin was prevented from converting into AMK, the positive effects on memory were lost. This suggests that AMK plays a vital role in enhancing memory formation.
What makes these findings particularly exciting is that the benefits were observed across all ages of mice, including older ones. Given that cognitive decline is often associated with aging, the researchers are hopeful that these results could translate to humans as well.
If future studies confirm similar effects in people, AMK could become a valuable tool in reducing the severity of Mild Cognitive Impairment (MCI), a condition that can sometimes progress to Alzheimer’s disease.
This research, published in the Journal of Pineal Research , opens up new avenues for potentially slowing or even reversing cognitive decline through melatonin’s metabolites.
The prospect of using AMK therapy to support memory and protect against diseases like Alzheimer’s is an encouraging development in the field of cognitive health.
As studies continue, this could one day lead to effective treatments for preserving memory and maintaining cognitive function as we age.
If you care about dementia, please read studies about Vitamin B9 deficiency linked to higher dementia risk , and flavonoid-rich foods could help prevent dementia .
For more information about brain health, please see recent studies that cranberries could help boost memory , and how alcohol, coffee and tea intake influence cognitive decline .
Copyright © 2024 Knowridge Science Report . All rights reserved.
Ultrasound Brain Stimulation Boosts Mindfulness
2 min read
Study participants felt time distortion, fewer negative thoughts and greater detachment from feelings with a noninvasive ultrasound intervention
By Lucy Tu janiecbros/Getty Images Even when you aren’t doing anything, your brain is relentlessly active— daydreaming, ruminating, contemplating the past or future . How this mind wandering functions can significantly shape a person’s internal conscious experience.
In a recent study of 30 participants, researchers applied low-intensity ultrasound waves to a brain region associated with introspection and off-task mind wandering. Participants who underwent five minutes of ultrasound stimulation reported significantly heightened mindfulness—the ability to be fully present in the moment, without judgment toward others or the self. The results were published in Frontiers in Human Neuroscience .
“I haven’t seen ultrasound technology used in this way, but this type of neuromodulation has significant potential to change how we think about and enhance mindfulness,” says University of Wisconsin–Madison social psychologist Hadley Rahrig, who also studies that state of mind. On supporting science journalism
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The researchers targeted the brain’s default mode network (DMN), a constellation of interconnected areas that become particularly active when the mind disengages with the outside world and drifts into activities such as reminiscing or envisioning the future. Abnormal DMN activity and connectivity have been linked to anxious rumination and depressive symptoms. “You get stuck, where your mind just keeps going and you can’t stop it. We hypothesized that we could use ultrasound stimulation to remove some stickiness and let the network cool off,” says the new study’s lead author, Brian Lord, a cognitive neuroscientist at the University of Arizona.
Since the DMN was described in 2001, scientists have sought to manipulate it through broad-brush methods such as meditation and psychedelic drug therapy . But it remained difficult to precisely adjust DMN function because of its deep-brain location.
To overcome this challenge, Lord and his team used transcranial-focused ultrasound, a technique that converts electric current into concentrated and localized acoustic waves. (Half the participants received sham ultrasound as a control.) These waves can penetrate brain regions with millimeter-level precision and with greater depth than other noninvasive stimulation methods, which typically use magnetic fields or scalp-attached electrodes to induce electric currents spread over several centimeters.
Functional MRI scans showed that the researchers successfully inhibited activity in the posterior cingulate cortex, a key area in the DMN linked to emotional regulation and concentration during meditation. Through questionnaires and an interview, participants in the treatment group reported at least 30 minutes of subjective effects akin to entering a deep meditative state: a distorted sense of time, fewer negative thoughts and an improved ability to detach from their feelings. Other scientists at the University of Arizona are testing this technique to treat mood disorders such as depression.
“One of the greatest barriers to meditation and mindfulness is the steep learning curve. Brain stimulation can act like training wheels for the mind, helping people achieve that deep state of consciousness,” Lord says. “That’s our larger goal.”
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Lucy Tu is a freelance writer and a Rhodes Scholar studying reproductive medicine and law. She was a 2023 AAAS Mass Media Fellow at Scientific American .
Communist-funded vaccine incentives plan used in Walz’s Minnesota plandemic may be NATIONWIDE SCAM to vax to death children for “Bird Flu” in 2025
Who wants a government-funded “incentive” to poison themselves? Step right up and get your $200 visa gift cards and college scholarships for all kids ages 5 – 11 who get the next scamdemic mRNA nanoparticle jabs that cause heart attacks , strokes, infertility, turbo cancer, deranged thinking, loss of appetite and 3-foot-long vascular clots. That’s exactly what Commie Minnesota Governor Walz , the current VP candidate for the Dems, did during the Covid scamdemic.
Should the communists in DC maintain control in November (steal the election again), the other choice will most likely involve heavy fines and prison time (in “re-education camps by FEMA/DHS) for those who do not comply with the next round of “novel” mRNA clot shots for the lab-made-whatever-disease that’s supposedly spreading everywhere like wildfire. White Clot Syndrome: 40 trillion mRNA spike prions clog the entire vascular system, limiting oxygen, blood flow, and nutrients to vital organs, including the liver, lungs and brain
Now it’s being revealed that Covid boosters may help generate up to 100 trillion spike proteins in your blood, clogging up the liver, the lungs and the brain. This is modified RNA. Your DNA has been hijacked to produce deadly prions , and you can’t even sue the manufacturers because they have their own “immunity,” and it’s 100% resistant to your lawyers and your limited wallet of funds.
Prions are misfolded proteins, like the spike proteins that mRNA instructs human cells to produce, that can cause severe neurodegenerative diseases . They can spread throughout the entire vascular system and end up lodging in the brain, ovaries, liver, pancreas and lungs. The clots from mRNA “vaccines” should be viewed as a radical new form of prion disease, also known as White Clot Syndrome.
Because Covid-19 was not a danger to teens, children or babies, the Vaccine Industrial Complex had to conjure up ways to coerce parents into having the deadly, experimental prion injections given to their young. Do you remember any other “medicine” or “vaccination” that the government literally PAID you to take? Major red flags should go up here for every American, whether you believe in vaccination or not. Shocking research reveals 90% of the U.S. population suffers from vaccine-induced spike prion clogging of the vascular system, a combination of CKM and WCS syndromes
New data reveals nearly every person who got an mRNA jab or two (or three) is now suffering from some level of heart strain from the trillions of prions ModRNA creates in the bloodstream, also known as White Clot Syndrome. Medical doctors are befuddled. They all got the wool pulled over their eyes with this Covid jab frenzy, just like Democrats who thought Biden wasn’t senile. Who knew? Independent truth media advocates and natural health advocates knew, that’s who.
Less than one year ago, the American Heart Association published a report about the frightening skyrocketing numbers of people suffering from cardiovascular disease, that overlaps type 2 diabetes, obesity and kidney disease. The AMA called the overlap CKM syndrome (cardiovascular-kidney-metabolic syndrome).
CKM and WCS (White Clot Syndrome) are now a combination serial killer, with the worst damage occurring in blood vessels, the heart muscle and the cardiovascular system. That is why Covid-vaxxed athletes, military members and pilots are dropping dead or having massive heart attacks out of the blue. Medical doctors are realizing this too, but cannot point the finger at the mRNA WCS jabs or they will lose their medical license instantly, and forever.
Beware of the next round of mRNA death jabs, most likely under a new plandemic name, like Bird Flu or Monkey Pox. Bookmark Vaccines.news to your favorite independent websites for updates on Long-Vax-Syndrome that’s about to get a million times worse when the next round of ModRNA jabs infect the masses. #WhiteClotSyndrome
Sources for this article include:
NaturalNews.com
BigLeaguePolitics.substack.com
WMCresearch.substack.com
THC Could Protect Brain From Aging, Study Finds
Two senior girlfriends 83 years old smoke medicinal marijuana together. One of them shows the other A promising new study suggests that long-term, low-dose THC intake may protect the brain from aging, improve cognitive function in older age, and promote overall longevity.
