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How Cancer Hijacks the Brain to Benefit Itself
Key points
Some natural mechanisms in the body can prevent the formation of cancer in its early stages.
Increasing the tumor mass beyond a certain threshold renders these mechanisms ineffective.
The nervous system and cancer have a reciprocal interplay.
Cancer cells manipulate the nervous system to enhance their growth and development.
In the last two centuries, complete treatments for many diseases, mostly infectious illnesses, have been discovered. The therapeutic targets for these diseases were clear and distinct from body cells. Therefore, targeting these pathogens had no adverse effects on the body. However, despite significant efforts to find new medications for cancer treatment, these therapeutic agents often result in large amounts of side effects. It appears that cancer cells are part of our body, and fighting cancer is essentially fighting against the body itself. Therefore, the body resists these treatments to neutralize the effects of therapeutic methods.
Natural anticancer mechanisms of the body are bypassed by cancer
The body has physiological mechanisms to prevent cancer formation. At the cellular level, tumor suppressors effectively hinder neoplastic alterations. At the systemic level, the tumor microenvironment, including proteins involved in extracellular skeleton and neighboring stromal cells, prevents the transformation of cells into a cancerous state. The immune system is also the most potent anti-cancer system that effectively removes and destroys cancer cells at early stages. However, if cancer cells grow beyond a certain threshold, they can evade the normal immune response to tumors.
When cancer size crosses a threshold, they can evade the normal anti-cancer mechanisms and also utilize the body’s systems to keep themselves and grow more aggressively. Several mechanisms are suggested for these normal systems that are hired by tumors. While normal cells that detach from normal extracellular framework easily die, cancer cells possess tools that allow them to detach from the extracellular matrix and migrate to neighboring or distant tissues. Additionally, tumor cells prompt neighboring stromal cells such as endothelial cells or fibroblasts to generate new blood vessels and facilitate their growth and migration.
Interestingly, cancer cells can manipulate the immune system to promote their growth and development. While immune cells are designed to fight off infections and remove abnormal cells, cancer cells can escape these defenses. They can release chemical compounds that suppress the activity of immune cells, preventing them from recognizing and attacking the tumor cells. Cancer cells can produce proteins that make them invisible to immune cells, allowing them to escape detection. Some immune cells, like macrophages, can be tricked by cancer cells into aiding in tumor growth, angiogenesis (formation of new blood vessels), and migration to other tissues. While some types of T cells destroy cancerous cells, others help in further development [1]. Therefore, cancer along with its development not only neutralizes the defense systems but also recruits them to work for itself.
Interaction between cancer and the nervous system
The nervous system controls movement and sensory perception and also supplies nerve connections to tissue stem cell microenvironments. This implies the role of the central nervous system in tissue development, maintenance, and repair. The nervous system also interacts with tumor cells reciprocally. Nerves can both promote and suppress cancer growth. For instance, it has been shown that the sympathetic nervous system (SNS) has been shown to accelerate breast cancer growth and progression, while parasympathetic nerves (PNS) have been observed to reduce breast cancer growth and progression. The SNS can influence tumor growth and metastasis. Studies suggest that the SNS, through the release of norepinephrine, can activate beta-adrenergic signaling pathways, which can lead to increased tumor cell proliferation, formation of new blood vessels, and metastasis. These studies highlight the importance of stress in activating the SNS and promoting cancer progression. In advanced tumors, SNS innervation increases around tumor cells [2].
In contrast, cancer cells stimulate the production of new nerves around them and increase neuronal excitability. Some types of cancer, such as head and neck cancer, prostate cancer, and colorectal cancer, tend to attack the space surrounding a nerve to spread to distant tissues. It is as if the nerves attract them.
These observations prompted some researchers to pay more attention to the interaction between cancer and the nervous system. In a recent article, Douglas Hanahan—along with Robert Weinberg, the first to identify hallmarks of cancer in a landmark paper published in 2000 and 2011—explores the intricate relationship between cancer biology and neuroscience. The article emphasizes how cancer cells can modify neuronal signaling and how the nervous system can affect tumor behavior. This two-way interaction is essential for comprehending tumor biology and creating new treatment approaches [3].
Recently, much attention has been drawn to the role of cancer in manipulating the nervous system to benefit itself. Like a parasite, cancer cells hijack the nervous system to evade the immune system, create new blood vessels, facilitate their migration, promote inflammation, and cause pain. This is an interesting example of tissues that apparently should be under the control of the nervous system, but they cleverly influence the commander-in-chief and consequently take over entire systems in the body. This reciprocal interplay between cancer and the nervous system indicates that new therapeutic strategies should consider the nervous system as an indirect target to get better treatment outcomes. Additionally, psychotherapeutic approaches including cognitive behavioral therapy , mindfulness -based cognitive therapy, and psychodynamic therapy aimed at reducing stress and anxiety in cancer patients may offer an advantage in conjunction with traditional medications.
References
1. Zand H, Pourvali K. The Function of the Immune System, Beyond Strategies Based on Cell-Autonomous Mechanisms, Determines Cancer Development: Immune Response and Cancer Development. Adv Biol (Weinh). 2024 Apr;8(4):e2300528
2. Cole SW, Nagaraja AS, Lutgendorf SK, Green PA, Sood AK. Sympathetic nervous system regulation of the tumour microenvironment. Nat Rev Cancer. 2015 Sep;15(9):563-72.
3. Hanahan D, Monje M. Cancer hallmarks intersect with neuroscience in the tumor microenvironment. Cancer Cell. 2023 Mar 13;41(3):573-580. Image by LillyCantabile from Pixabay Rommel Canlas / Shutterstock
Melatonin Receptor is Key to REM Sleep and Memory
Summary: Scientists have identified the melatonin MT1 receptor as a key regulator of REM sleep, crucial for memory, dreaming, and emotional regulation. This discovery may pave the way for targeted treatments for sleep disorders and conditions like Parkinson’s and dementia, which are linked to REM disruptions.
Using a novel drug, researchers enhanced REM sleep duration in animal studies without negatively impacting overall sleep. The findings offer promising clinical potential for future therapies.
Key Facts : The melatonin MT1 receptor regulates REM sleep.
REM sleep is essential for memory consolidation and emotional regulation.
The discovery could lead to targeted treatments for sleep disorders and neuropsychiatric conditions.
Source: McGill University
A significant breakthrough in the understanding of sleep mechanism opens new promise for treating sleep disorders and associated neuropsychiatric conditions: Scientists have pinpointed the melatonin receptor MT1 as a crucial regulator of REM (Rapid Eye Movement) sleep.
REM sleep is crucial for dreaming, memory consolidation, and emotional regulation. In the brain, the melatonin MT1 receptor affects a type of neuron that synthesizes the neurotransmitter and hormone noradrenaline , found in an area known as the Locus Coeruleus, or “blue spot” in Latin. The new study has identified the melatonin MT1 receptor as an important regulator of this sleep stage. Credit: Neuroscience News During REM sleep, these neurons quiet down and stop their activity. Serious conditions such as Parkinson’s disease and Lewy body dementia — which currently lack effective treatments — are linked to disruptions in REM sleep.
“This discovery not only advances our understanding of sleep mechanisms but also holds significant clinical potential,” said Gabriella Gobbi, principal investigator of a new study published in the Journal of Neuroscience .
She is a Professor of Psychiatry at McGill University, clinician-scientist at the Research Institute of the McGill University Health Centre, and Canada Research Chair in Therapeutics for Mental Health. The science of snoozing
Human sleep unfolds in a precise sequence of non-REM and REM stages, each serving distinct physiological functions. REM sleep plays a pivotal role in memory consolidation and emotional regulation. Non-REM sleep supports physical recovery and repair processes. Disruptions in this cycle can impair cognitive function and increase vulnerability to neuropsychiatric diseases.
Until now, the specific receptor triggering REM sleep had eluded scientists. The new study has identified the melatonin MT1 receptor as an important regulator of this sleep stage.
Using a novel drug targeting MT1 receptors, researchers successfully enhanced REM sleep duration in experimental animals, while simultaneously reducing neuronal activity.
“Currently, there are no drugs specifically targeting REM sleep. Most hypnotic drugs on the market, while extending total sleep duration, tend to adversely affect REM sleep,” said Dr. Stefano Comai, co-senior author of the study and Professor at the University of Padua and Adjunct Professor at McGill University.
Further research into the neurobiology and pharmacology of REM sleep is crucial for developing targeted treatments that could improve the quality of life for patients affected by these debilitating diseases, according to the researchers.