A group of researchers from the University of Bonn in Germany recently published a study in the journal ACS Pharmacology & Translational Science that investigates the impact of long-term THC treatment, the main psychoactive compound of cannabis, on brain aging.
The study centers on a key cellular pathway known as mTOR, a protein that plays a crucial role in aging by regulating how cells manage energy and create new structures, such as synapses in the brain, essential for learning and memory.
The researchers aimed to determine whether long-term, low-dose THC could affect the aging brain by influencing mTOR activity and overall metabolism.
They found that THC had a dual effect. Initially, in the brain, THC enhanced mTOR activity, which in turn raised the production of energy and important proteins required for brain function. This resulted in an increase in synaptic proteins, crucial for establishing and sustaining connections between neurons. However, following this initial increase, mTOR activity and metabolic processes in other parts of the body, such as fat tissue and blood, decreased. This reduction resembled the effects seen during a low-calorie diet, which is recognized for its potential anti-aging benefits.
The study, therefore, suggests that this dual effect—enhancing brain activity while lowering metabolism in other parts of the body—might help explain why THC could be advantageous for brain aging.
To achieve these results, the researchers conducted experiments using mice treated with low doses of THC over a long period to see how this treatment affected the mice as they aged, particularly in relation to their brain function and overall metabolism.
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Researchers conducted long-term experiments on mice treated with low doses of THC to examine its effects on brain function and metabolism as the mice aged. They focused on how THC influenced mTOR activity in the brain and also investigated its impact on fat tissue and blood. Compared to untreated mice, those receiving THC showed increased mTOR activity, which supported higher energy production and synaptic protein creation in the brain. Passport: Explore the finest destinations and experiences around the world in the Forbes Passport newsletter.
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This suggests that THC treatment might help the brain better manage aging. THC could offer therapeutic benefits for cognitive decline associated with aging. This perspective challenges conventional views on cannabis and suggests new medical applications, especially for age-related brain disorders such as Alzheimer’s disease .
Researchers point out that most studies examine the short-term effects of high cannabis doses, which frequently show negative results. However, this study indicates that a carefully controlled low-dose regimen could have beneficial effects, especially related to aging.
Although the study was done in mice, its findings might have implications for human aging. If similar effects are seen in people, this could lead to new methods for managing aging and cognitive decline.
While the study highlights the potential benefits of long-term THC use, it also raises concerns about its long-term safety and balance of effects. Limitations include reliance on mouse models, which may not fully represent human aging and brain function. Uncertainties remain regarding dosage, long-term safety, and overall health impacts. Furthermore, the focus on low-dose THC does not address potential side effects or differences in individual responses, which are important factors for considering therapeutic use in humans.
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Dario Sabaghi is a freelance journalist specializing in international news and the cannabis industry.
Since 2021, he has been contributing to Forbes,
…
The Hidden Risks of Hearing Loss
Woman doctor examining an elderly man’s ear Hearing loss is frustrating for those who have it and for their loved ones. But recent research from Johns Hopkins reveals that it also is linked with walking problems, falls and even dementia.
In a study that tracked 639 adults for nearly 12 years, Johns Hopkins expert Frank Lin, M.D., Ph.D . , and his colleagues found that mild hearing loss doubled dementia risk. Moderate loss tripled risk, and people with a severe hearing impairment were five times more likely to develop dementia. The Links Between Hearing and Health
“Brain scans show us that hearing loss may contribute to a faster rate of atrophy in the brain,” Lin says. “Hearing loss also contributes to social isolation. You may not want to be with people as much, and when you are you may not engage in conversation as much. These factors may contribute to dementia.”
As you walk, your ears pick up subtle cues that help with balance. Hearing loss mutes these important signals, Lin notes. “It also makes your brain work harder just to process sound. This subconscious multitasking may interfere with some of the mental processing needed to walk safely.” Research Shows Many Causes, Early Symptoms
Everything from genes and noise exposure to medications, head injuries and infections can play a role in hearing loss. Trouble detecting soft or high-pitched sounds is often the first sign that stereocilia — the delicate hair cells that convert sound waves into electrical signals within the ear — have been damaged. Soft sounds include phone conversations or background noise in settings such as restaurants. High-pitched sounds may include children’s voices. Ringing in the ears, called tinnitus, is another early signal of possible hearing loss. Hearing Aid Myths That Hold You Back
Can hearing aids reduce these risks? Lin hopes to find out in a new study, still in the planning stages. “These studies have never been done before,” he notes. “What we do know is that there’s no downside to using hearing aids. They help most people who try them. And in those people, they can make all the difference in the world—allowing people to reengage with friends and family and to be more involved again.”
Although nearly 27 million Americans age 50 and older have hearing loss, only one in seven uses a hearing aid. If you think your hearing has diminished, it’s worth making an appointment with an audiologist for a hearing check, Lin says. If you have hearing loss, don’t let the following myths keep you from getting help. “My hearing’s not that bad.”
Hearing aid users wait, on average, 10 years before getting help for hearing loss. But during that time, communication with loved ones becomes more difficult, and isolation and health risks increase. “Our findings emphasized just how important it is to be proactive in addressing any hearing declines over time,” says Lin. “Wearing hearing aids means I’m old, and I’m not ready for that.”
It’s normal to feel worried that hearing loss means you’re aging—and to want to hide it. Plenty of people with a hearing impairment sit silently rather than joining in conversations and activities, because they fear that hearing problems will make them seem helpless or less than competent. The truth: Connecting with others can help your brain stay younger and keep you involved with life. “I don’t like the way hearing aids look.”
Forget the old days of big, whistling earpieces. Today’s hearing aids and cochlear implants are smaller (and less conspicuous) than ever before. Even celebrities (like former president Bill Clinton and football Hall of Famer Mike Singletary) are wearing them proudly. “I heard that hearing aids are difficult to use.”
There is a breaking-in period as you—and your central auditory system and brain—adjust to life with hearing aids. That’s why most doctors and hearing centers include a trial period, so you can be sure the type you’ve chosen—whether it’s a miniature behind-the-ear model or one that fits into your ear—is right for you. Definitions
Social isolation : Loneliness that can affect health. People who are socially isolated have little day-to-day contact with others, have few fulfilling relationships and lack a sense of belonging. Social isolation can increase the risk for poor eating, smoking, alcohol use, lack of exercise, depression, dementia, poor sleep and heart disease.
Dementia (di-men-sha) : A loss of brain function that can be caused by a variety of disorders affecting the brain. Symptoms include forgetfulness, impaired thinking and judgment, personality changes, agitation and loss of emotional control. Alzheimer’s disease, Huntington’s disease and inadequate blood flow to the brain can all cause dementia. Most types of dementia are irreversible.
Cochlear (koe-klee-er) implant : A device implanted into the inner ear to stimulate the auditory (hearing) nerve. It’s used to help restore sound perception in children and adults with profound hearing loss. The Food and Drug Administration’s recent rule has expanded access to hearing aids by creating a new category of hearing aids: over-the-counter (OTC) hearing aids. Here are the answers to some of the most commonly asked questions about over-the-counter hearing aids.
Kynurenine pathway blockade shows promise for restoring brain metabolism in Alzheimer’s
Among the many ways neuroscientists think Alzheimer’s disease may strip away brain function is by disrupting the glucose metabolism needed to fuel the healthy brain. In essence, declining metabolism robs the brain of energy, impairing thinking and memory.
Against that backdrop, a team of neuroscientists at the Knight Initiative for Brain Resilience at Stanford’s Wu Tsai Neurosciences Institute have zeroed in on a critical regulator of brain metabolism known as the kynurenine pathway. They hypothesize that that the kynurenine pathway is overactivated as a result of amyloid plaque and tau proteins that accumulate in the brains of patients with Alzheimer’s disease.
Now, with support from research and training grants from the Knight Initiative, they have shown that by blocking the kynurenine pathway in lab mice with Alzheimer’s Disease, they can improve, or even restore, cognitive function by reinstating healthy brain metabolism. We were surprised that these metabolic improvements were so effective at not just preserving healthy synapses, but in actually rescuing behavior. The mice performed better in cognitive and memory tests when we gave them drugs that block the kynurenine pathway.” Katrin Andreasson, senior author, neurologist at the Stanford School of Medicine and member of the Wu Tsai Neurosciences Institute The study, which included collaborations with researchers at the Salk Institute for Biological Studies, Penn State University, and others, appeared August 22, 2024 in the journal Science . Hungry neurons
In the brain, kynurenine regulates production of the energy molecule lactate, which nourishes the brain’s neurons and helps maintain healthy synapses. Andreasson and her fellow researchers specifically looked at the enzyme indoleamine-2,3-dioxygenase 1 -; or IDO1, for short -; which generates kynurenine. Their hypothesis was that increases in IDO1 and kynurenine triggered by accumulation of amyloid and tau proteins would disrupt healthy brain metabolism and lead to cognitive decline.
“The kynurenine pathway is over activated in astrocytes, a critical cell type that metabolically supports neurons. When this happens, astrocytes cannot produce enough lactate as an energy source for neurons, and this disrupts healthy brain metabolism and harms synapses” Andreasson said. Blocking production of kynurenine by blocking IDO1 restores the ability of astrocytes to nourish neurons with lactate.
Best of all for Andreasson, and for Alzheimer’s patients, IDO1 is well known in oncology and there are already drugs in clinical trials to suppress IDO1 activity and production of kynurenine. That meant Andreasson could circumvent the time-intensive work of identifying new drugs and to begin testing in lab mice almost immediately.
In those tests, in which mice with Alzheimer’s Disease must navigate an obstacle course before and after drug intervention, Andreasson and team found that the drugs improved hippocampal glucose metabolism, corrected deficient astrocytic performance, and improved the mice’s spatial memory. Promise kept
“We also can’t overlook the fact that we saw this improvement in brain plasticity in mice with both amyloid and tau mice models. These are completely different pathologies, and the drugs appear to work for both,” Andreasson noted. “That was really exciting to us.”
Better yet, this intersection between neuroscience, oncology, and pharmacology could help speed drugs to market if proved effective in ongoing human clinical trials for cancer.
“We’re hopeful that IDO1 inhibitors developed for cancer could be repurposed for treatment of AD,” Andreasson stressed.
The next step is to test IDO1 inhibitors in human Alzheimer’s patients to see if they show similar improvements in cognition and memory. Prior clinical tests in cancer patients tested the effectiveness of IDO1 inhibitors on cancer but did not anticipate or measure improvements in cognition and memory. Andreasson is hoping to investigate IDO1 inhibitors in human trials for Alzheimer’s disease in the near future.
Source:
Stanford University
Journal reference:
Minhas, P. S., et al. (2024) Restoring hippocampal glucose metabolism rescues cognition across Alzheimer’s disease pathologies . Science . doi.org/10.1126/science.abm6131 .
Gen Z blames social media for mental health struggles, yet few are ready to disconnect
Tags: addiction , Anxiety , badhealth , badscience , computing , cyber war , Dangerous , depression , future tech , Gen Z , Glitch , health science , honest , information technology , internet , inventions , mental health , Mind , mind body science , research , smartphone addiction , Social media , truth A recent survey reveals that three out of four Gen Z individuals with internet access in the United States believe social media negatively impacts their mental health .
The survey, which gathered responses from 2,000 Gen Z social media users, found that Instagram and TikTok (both at 20 percent) and Facebook (13 percent) were the platforms most often linked to declines in mental well-being.
For older members of Generation Z, born between 1998 and 2004, growing up with nearly a decade of social media exposure may have contributed to what one expert referred to as ” problematic internet use .” (Related: How smartphone addiction affects brain function and mental health .)
Commissioned by LG Electronics, this survey was carried out online by Talker Research between June 20 and June 24.
The study shows that people start to feel negative emotions just 38 minutes after using social media. This is often because they encounter upsetting content (51 percent), feel unproductive with their time (49 percent) or experience “fear of missing out,” or FOMO (36 percent). On average, individuals spend about five and a half hours each day on social media and 45 percent believe they use it more than their friends do.
Louis Giagrande, LG Electronics head of U.S. marketing, pointed out that spending a lot of time online can leave people feeling drained. He said people should be mindful of the content they engage with to improve their overall well-being and focus on positive content to help manage life’s challenges better and find more happiness.
Interestingly, 62 percent of Gen Zers wish they could reset their social media feeds. Many are frustrated with the content they see, with 53 percent saying it doesn’t match their interests and 54 percent feeling they have little control over what appears in their feeds. Only 16 percent believe they have full control.
Despite these issues, 80 percent of respondents also find that social media can positively impact their mood. Content that tends to lift people’s spirits includes comedy (65 percent), animals (48 percent), beauty-related posts (40 percent) and prank videos (34 percent). Conversely, content related to violence (50 percent), politics (40 percent) and sexual themes (32 percent) often leads to negative feelings.
The study found that two-thirds of people have managed to turn a bad day into a good one thanks to social media. They are also 70 percent more likely to use social media when they’re in a good mood and 44 percent believe it has a positive effect on their outlook on life. Looking ahead, 38 percent think social media platforms will improve their impact on mental health over the next five years.
Gen Zers use social media daily for various reasons, according to the study. Sixty-six percent do it out of boredom, 59 percent seek laughs or smiles, 55 percent need a distraction or break, 49 percent want to stay updated on global events, 44 percent check in on friends, 42 percent seek connections with others, 33 percent look for relaxation and 32 percent search for specific information. How smartphone addiction affects mental health
Recent findings reveal a concerning link between excessive smartphone use and serious mental health issues. Teens who spend more than three hours daily on social media face an increased risk of developing mental health issues, especially those related to internal stress and anxiety.
Research from JAMA Psychiatry , which studied nearly 6,600 U.S. adolescents, suggests that boosting media literacy, limiting social media time and redesigning social media platforms could help alleviate these mental health issues.
A study published in the Canadian Medical Association Journal consolidates evidence from numerous research efforts – showing that heavy smartphone and social media use is associated with greater mental distress, self-harm and suicidal thoughts among young people. This effect is particularly pronounced in girls and follows a pattern where more screen time correlates with more severe problems.
Experts also point out that social media negatively influences teenagers’ self-esteem and their relationship with others. Problems, such as cyberbullying, social comparison and the glorification of self-harm and suicide are prevalent. Furthermore, heavy smartphone use and multitasking contribute to chronic sleep issues – impacting academic performance, cognitive abilities and emotional stability.
San Diego-based psychologist Dr. Jean Twenge and her colleagues have documented a significant rise in anxiety, depression and loneliness among American adolescents. Her latest research shows that high school seniors now spend about an hour less each day engaging in face-to-face social activities compared to their peers from the 19080s. This decrease in personal interaction – such as attending social events, dating and spending time with family – correlates with increased feelings of loneliness, especially since smartphones have become widespread.
Visit Mental.news for more stories about social media and smartphone use and mental health.
Watch this video from SciShow discussing how people can overcome FOMO and lessen their social media addiction .