As scientists continue to explore the complexities of sleep regulation, the hope for effective interventions in neurological disorders grow increasingly promising. About this sleep, memory, and neuroscience research news
Author: Claire Loewen
Source: McGill University
Contact: Claire Loewen – McGill University
Image: The image is credited to Neuroscience News
Original Research: Open access.
“ Selective Enhancement of REM Sleep in Male Rats through Activation of Melatonin MT1 Receptors Located in the Locus Ceruleus Norepinephrine Neurons ” by Gabriella Gobbi et al. Journal of Neuroscience
Abstract
Selective Enhancement of REM Sleep in Male Rats through Activation of Melatonin MT1 Receptors Located in the Locus Ceruleus Norepinephrine Neurons
Sleep disorders affect millions of people around the world and have a high comorbidity with psychiatric disorders.
While current hypnotics mostly increase non-rapid eye movement sleep (NREMS), drugs acting selectively on enhancing rapid eye movement sleep (REMS) are lacking.
This polysomnographic study in male rats showed that the first-in-class selective melatonin MT 1 receptor partial agonist UCM871 increases the duration of REMS without affecting that of NREMS.
The REMS-promoting effects of UCM871 occurred by inhibiting, in a dose–response manner, the firing activity of the locus ceruleus (LC) norepinephrine (NE) neurons, which express MT 1 receptors.The increase of REMS duration and the inhibition of LC-NE neuronal activity by UCM871 were abolished by MT 1 pharmacological antagonism and by an adeno-associated viral (AAV) vector, which selectively knocked down MT 1 receptors in the LC-NE neurons.In conclusion, MT 1 receptor agonism inhibits LC-NE neurons and triggers REMS, thus representing a novel mechanism and target for REMS disorders and/or psychiatric disorders associated with REMS impairments.Join our Newsletter I agree to have my personal information transferred to AWeber for Neuroscience Newsletter ( more information )Sign up to receive our recent neuroscience headlines and summaries sent to your email once a day, totally free.We hate spam and only use your email to contact you about newsletters. You can cancel your subscription any time.
Could Antidepressants Give Memory a Boost?
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Sep 23, 2024, 9:46 am Key Takeaways
Antidepressants have the potential to boost brain function
People responding to an SSRI antidepressant did better on cognitive tests
Researchers think stimulating a specific brain receptor provided the benefits
MONDAY, Sept. 23, 2024 (HealthDay News) — Antidepressants have the potential to improve memory and thinking skills, a new study suggests.
Some patients experienced a boost on brain tests after taking the SSRI antidepressant escitalopram (Lexapro), researchers report.
The drug appeared to affect a serotonin receptor in the brain called the 5HT4 receptor, according to results published recently in the journal Biological Psychiatry .
Serotonin is described as a “feel good” hormone, researchers said in background notes. Higher levels of serotonin in the brain contribute to a sense of well-being and have been shown to ease clinical depression.
“It seems that the SSRI medication contributes to an improvement on cognitive function, at the same time as helping improve mood,” said lead investigator Vibeke Dam , a senior researcher in neurology and neurobiology with Copenhagen University Hospital in Denmark.
“Our work ties the improvement in cognitive function to the specific 5HT4 receptor and suggest that direct serotonin 4 receptor stimulation may be an important pro-cognitive target to consider in optimizing outcomes of antidepressant treatment,” Dam added in a journal news release. “It also reinforces the idea that serotonin is crucial to mood improvement.”
For the study, researchers scanned the brains of 90 depressed patients to measure 5HT4 receptor function in their brains. The patients also were tested for mood problems and cognitive abilities.
Then the patients were given daily escitalopram (Lexapro) for eight weeks. At the end of the study, 40 patients were rescanned and retested.
What did they find? The patients’ performance on cognitive tests had improved — particularly their ability to recall words — and this performance appeared to be linked to higher activity with the 5HT4 receptor.
“This work points to the possibility of stimulating this specific receptor so that we can treat cognitive problems, even aside from whether or not the patient has overcome the core symptoms of depression,” said lead researcher Dr. Vibe Froekjaer , a clinical professor of neuropsychiatry with Copenhagen University Hospital in Denmark.
The team’s next step will be to treat patients with drugs that specifically target the 5HT4 receptor, and then assess the effect on their brain function. Serotonin is found in the gut, and there are irritable bowel syndrome drugs that specifically bind to and stimulate 5HT4 receptors, researchers said.