This video is from the Daily Videos channel on Brighteon.com . More related stories:
Study: Teens with “problematic smartphone use” more likely to experience anxiety and depression .
Are you feeling down? A digital detox can help improve your well-being, says experts .
The link between social media and depression: How to care for your mental health .
Mobile devices rewire your brain, turning you into a reward addict who craves more food .
The miserable generation: Smartphones make children unhappy, screen time should be limited to 2 hours per day, study finds .
Sources include:
StudyFinds.org
ScienceDirect.com SWNSDigital.com JAMANetwork.com NCBI.NLM.NIH.gov PsychologyToday.com Brighteon.com Take Action:Support Natural News by linking to this article from your website.Permalink to this article:CopyEmbed article link:CopyReprinting this article:Non-commercial use is permitted with credit to NaturalNews.com (including a clickable link). Please contact us for more information.
Oxford study reveals COVID-19 mRNA vaccines as the sole cause of heart inflammation and heart failure in children
Researchers at the University of Oxford have uncovered one of the most significant data points with the COVID-19 vaccines. The COVID-19 mRNA vaccines are the sole cause of myocarditis, pericarditis and heart failure among children and adolescents.
This revelation challenges the narrative pushed by the Food and Drug Administration , the Centers for Disease Control and Prevention and mainstream media, which have downplayed or outright denied the risks associated with these vaccines. Children should have never been injected with these instruments of medical fraud, and some suffered heart inflammation and death as a result. (Related: Science behind the CDC’s childhood vaccines lacks double blind, placebo-controlled studies and conceals adverse events .) Myocarditis, pericarditis and heart failure occurred only in the vaccinated adolescents
The extensive study, which analyzed official government data from over one million children and adolescents aged five to 15 in England, found that myocarditis and pericarditis were exclusively linked to COVID-19 vaccinations. No cases of heart inflammation were recorded among unvaccinated children or those infected with COVID-19.
This finding contradicts previous claims linking these serious health issues to COVID-19 infection, sugar intake, video games, or even climate change. Health officials tried to scare parents into vaccinating , claiming their kids would contract COVID-19 and have heart problems from the virus. It turns out that the opposite is true.
According to the Oxford study, all reported cases of myocarditis and pericarditis occurred in children who had received at least one dose of the vaccine. Myocarditis and pericarditis cases were documented exclusively in the vaccinated groups, with a rate of 27 cases per million after the first dose and 10 cases per million after the second dose.
“All myocarditis and pericarditis events during the study period occurred in vaccinated individuals,” the study authors wrote.
Over half of the adolescents affected by myocarditis were hospitalized for their serious vaccine injury. Nearly 60% of children in the first vaccination group never received a second dose, so obviously there were widespread concerns about continuing with the harmful vaccine protocol. How many more children would have been injured had parents or doctors not stepped in and stopped the protocol? The COVID-19 vaccines were completely unnecessary for adolescents
The study also highlighted that hospitalization rates due to COVID-19 were exceedingly rare in the study group, and there were no recorded deaths from the virus. In fact, both the unvaccinated and vaccinated children tested positive for the virus at similar rates, so there’s no solid data proving that the vaccine prevented anything.
This data point also contradicts the fear-based narratives put out by governments and mainstream media authorities. The vaccine was unnecessary from the start and provided no known benefits for adolescents – only heart damage.
Dr. John Campbell, a well-known commentator on medical issues, has condemned the results as “deeply troubling,” stressing that this revelation could have catastrophic implications for public health. “This could not be a more serious report,” Campbell warned, urging immediate action to address the public health crisis revealed by the study. He describes how the vaccine causes stroke in the following video .
To make matters worse, a recent study by Harvard Medical School has linked COVID-19 mRNA vaccines to a sharp increase in sudden deaths worldwide , including fatal cerebral ischemia.
The Harvard researchers specifically implicated Moderna’s vaccine in the recent spike in this deadly brain disorder, which shuts off blood flow to the brain. This serious health issue is more prominent in studies that investigate health outcomes up to a year after vaccination.
The study is also limited, because the control group is centered around unvaccinated populations that were subject to COVID-19 tests, an instrument of medical fraud that was used to forcibly admit children to hospitals and subject them to further deleterious protocol. The study doesn’t look at the large pool of adolescents who didn’t take the tests, who got mildly ill and easily recovered at home.
Sources include:
Medrxiv.com [PDF]
Youtube.com
NCBI.NLM.NIH.gov 1
NCBI.NLM.NIH.gov 2
NaturalNews.com
Reverse ‘TikTok Brain’ With These 8 Dopamine-Boosting Tips
Photo Illustration by Joules Garcia for Verywell Health; Getty Images Key Takeaways
Rapid-fire, reward-driven content like social media videos can interfere with dopamine regulation and make it challenging to maintain focus on tasks lacking immediate gratification.
Incorporating strategies such as regular exercise, adequate sleep, and stress management can help maintain healthy dopamine levels and improve cognitive function.
It’s important to tailor your approach to what works best for you, as everyone’s needs and responses to different strategies can vary.
Your ability to focus is under siege.
Digital distractions are everywhere, supplying small doses of pixelated pleasure at the expense of your brain’s ability to concentrate. Apps like TikTok, for example, are designed to deliver rapid dopamine hits as you intake video after video, triggering a sense of addiction.
There’s nothing inherently wrong with dopamine . Often called the “feel-good” neurotransmitter, dopamine is central to your experience of pleasure, reward, concentration, and motivation.1 It lights up in anticipation of completing a task, driving your focus and motivation toward achieving it. This reward system is crucial for maintaining attention, particularly with tasks that demand more cognitive effort.
While dopamine is essential for motivation and goal-directed behavior, an excess of rapid, shallow dopamine hits—like watching TikTok videos—can erode your capacity for extended focus.1
Experts like Gloria Mark, PhD , a psychologist and expert in attention spans and human/computer interactions, now call this phenomenon “TikTok Brain.”
“People’s attention spans on screens have shortened over the 20 years I’ve been looking at this,” she told Verywell.
TikTok operates on the psychological principle of random reinforcement, where rewards—entertaining clips—come at unpredictable intervals. This unpredictability—never knowing if the next video will delight or disappoint—keeps users hooked, much like gambling, where the anticipation of the next reward fuels the addiction.
Over time, the brain starts craving these quick dopamine hits, triggered by the anticipation of an imminent reward. That makes it increasingly difficult to focus on tasks that don’t offer immediate gratification, such as reading or long-term projects. Studies support these observations, showing that excessive screen time reduces attention spans and disrupts dopamine regulation.2
It is possible to reap the benefits of dopamine in a more sustainable way and rewire your attention span. In addition to working to break your digital dependencies, you’ll need to incorporate dopamine-boosting nutrients, activities, and habits into your daily routine.
Here are some practical strategies you can start implementing today. Broaden Your Supplement Regimen
Several supplements can enhance dopamine production and support cognitive health: Velvet beans ( Mucuna pruriens ) are rich in L-dopa, a direct precursor to dopamine production, and have been shown to significantly boost dopamine levels, especially in individuals with Parkinson’s disease.3
Glutathione , a potent antioxidant, protects the brain from oxidative stress, which is essential for upholding dopamine levels. However, it is best taken intravenously or sublingually due to poor absorption in the gastrointestinal tract.4
Rhodiola and ginkgo biloba improve focus and mental clarity by supporting dopamine pathways.5
L-tyrosine , an amino acid, also enhances dopamine, particularly when you’re under stress.6
“Supplements can be a powerful tool in maintaining brain health, but they should be used thoughtfully and ideally under the guidance of a healthcare provider, particularly when it comes to supporting neurotransmitter balance,” Rachel Goldman, PhD , a licensed psychologist and clinical assistant professor at NYU Grossman School of Medicine, told Verywell. Commit to Daily Movement
Goldman said physical activity is one of the most effective ways to boost dopamine levels. Regular exercise—whether it’s running, cycling, dancing, or even walking—triggers the release of dopamine and other neurotransmitters that elevate mood and sharpen focus. The “runner’s high” often chased by athletes is a direct result of this dopamine surge, leading to enhanced motivation and a greater sense of well-being.
“Exercise can feel overwhelming for some, so I like to keep it realistic,” said Goldman. “Any movement or physical activity is a great start and can significantly boost dopamine levels, along with offering numerous other health benefits.” Prioritize Quality Sleep
During sleep, the brain not only replenishes its dopamine stores but also undergoes crucial processes that support overall cognitive function, like memory consolidation and the removal of toxins accumulated throughout the day.
Adequate, deep sleep is vital for preserving healthy dopamine levels and ensuring that your brain functions optimally. On the other hand, sleep deprivation doesn’t just reduce dopamine receptor sensitivity—it can also impair the brain’s ability to produce dopamine altogether, leading to decreased motivation, impaired focus, and heightened stress levels.7 Opt for Dopamine-Rich Foods
Foods that increase dopamine levels play a significant role in supporting a healthy relationship between your gut health and your brain health (known as the gut-brain axis). Foods rich in tyrosine, an amino acid that’s a precursor to dopamine production, are particularly beneficial.8 These include bananas, avocados, almonds, eggs, and lean meats.
A study in the journal Genes & Nutrition found that flavonoid-rich foods can also improve cognitive function and potentially increase dopamine production, highlighting the importance of diet in supporting optimal dopamine levels.9 You can find flavonoids in berries, dark chocolate, parsley, kale, and green tea. Manage Stress Effectively
Chronic stress is one of the most significant barriers to healthy dopamine levels. Mitigating stress through techniques like mindfulness, meditation, journaling, breathing exercises, or yoga can protect and even boost dopamine production.Regular meditation, in particular, has been shown to enhance dopamine levels, improving focus and reducing anxiety.10Mark also suggests that spending time outdoors can lower stress and restore attention, as nature offers diverse stimuli that can help rejuvenate your mental resources. Try Cold Exposure Cold exposure, such as taking cold showers, ice baths, or using a cryotherapy chamber, is an unconventional but potentially effective way to boost dopamine levels.More research on the topic is needed to support its mental health benefits, but it’s intended to work by stimulating your vagus nerve .“In cryotherapy, it’s vital that the machine includes your head, as this allows the cold to stimulate the vagus nerve, triggering the release of dopamine, epinephrine, and norepinephrine,” Julio Orta, RN, the lead nurse at Restore Hyper Wellness, told […]
A drug that restores brain metabolism could help treat Alzheimer’s
ARI SHAPIRO, HOST:
Scientists are experimenting with a novel approach to treating Alzheimer’s disease in mice. They’re using a drug that helps the brain make energy. NPR’s Jon Hamilton says in a mouse, at least, the treatment can reverse memory loss.
JON HAMILTON, BYLINE: The brain is powered by sugar in the form of glucose. And in a young, healthy person, brain cells are really good at transforming glucose into energy. But Dr. Katrin Andreasson of Stanford University says in someone with Alzheimer’s…
KATRIN ANDREASSON: The energy metabolism really tanks. It really drops.
HAMILTON: So Andreasson and a team of scientists did an experiment with mice that develop a form of Alzheimer’s. They altered the animal’s genes in a way they thought would make glucose metabolism even worse and, as a result, accelerate the disease.
ANDREASSON: We expected to see everything much, much, much worse. But, no, it was the complete flip opposite.
HAMILTON: Eventually, the team found an explanation. The genetic tweak had altered the behavior of cells called astrocytes. Usually, these cells help provide energy to neurons, the cells involved in memory and thinking. But Andreasson says when Alzheimer’s plaques and tangles begin to appear in the brain, astrocytes stop doing this job.
ANDREASSON: The astrocytes are kind of put to sleep, but you got to wake them up, you know, to get them to help the neurons.
HAMILTON: The genetic tweak seemed to get the astrocytes back on track. To test that idea, the team did another experiment. Andreasson says they would place a mouse in the center of a shiny, white disc under a bright light.
ANDREASSON: It really doesn’t like it. It wants to get out of there, but it has to learn where the escape hole is.
HAMILTON: By following visual cues. Andreasson says healthy mice learned how to find the exit almost instantly.
ANDREASSON: But in the Alzheimer mice, the time to find the escape hole really skyrocketed.
HAMILTON: Until the team gave those mice an experimental cancer drug. It woke up the astrocytes the same way the genetic tweak had. It also restored normal glucose metabolism in the hippocampus, an area that’s critical to memory and navigation. And once a mouse had been treated, it could escape the bright light as quickly as a healthy animal. Another experiment showed that the drug also restored human astrocytes and neurons derived from Alzheimer’s patients. The results appear in the journal Science, and Shannon Macauley of the University of Kentucky says they show that Alzheimer’s involves a lot more than just plaques and tangles.
SHANNON MACAULEY: The thought that we can have these metabolic changes in our brain but they’re reversible, to me, is a very exciting development and can kind of change how we think about targeting this disease.
HAMILTON: Macauley, who wrote an editorial accompanying the study, says the research adds to the evidence that cells other than neurons play an important role in Alzheimer’s. She says the brain is a bit like a beehive. Neurons may be the queen bees, but they’re kept alive by worker bees like astrocytes.
MACAULEY: And those worker bees are getting unbelievably taxed from all the things that they’re being asked to do, and so when that happens, the whole system doesn’t work well. And I think that’s what’s happening kind of in the Alzheimer’s brain.
HAMILTON: Macauley says treatments aimed at those worker bees could eventually help Alzheimer’s patients, including those who are already taking new drugs that remove amyloid plaques. She says amyloid drugs can slow down the disease, but a metabolic drug might actually reverse some symptoms.
MACAULEY: Maybe this can make your astrocytes and your neurons work a little bit better so that you can function a little bit better. Maybe you can plateau those memory declines or get a little executive function back.
HAMILTON: If the approach works in people, she says, not just mice.
Jon Hamilton, NPR News. Transcript provided by NPR, Copyright NPR.
NPR transcripts are created on a rush deadline by an NPR contractor. This text may not be in its final form and may be updated or revised in the future. Accuracy and availability may vary. The authoritative record of NPR’s programming is the audio record.
Low-dose THC reverses brain aging and enhances cognition in mice, research suggests
Abstract. Credit: ACS Pharmacology & Translational Science (2024). DOI: 10.1021/acsptsci.4c00002, https://pubs.acs.org/doi/10.1021/acsptsci.4c00002 Bonn researchers have clarified the influence of treatment with tetrahydrocannabinol on the metabolic switch mTOR: A low-dose long-term administration of cannabis can not only reverse aging processes in the brain, but also has an anti-aging effect.
Researchers from the University Hospital Bonn (UKB) and the University of Bonn together with a team from Hebrew University (Israel) have now been able to show this in mice. They found the key to this in the protein switch mTOR, whose signal strength has an influence on cognitive performance and metabolic processes in the entire organism. The results are now presented in the journal ACS Pharmacology & Translation Science .
Information about the availability or scarcity of resources is of crucial importance for the regulation of metabolism. The so-called metabolome is a complex reaction network that summarizes all metabolic properties of a cell or tissue. In higher organisms, the protein mTOR [Mechanistic Target of Rapamycin] is the central hub for cell growth and metabolism.
As a sensitive intracellular energy sensor system, its activity has a major influence on aging by regulating cell metabolism. A reduction in mTOR activity through a low-calorie diet, intensive physical activity or pharmacological treatment therefore has a general anti-aging effect.