Researchers also presented these findings Monday at the European College of Neuropsychopharmacology’s annual meeting in Milan.
The study “demonstrates the intimate role of brain 5HT4 receptors in cognitive function,” said Philip Cowen , a professor of psychopharmacology with the University of Oxford.
“This confirms recent work from Oxford showing that the 5HT4 receptor stimulant, prucalopride — a drug licensed for the treatment of constipation — improves memory in both healthy participants and people at risk of depression,” said Cowen, who was not involved in the study.
More information
The National Institutes of Health has more on antidepressants .
SOURCE: European College of Neuropsychopharmacology, news release, Sept. 23, 2024 What This Means For You
Drugs targeting specific serotonin receptors could one day help improve people’s memory and brain function.
MIND Diet Linked with Sharper Memory, Lower Risk of Cognitive Decline
Health News
The MIND diet (a blend of the Mediterranean and DASH diets) can help slow cognitive decline as you grow older, especially for women. Ascent Xmedia/Getty Images A study says the MIND diet could reduce the risk of cognitive problems during aging.
Following the MIND diet especially predicted a better trajectory for Black people.
This diet emphasizes brain-healthy foods and discourages those harmful to the brain.
Dietitians say to eat more foods like leafy greens, nuts, berries, and fatty fish.
At the same time, cut down on foods high in saturated fat and sugar.
According to a new study published in Neurology , the Mediterranean-Dietary Approaches to Stop Hypertension Intervention for Neurogenerative Delay (MIND) diet could reduce people’s risk of cognitive impairment as they grow older.
The Alzheimer’s Society explains that it is normal to become more forgetful or have greater difficulty thinking as we age.
However, people with dementia can have more severe deficits in memory, thinking, language, orientation, perception, mood , and behavior.
Diet is one factor that could influence the likelihood of cognitive decline , according to the study authors.
They specifically wanted to look at whether this was equally true for both Black and white Americans.
While they found that there was no racial difference in how protective the diet was, they did find that there was a difference between women and men, with only women experiencing a decreased risk of cognitive impairment.
However, better adherence to the MIND diet was a predictor of cognitive trajectory (changes in cognitive function over time) in Black study participants. How the link between MIND diet and cognitive decline risk was studied
The study included over 14,000 people who were, on average, 64 years old. Among these, 30% were Black and 70% were white.
These individuals were asked to complete a questionnaire examining their dietary patterns over the previous year. The researchers then looked to see how closely their diets matched with the MIND diet.
Points were given based on whether they ate certain foods in the designated amounts. For example, if they ate three or more servings each day of whole grains, they received 1 point. Twelve points was the highest possible score, meaning that their diet was a perfect match for the MIND diet.
These scores were then used to divide the participants into three groups: low, with an average score of 5
middle, with an average score of 7
high, with an average score of 9
People were followed for an average of 10 years. Thinking and memory were assessed at the beginning and end of the study.
It was found that 12% of the low group developed cognitive impairment, compared to 11% of the middle group and 10% of the high group.
However, after adjusting for various factors, people in the high group had a 4% decreased risk of cognitive impairment compared to the low group.
Additionally, women had a 6% decreased risk of cognitive impairment in the high group, but no decrease in risk was seen in men.
Finally, the scientists found that people who more closely followed the MIND diet had a slower decline in their cognitive abilities and this association was most prominent in Black individuals.
However, more research is needed to understand why there was a racial difference. What is the MIND diet?