In addition to an altered metabolism, the aging of the brain is also accompanied by a reduced ability to change neuronal connections, known as synaptic plasticity . Reduced mTOR activity can therefore also have a negative effect on the aging brain by reducing the formation of new synapses on a nerve cell and thus also cognitive abilities.
“Therefore, anti-aging strategies based on the reduction of mTOR activity might not only be ineffective but even counterproductive against brain aging. In our current work, we have now found a strategy to solve this dilemma,” says Prof. Dr. Andreas Zimmer, Director of the Institute of Molecular Psychiatry at the UKB and member of the Cluster of Excellence ImmunoSensation2 at the University of Bonn. Cannabis reverses the aging process in the brain
In a previous study , the Bonn researchers, together with a team from the Hebrew University of Jerusalem, were able to show that long-term, low-dose administration of tetrahydrocannabinol (THC), the active ingredient in cannabis, has an anti-aging effect on the brain by restoring cognitive abilities and synapse density in old mice. Whether changes in mTOR signaling and the metabolome are linked to the positive effects on the aging brain had remained an open question.
“We have now been able to show that treatment with THC has a tissue-dependent and dual effect on mTOR signaling and the metabolome,” says Dr. Andras Bilkei-Gorzo from the Institute of Molecular Psychiatry at the UKB, who is also a researcher at the University of Bonn.
Thus, THC treatment in the brain led to a transient increase in mTOR activity and levels of intermediates involved in energy production and amino acids. The latter enabled an increased synthesis of synaptic proteins and thus the formation of new synapses.
Unexpectedly, on the other hand, the Bonn researchers found a similarly strong reduction in mTOR activity of mice in adipose tissue and in the content of amino acids and carbohydrate metabolites in blood plasma as after a low-calorie diet or after intensive physical activity.
“We concluded that long-term THC treatment initially has a cognition-enhancing effect by increasing energy and synaptic protein production in the brain , followed by an anti-aging effect by decreasing mTOR activity and metabolic processes in the periphery,” says Bilkei-Gorzo.
“Our study suggests that a dual effect on mTOR activity and the metabolome could be the basis for an effective anti-aging and cognition-enhancing drug.”
More information: Bilkei-Gorzo et al. Bidirectional Effect of Long-Term Δ 9 -Tetrahydrocannabinol Treatment on mTOR Activity and Metabolome, ACS Pharmacology & Translational Science (2024). DOI: 10.1021/acsptsci.4c00002 . pubs.acs.org/doi/10.1021/acsptsci.4c00002
Provided by University of Bonn
Five ways the brain can age: 50,000 scans reveal possible patterns of damage
Results raise hopes that methods could be developed to detect the earliest stages of neurodegenerative disease. Facebook
Some parts of the brain tend to atrophy and deform in concert with other regions.Credit: Zephyr/SPL An analysis of almost 50,000 brain scans 1 has revealed five distinct patterns of brain atrophy associated with ageing and neurodegenerative disease . The analysis has also linked the patterns to lifestyle factors such as smoking and alcohol consumption, as well as to genetic and blood-based markers associated with health status and disease risk.
The work is a “methodological tour de force” that could greatly advance researchers’ understanding of ageing, says Andrei Irimia, a gerontologist at the University of Southern California in Los Angeles, who was not involved in the work. “Prior to this study, we knew that brain anatomy changes with ageing and disease. But our ability to grasp this complex interaction was far more modest.”
The study was published on 15 August in Nature Medicine . Wrinkles on the brain
Ageing can induce not only grey hair, but also changes in brain anatomy that are visible on magnetic resonance imaging (MRI) scans, with some areas shrivelling or undergoing structural alterations over time. But these transformations are subtle. “The human eye is not able to perceive patterns of systematic brain changes” associated with this decline, says Christos Davatzikos, a biomedical-imaging specialist at the University of Pennsylvania in Philadelphia and an author of the paper.
Previous studies have shown that machine-learning methods can extract the subtle fingerprints of ageing from MRI data. But these studies were often limited in scope and most included data from a relatively small number of people. Older mouse brains rejuvenated by protein found in young blood To identify broader patterns, Davatzikos’s team embarked on a study that took roughly eight years to complete and publish. They used a deep-learning method called Surreal-GAN that was developed by first author Zhijian Yang while he was a graduate student in Davatzikos’s laboratory. The scientists trained the algorithm on brain MRIs from 1,150 healthy people aged between 20 and 49, and 8,992 older adults, including many experiencing cognitive decline. This taught the algorithm to recognize recurring features of ageing brains, allowing it to create an internal model of anatomical structures that tend to change at the same time versus those that tend to change independently.
The researchers then applied the resulting model to MRI scans from almost 50,000 people participating in various studies of ageing and neurological health. This analysis yielded five discrete patterns of brain atrophy. The scientists linked various types of age-related brain degeneration to combinations of the five patterns, although there was some variability between individuals with the same condition. Patterns of ageing
For example, dementia and its precursor, mild cognitive impairment , had links to three of the five patterns. Intriguingly, the researchers also found evidence that the patterns they identified could potentially be used to reveal the likelihood of more brain degeneration in the future. “If you want to predict progression from cognitively normal status to mild cognitive impairment, one [pattern] was the most predictive by far,” says Davatzikos. “At later stages, the addition of a second [pattern] enriches your prediction, which makes sense because this kind of captures the propagation of the pathology.” Other patterns were linked to conditions including Parkinson’s disease and Alzheimer’s disease , and one combination of three patterns was highly predictive of mortality.
The authors found clear associations between certain patterns of brain atrophy and various physiological and environmental factors, including alcohol intake and smoking, as well as various health-associated genetic and biochemical signatures. Davatzikos says that these results probably reflect the effect of overall physical well-being on neurological health, because damage to other organ systems can have consequences for the brain.
Davatzikos cautions that the study “doesn’t mean that everything can be boiled down to five numbers”, however, and his team is looking to work with data sets that include a broader range of neurological conditions and have greater racial and ethnic diversity. News & Views 14 AUG 24 How the human brain creates cognitive maps of related concepts News 14 AUG 24 One-quarter of unresponsive people with brain injuries are conscious
Newly Discovered Brain Wave Helps Lock in Memories While We Sleep
Sleep works magic on memory.
You might’ve felt these frustrations before: Trying to learn a guitar riff, shoot a free-throw, or nail a difficult phrase in a new language, but despite hours of practice, you’re just not getting it right. Then with a good night’s sleep—voilà, somehow, you’ve nailed the skills.
Neuroscientists have long known that brain waves during sleep etch learnings from the previous day into neural circuits for long-term storage. As we drift off, our brains remain hard at work. One region, a seahorse-shaped structure called the hippocampus, especially sparks with activity. This area is essential for translating what we learn into long-term memories during sleep.
Disruptions to electrical activity in the hippocampus can lead to memory problems in multiple neurological disorders, including schizophrenia and Alzheimer’s disease. But one question has always troubled neuroscientists.
Brain cells, or neurons, need to stay in a “Goldilocks zone” of activity to encode and store memories. Learning new things spikes activity in a specific set of neurons. But when they further increase their activity during sleep—like a car with a gas pedal and no brake—what’s to prevent them from hyperactivating and, in turn, destroying the brain’s ability to learn?
A new study from Cornell University suggests a way the brain balances itself during sleep. In recordings from multiple areas of the hippocampus in mice and rats, the team discovered a previously undetected brain wave that keeps brain cells in check. Dubbed BARR (for barrage of action potentials), these brain waves reset neurons so they can encode new experiences the next day, while enhancing memories during sleep.
“Sleep is not just a time for the body to rest but also for the mind to solidify memories,” wrote Drs. Xiang Mou and Daoyun Ji at Baylor College of Medicine in Houston, Texas, who were not involved in the study.
The results help explain why sleep promotes memory, and how its disruption can lead to brain disorders in schizophrenia , Alzheimer’s disease , and other neurological conditions associated with memory problems.
“This mechanism could allow the brain to reuse the same resources, the same neurons, for new learning the next day,” said study author Dr. Azahara Oliva at Cornell University in a press release. Under the Sea
As we drift into unconsciousness every night during sleep, the hippocampus is hard at work. Shaped like a seahorse, this brain region has long been known as a hub for memory.
Patients with damage to the hippocampus lose their ability to create new memories. And decades of research shows the area processes the day’s learnings for long-term storage in other parts of the brain—and holds the key to retrieving those memories when needed.
But the region is hardly a one-trick pony. Imagine it as a town with multiple neighborhoods and highways connecting it to other brain regions. Each neighborhood plays a slightly different role. Some encode new memories, which are then shuffled to the cortex—the outer part of the brain—for longer storage and retrieval. Others link specific memories to joy, sadness, and other feelings through wiring connected to regions of the brain associated with emotion.
Scientists have already mapped out these neighborhoods. CA1, sitting at the front, extensively connects to other parts of the brain involved in reasoning and memory. CA3 encodes memories and potentially helps separate similar ones—for example, did I get that cup of coffee yesterday at that café, or was that a memory from a few days ago?
But the role of the middle child, CA2, has always been mysterious. Sing Me to Sleep
Every night we cycle through several stages of sleep. One stage, called non-rapid eye movement, occurs when we drift off to sleep and eventually transition from light sleep into deeper slumber.
This is when CA1 perks up. Neurons encoding memories from the day reactivate—kind of like replaying a memory on video, but at a faster rate.
These patterns, called sharp-wave ripples, help etch memories into the brain. Like waves on the ocean, they “splash” across other brain regions in electrical ebbs and flows that reconfigure neural connections. These waves help the hippocampus send learning to other regions where it can be stored in memory. But without a way to dampen the waves down, neurons hyperactivate, meaning they can no longer learn or store new information.
To study how sleep changes the brain, the team implanted electrodes into multiple parts of the hippocampus in mice and rats to monitor their brain activity.
The rodents then learned several tasks, for example, figuring out if an object had been removed. A bit like finding your favorite couch wasn’t where you expected it to be, this requires memory of its location. Other tests challenged the critters to navigate a maze and have social interactions—that is, remembering whether they’d met a previous acquaintance.
As the mice fell asleep, their brain activity showed signs of sharp-wave ripples. But surprisingly, CA2, the middle child, also sparked, with long-lasting bursts of activity spreading through the hippocampus. These BARR brain waves—never seen before—flared up in neurons that encode learning, which usually have higher levels of activity, to tamp them down in sleep.
In a way, as we sleep, our brain is in a kind of civil war. Neurons encoding memories reactivate to consolidate learning, while BARR brain waves keep them at bay so that they don’t overactivate. A Brainy Scale
The team focused on a type of brain cell that triggers BARR brain waves during sleep.
Using optogenetics—a way to turn neurons on or off using light—in rodents, they artificially disrupted BARR activity as the critters slept after learning several memory tasks. As a result, sharp-wave ripples, the type of brain activity usually associated with solidifying memory, lasted far longer.
Surprisingly, it made memory worse. On the surface, it doesn’t make sense: Wouldn’t more activity during sleep be better for memory? Not so much, explained the team. It’s all about balance.
“BARRs serve as a passive brake” that lowered increased neural activity in sleep, wrote Mou and Ji. The brain resets balance after a day of hard work. Disrupting BARR during sleep altered the animals’ memory, likely because their neural […]
New Research Reveals That Your Brain’s Memory “Resets” Every Night
A new study from Cornell University reveals that sleep not only consolidates memories but also resets the brain’s memory storage mechanism. This process, governed by specific regions in the hippocampus, allows neurons to prepare for new learning without being overwhelmed. This insight opens potential pathways for enhancing memory and treating neurological disorders like Alzheimer’s and PTSD. Cornell University research demonstrates that sleep resets the hippocampus, enabling continuous learning and offering new strategies for treating memory-related disorders.
While everyone knows that a good night’s sleep restores energy, a new Cornell University study finds it resets another vital function: memory.
Learning or experiencing new things activates neurons in the hippocampus, a region of the brain vital for memory. Later, while we sleep, those same neurons repeat the same pattern of activity, which is how the brain consolidates those memories that are then stored in a large area called the cortex. But how is it that we can keep learning new things for a lifetime without using up all of our neurons? Mechanisms of Memory Resetting
A new study published in the journal Science , finds at certain times during deep sleep, certain parts of the hippocampus go silent, allowing those neurons to reset.
“This mechanism could allow the brain to reuse the same resources, the same neurons, for new learning the next day,” said Azahara Oliva, assistant professor of neurobiology and behavior and the paper’s corresponding author.
The hippocampus is divided into three regions: CA1, CA2 and CA3. CA1 and CA3 are involved in encoding memories related to time and space and are well-studied; less is known about CA2, which the current study found generates this silencing and resetting of the hippocampus during sleep.
The researchers implanted electrodes in the hippocampi of mice, which allowed them to record neuronal activity during learning and sleep. In this way, they could observe that, during sleep, the neurons in the CA1 and CA3 areas reproduce the same neuronal patterns that developed during learning during the day. But the researchers wanted to know how the brain continues learning each day without overloading or running out of neurons.
“We realized there are other hippocampal states that happen during sleep where everything is silenced,” Oliva said. “The CA1 and CA3 regions that had been very active were suddenly quiet. It’s a reset of memory, and this state is generated by the middle region, CA2.” Implications for Memory Enhancement and Treatment
Cells called pyramidal neurons are thought to be the active neurons that matter for functional purposes, such as learning. Another type of cell, called interneurons, has different subtypes. The researchers discovered that the brain has parallel circuits regulated by these two types of interneurons – one that regulates memory, the other that allows for resetting of memories.
The researchers believe they now have the tools to boost memory, by tinkering with the mechanisms of memory consolidation, which could be applied when memory function falters, such as in Alzheimer’s disease. Importantly, they also have evidence for exploring ways to erase negative or traumatic memories, which may then help treat conditions such as post-traumatic stress disorder.
The result helps explain why all animals require sleep, not only to fix memories, but also to reset the brain and keep it working during waking hours. “We show that memory is a dynamic process,” Oliva said.
Reference: “A hippocampal circuit mechanism to balance memory reactivation during sleep” by Lindsay A. Karaba, Heath L. Robinson, Ryan E. Harvey, Weiwei Chen, Antonio Fernandez-Ruiz and Azahara Oliva, 15 August 2024, Science .
DOI: 10.1126/science.ado5708
The study was funded by the National Institutes of Health, a Sloan Fellowship, a Whitehall Research Grant, a Klingenstein-Simons Fellowship and a New Frontiers Grant.
Brain cells ‘reset’ during sleep to prepare for tomorrow’s memories
A good night’s sleep is crucial for helping people make new memories: Neurons that capture new memories during the day reset while you sleep, researchers reported. Photo by Adobe Stock/HealthDay News A good night’s sleep is crucial for helping people make new memories, a new study says.
Neurons that capture new memories during the day reset while you sleep, researchers reported Thursday in the journal Science .
“This mechanism could allow the brain to reuse the same resources, the same neurons, for new learning the next day,” said researcher Azahara Oliva , an assistant professor of neurobiology and behavior at Cornell University, in Ithaca, N.Y.
The process revolves around the hippocampus, a brain region vital to humans’ ability to create memories. Related
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Learning something or engaging in a new experience activate neurons in the hippocampus, storing those events as memories.