Johanna Angman , a Registered Dietician Nutritionist with Glowbar LDN , who was not involved in the study, described the MIND diet as a “scientifically curated eating plan.”It blends the Mediterranean and the Dietary Approaches to Stop Hypertension ( DASH ) diets with a focus on brain health, she explained.The MIND diet is centered on ten food groups that promote cognitive function, including leafy greens, berries, nuts, and fish .At the same time, it discourages consumption of red meat , butter, and sugary foods, said Angman.“What sets the MIND diet apart is its laser focus on reducing neurodegeneration, targeting foods that specifically protect the brain from oxidative stress , inflammation, and vascular damage, which are key contributors to cognitive decline,” she said. Why the MIND diet might help prevent cognitive decline Akanksha Kulkarni , a Registered Dietitian Nutritionist at Prowise Healthcare , who was not involved in the study, said the way that the MIND diet helps prevent cognitive decline is through the nutrients it contains.“In particular, leafy greens and berries contain many antioxidants, while omega-3 fatty acids, mostly found in fish and nuts, are believed to be essential for brain health,” she said.These nutrients can help us with memory and other aspects of cognition as we age, according to Kulkarni.She further noted that the MIND diet’s emphasis on good fats can play an important role in maintaining brain health.“Healthy fats from olive oil and fish also aid in offering protection from inflammation of the brain, which has been associated with Alzheimer’s disease and other content degenerative diseases,” said Kulkarni.She said the diet also reduces the consumption of saturated fats, which can contribute to the formation of plaques in the brain.“Because the MIND diet aids in maintaining healthy blood vessels and prevents factors that put a person at risk of dementia, it helps prevent the onset of diseases such as Alzheimer’s,” said Kulkarni. “This has also been positively correlated with slower cognitive decline.” Easy ways to begin adopting the MIND diet Angman suggests starting with “small, sustainable changes.”“Incorporating one serving of leafy greens daily can be a powerful first step, as these are linked most strongly to cognitive benefits,” she said.Angman also suggests replacing snacks with a handful of nuts. You can also include berries in your breakfast or incorporate them into a smoothie.“Fish, particularly fatty fish like salmon , should be on your plate at least once or twice a week,” she added.Also, Angman advises reducing the amount of red meat you eat and substituting it with more plant-based proteins like legumes.“By slowly reshaping daily habits, you’ll be aligning your diet more closely with the MIND approach,” said Angman, “giving your brain long-term protection without feeling overwhelmed by change.” Takeaway […]
MIND diet linked to lower cognitive decline risk, especially in women
New research confirms the brain-protective benefits of the MIND diet. Image credit: Nadine Greeff/Stocksy. Closely following a MIND diet was associated with a reduced risk of cognitive impairment and slower rates of decline with aging in a new study.
The observed effects on cognitive aging were more prominent in women in the study, with adherence to the diet having no association with the risk of cognitive impairment, and lesser associations with the rate of cognitive decline in men.
The study also found the association between greater diet adherence and slower cognitive decline held true for Black and white participants but was more apparent for Black participants.
The right diet may be a way to slow one’s rate of cognitive impairment or decline while growing older, according to a new study published in Neurology . The research does not prove a definitive link, but finds a consistent correspondence between a person’s diet and a slower rate of cognitive loss over time.
The study found an association between a closer adherence to the MIND diet and a decreased risk of cognitive impairment and slower rates of cognitive decline in women.
The researchers detected no such association between the MIND diet adherence and the risk of cognitive impairment in men. However, it was associated with a slower rate of cognitive decline in men, though the link was still stronger in women.
The MIND diet is a modified combination of the Mediterranean and DASH diets.
While other studies track the development of dementia, the authors of this study investigated impairment and decline, two particularly universal phenomena that occur with time. They were also interested in seeing if there were differences between White and Black Americans in this process.
Greater adherence to the MIND diet correlated to a decreased risk of cognitive impairment and slowed decline for both white and Black participants. However, it more strongly predicted cognitive decline in Black participants.
The research encompassed data from 14,145 white and Black adults who participated in the Food Frequency Questionnaire in the Reasons for Geographic and Racial Differences in Stroke ( REGARDS) study.
Individuals had a mean age of 64, give or take 9 years, and were followed for an average of 10 years. Of the participants, 56.7% were female, 70% were white, and 30% were Black. How the MIND diet affects brain aging
Scott Kaiser, MD , who was not part of the study, is a board-certified geriatrician and Director of Geriatric Cognitive Health for the Pacific Neuroscience Institute in Santa Monica, CA.
Commenting on the study results for Medical News Today , he noted that “the Mediterranean-DASH Intervention for Neurodegenerative Delay (MIND) diet has been demonstrated to slow brain aging by something on the order of 7.5 years , and significantly reduce one’s risk of developing Alzheimer’s disease.”
Michelle Routhenstein, MS, RD, CDCES , preventive cardiology dietitian at EntirelyNourished.com, also not involved in the study, explained that “the MIND diet was created by researchers at Rush University Medical Center in 2015 , based on findings that certain foods can enhance brain health and lower the risk of cognitive decline, especially Alzheimer’s disease.”
Kaiser further added that the MIND diet includes “two key layers of vegetables and fruits at its broad base — the biggest, most fundamental layer being reserved for green, leafy vegetables because they are that important.”
Nuts and whole grains are key elements of the MIND diet as well. It also includes nutrient-dense proteins such as fish and poultry, although the jury, according to Kaiser, is still out on red meats.
“While there is a lot of debate regarding red meat intake among nutritional and lifestyle medicine experts,” he said, “the MIND diet does not call for its elimination altogether.”
Kaiser cited concerns among some that eliminating meat altogether may deprive one of beneficial minerals, such as zinc, or result in an over-reliance on carbohydrates.
Still, Kaiser said, “the MIND diet does suggest limiting red meat intake — including all beef, lamb, and pork — to no more than 3 servings each week.” Foods to avoid on the MIND diet
Kaiser also pointed out that there are certain types of foods the MIND diet encourages people not to eat.
“The MIND diet, and other brain-healthy diets, encourage the intake of fresh whole foods and the avoidance of highly processed and refined foods,” he said.
Highly processed and refined foods tend to be low in fiber, are digested too quickly, and cause rapid fluctuations in blood sugar levels.
These level changes may result in, Kaiser said, a “broad constellation of physiological consequences,” including inflammation and oxidative stress , which can negatively affect brain health over the long term.
Fast foods, especially fried foods rich in trans fats, are particularly unwelcome in the MIND diet, as they have been linked to a wide range of health conditions.
“Sugars are Enemy Number One,” Kaiser emphasized. What are the best foods for brain health?
“While no single food can guarantee better brain health,” said Kaiser, “an extensive and growing body of research demonstrates the brain health benefits of certain foods — especially those rich in certain antioxidants and other ‘neuroprotective’ compounds.” For example, the MIND diet promotes berries over the consumption of other fruits. Routhenstein explained why. It is “due to their unique anthocyanin and flavonoid makeup, which adds a rich antioxidant component to your diet, known to help support brain health,” she told us. “Research suggests,” said Routhenstein, “that these particular compounds may enhance cognitive function, improve memory, and potentially reduce the risk of cognitive decline as people age.”Kaiser further noted that: “These ‘phytonutrients,’ chemicals that plants produce to keep themselves healthy, can actually reduce inflammation in our brains, protect brain cells from injury, support learning and memory, and deliver other obvious benefits for brain health.” Routhenstein illustrated that one day on a MIND diet might look like having “blueberry-pecan oatmeal for breakfast, a salad with cherry tomatoes, chickpeas, and olive oil dressing for lunch, baked salmon with quinoa and mixed vegetables for dinner, and an apple […]
Do nootropics really boost focus and memory? Experts weigh in on ‘smart drugs’
Getty Images If you’ve ever put in long hours studying for final exams or perfecting a presentation for a client, you’ve probably found yourself wishing for an extra jolt of brain power. Nootropics are often touted as a way to help with that. Nicknamed “brain boosters” or “smart drugs,” they’re typically substances that purport to improve brain performance.
This cognitive boost is meant to be above our normal baseline, explains Dr. Scott Small , professor of neurology and Director of the Alzheimer’s Disease Research Center at Columbia University. Different parts of the brain govern different cognitive abilities, such as memory, abstract reasoning, decision making, and speed of processing. Nootropics are intended to target these areas, he tells Fortune .
“So in theory, if you wanted to improve memory above baseline, you would have a nootropic that improves the function of that area, somehow cranking up its functional capabilities,” adds Small, author of “ Forgetting: The Benefits of Not Remembering .”
But just how well do nootropics actually work? What are nootropics?
Nootropics fall into three different classes of drugs: eugeroics like Modafin and Nuvigil meant to promote alertness, stimulants like Ritalin and Adderall prescribed to those with ADHD, and dietary supplements. Because the first two classes of drugs are prescription-based, they are only formulated for—and should be used by—certain individuals.
But anyone can try a natural nootropic supplement, which can include one or a combination of several ingredients. They have the potential to reduce anxiety, enhance your mood, increase productivity, heighten your energy, improve your memory, and sharpen your focus. Some of the most common ingredients include: Lion’s mane
Rhodiola rosea
Ginkgo biloba
Ashwagandha
Panax ginseng
Alpha GPC
Caffeine
Citicoline
Phosphatidylserine
Huperzine A
L-theanine
Bacopa monnieri
You don’t always need to tap into the $9.2 billion brain health supplement market to get your fill of these. You can easily get a dose of caffeine with a cup of joe or drink some L-theanine, an amino acid known for boosting alertness, with a cup of green or black tea.