The same neurons later repeat the same pattern of activity while you sleep, transferring the day’s memories in a larger brain region called the cortex.
But what keeps the neurons of the hippocampus from filling up, thus preventing new learning, the researchers wondered.
Electrodes implanted into the hippocampi of mice provided a potential explanation.
It turns out that those neurons that captured the day’s memories undergo a reset after feeding the latest memories into the cortex, researchers found.
Two regions of the hippocampus that capture memories, CA1 and CA3, appear to reset during sleep under the direction of a third region called CA2, researchers said.
“We realized there are other hippocampal states that happen during sleep where everything is silenced,” Oliva said in a university news release. “The CA1 and CA3 regions that had been very active were suddenly quiet. It’s a reset of memory, and this state is generated by the middle region, CA2.”
It turns out the brain has parallel circuits regulated by two types of neurons, researchers said. One network of circuits regulates memory, and the other allows for resetting of memory.
This new understanding could help researchers come up with tools to boost memory, by tinkering with the mechanisms of memory consolidation.
The findings also could lay the foundation for new ways to treat problems caused by unwanted memories, like post-traumatic stress disorder (PTSD), or to fix memory disorders like Alzheimer’s disease
But overall, the findings help explain why sleep is so crucial for the brain health of all animals, researchers said.
“We show that memory is a dynamic process,” Oliva said.
More information
Harvard University has more about how memory works .
Copyright © 2024 HealthDay. All rights reserved.
Sleep resets neurons for new memories the next day
While everyone knows that a good night’s sleep restores energy, a new Cornell University study finds it resets another vital function: memory.
Learning or experiencing new things activates neurons in the hippocampus, a region of the brain vital for memory. Later, while we sleep, those same neurons repeat the same pattern of activity, which is how the brain consolidates those memories that are then stored in a large area called the cortex. But how is it that we can keep learning new things for a lifetime without using up all of our neurons?
A new study, “A Hippocampal Circuit Mechanism to Balance Memory Reactivation During Sleep,” that has just been published in Science , finds at certain times during deep sleep, certain parts of the hippocampus go silent, allowing those neurons to reset.
“This mechanism could allow the brain to reuse the same resources, the same neurons, for new learning the next day,” said Azahara Oliva, assistant professor of neurobiology and behavior and the paper’s corresponding author.
The hippocampus is divided into three regions: CA1, CA2 and CA3. CA1 and CA3 are involved in encoding memories related to time and space and are well-studied; less is known about CA2, which the current study found generates this silencing and resetting of the hippocampus during sleep.
The researchers implanted electrodes in the hippocampi of mice, which allowed them to record neuronal activity during learning and sleep. In this way, they could observe that, during sleep, the neurons in the CA1 and CA3 areas reproduce the same neuronal patterns that developed during learning in the day. But the researchers wanted to know how the brain continues learning each day without overloading or running out of neurons.
“We realized there are other hippocampal states that happen during sleep where everything is silenced,” Oliva said. “The CA1 and CA3 regions that had been very active were suddenly quiet. It’s a reset of memory, and this state is generated by the middle region, CA2.”
Cells called pyramidal neurons are thought to be the active neurons that matter for functional purposes, such as learning. Another type of cell, called interneurons, has different subtypes. The researchers discovered that the brain has parallel circuits regulated by these two types of interneurons — one that regulates memory, the other that allows for resetting of memories.
The researchers believe they now have the tools to boost memory, by tinkering with the mechanisms of memory consolidation, which could be applied when memory function falters, such as in Alzheimer’s disease. Importantly, they also have evidence for exploring ways to erase negative or traumatic memories, which may then help treat conditions such as post-traumatic stress disorder.
The result helps explain why all animals require sleep, not only to fix memories, but also to reset the brain and keep it working during waking hours. “We show that memory is a dynamic process,” Oliva said.
The study was funded by the National Institutes of Health, a Sloan Fellowship, a Whitehall Research Grant, a Klingenstein-Simons Fellowship and a New Frontiers Grant.
NHS data: Nearly 200,000 Brits currently awaiting autism assessment – 30,000 more than the previous year
Tags: ASD , autism , Autism spectrum disorder , badhealth , badmedicine , badscience , brain damaged , brain function , brain health , children’s health , disorders , health care , Mind , mind body science , National Health Service , neurodiversity , neurological health , NHS , United Kingdom New data from the United Kingdom’s National Health Service (NHS) reveals that a record number of British citizens are seeking autism assessment, with nearly 200,000 currently on the waiting list – 30,000 more than the previous year .
This figure marks a 22 percent rise from last year and is nine times higher than in 2019. The surge has created significant delays, with 90 percent of people waiting beyond the recommended 13 weeks. Notably, two-thirds of those awaiting assessment are children under 17 years old.
Experts are condemning the British health care system as “broken” and urging for immediate reform to prevent missing out on critical early support. National Autistic Society Head of Policy Mel Merritt pointed out that the lengthy waits mean many are missing out on essential assistance. In April, it was revealed that children across the U.K. could wait up to four years for an autism diagnosis. Merritt stressed the need to address the diagnostic delays to restore NHS effectiveness and support people in need.
Autism, a developmental condition, means the brain functions differently from birth although it may only be recognized in childhood or later. Understanding the surge in autism diagnoses
Experts remain divided on whether the surge in autism diagnoses reflects overdiagnosis or a genuine increase in cases . A study reported by The Guardian reveals that some NHS centers in the U.K. diagnose autism in adults at twice the rate of others.
Autism diagnoses have dramatically risen over the past decades. A 2021 study published by the Association for Child and Adolescent Mental Health, revealed a staggering 787 percent increase in U.K. diagnoses from 1998 to 2018 . Autism only affected one in 2,500 children 80 years ago. Today, it is estimated to affect one in 36.
This rise can be partly attributed to better understanding, heightened awareness and more professionals becoming qualified to diagnose the condition referred to as autism spectrum disorder (ASD). As a result, the criteria for diagnosing autism has expanded drastically, bringing in individuals who might not have been previously considered as being within the spectrum, particularly girls and women.
The reasons behind the increase in autism diagnoses remain a topic of debate, with experts and those in the neurodiversity movement unsure whether this rise is due to overdiagnosis or if more children genuinely have ASD.
The neurodiversity movement encourages people to see neurological differences, like autism, as natural variations instead of disorders or problems. This movement has played a big role in changing how autism is understood and diagnosed – pushing for more recognition of different ways people’s brains work.
The term “neurodiversity” was first used in the 1990s to help reduce the stigma faced by people with attention-deficit/hyperactivity disorder, autism and learning disabilities like dyslexia. Since then, it has grown into a movement that supports those who think and learn differently – focusing on their strengths and talents, instead of the challenges, particularly in their social environment.
Study author Dr. Ginny Russell, Mental Health and Development Disorders senior research fellow at the University of Exeter , said the criteria for diagnosing autism may continue to expand, believing that this expansion could eventually lead to almost everyone being categorized as “neurodiverse.”
Russell pointed out that while there might be a slightly higher number of children with mild autistic traits, there is no strong evidence to support a significant increase in ASD cases .
According to Russell, the rise in diagnoses is largely due to expanding assessment criteria that continue to include more people. The study author added that as the definition of autism broadens, it might eventually include individuals like herself who have some “borderline traits.”
Are autism and ADHD being over-diagnosed? Watch this video .
This video is from the Daily Videos channel on Brighteon.com . More related stories:
Autism rates in the US on the rise; California seeing record numbers .
CDC confirms aluminum in vaccines linked to childhood asthma and AUTISM .
Can sulforaphane help children with autism?
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TheGuardian.com
ACAMH.OnlineLibrary.Wiley.com
PsychologyToday.com
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