But you may not even need to turn to a drug at all, in Small’s view. He says nootropics “could be a drug, a pharmaceutical agent, a diet. It could be a behavior, like physical or cognitive exercise,” he says. At the end of the day, “it’s an intervention, behavioral or not, that improves your cognition above normal.” Are nootropics actually effective?
Research is limited on the effectiveness of nootropics. A study published in the National Library of Medicine finds that most nootropics don’t have an immediate effect after a single dose and need to be used for a longer period of time to measure improvement. It also concludes that there isn’t enough research on healthy individuals in the field.
Small has seen positive effects of behavioral interventions in reviving someone’s memory that has slid down a little bit with aging, but he says this is more focused on boosting a cognitive decline back to the baseline, rather than exceeding the cognitive baseline.
“In the strict definition of nootropic I don’t think there’s anything that meets that criteria—that you either do something or take something and all your cognitive abilities rise like a tide,” Small says, acknowledging his definition of a nootropic may be a little more orthodox than others’. “People have been searching for it. I’ve been searching for it.” Are nootropics safe?
Many products advertised as nootropic supplements haven’t been examined in terms of safety and efficacy, according to the American Medical Association. As with any drug, there can be side effects, such as insomnia, anxiety, allergic reactions, or interactions with medications.
Experts agree that when shopping for a supplement, you’ll want to consider whether the ingredients have been well researched, the dose efficacy, synergistic effects (some nootropics work better together), if the labeling is transparent, and whether it’s been tested by a third party.
Small says that if you’re going to try a nootropic, you need to do your due diligence. “Whether it’s a supplement or a drug, it’s a pill. And that you just never know.”
But if, for example, a young and healthy person is taking the GRE and looking to boost their scores, he says he wouldn’t recommend taking anything in good faith. It’s why he prefers behavioral interventions. “Anyone can do them, and anyone can access them,” he says. “They seem to be the safest and most effective.” Physical exercise is one of his go-to recommendations. “From a neurologist point of view, the part of the brain for physical exercise clearly improves the hippocampus, an area of the brain that is important for memory, and the frontal cortex, an area of the brain important for decision making.”He also suggests staying cognitively active , which can involve working on games and puzzles. And, in the middle of a loneliness epidemic , staying socially engaged is also important since depression can affect cognition. Sleep is, of course, critical in maintaining normal cognition, Small adds.As he puts it, it’s “all good cognitive hygiene.” More on nutrition and supplements: The 5 best supplements for healthy aging , according to a longevity expert It’s not 8 glasses a day anymore. Here’s how much water you should drink each day Do turmeric supplements work? Experts say, yes, for 2 conditions Does apple cider vinegar really help with weight loss? Here are the science-backed health benefits This story was originally featured on Fortune.com
MIND: The Diet for Brain Health That Could Slow Cognitive Decline
A diet developed for brain health might slow or prevent cognitive decline associated with dementia, Alzheimer’s and age-related memory loss, a study says.
“Following a MIND diet approach to meals can be a great way to boost brain health,” study lead author Dr. Russell Sawyer told Newsweek . He is an assistant professor in the Department of Neurology and Rehabilitation Medicine at the University of Cincinnati’s College of Medicine.
“What I like about the MIND diet is that it is more about what you should be eating and less about what you should not be eating,” he said. “As someone who enjoys food, I would much rather add a dark-green leafy salad with nuts, berries, beans and an olive oil-based dressing to my diet than severely limit what I should not be eating.”
The MIND diet is a combination of the Mediterranean diet —which has been linked to a plethora of positive health outcomes, from better heart health to general longevity—and the Dietary Approaches to Stop Hypertension (DASH) diet, developed to help lower blood pressure. “MIND” stands for Mediterranean-DASH intervention for neurodegenerative delay.
The MIND diet prioritizes whole grains, leafy green vegetables, berries, beans and nuts; encourages the consumption of other, non-leafy green vegetables, fish, seafood, poultry and olive oil; allows for limited consumption of red meat and wine; and limits the consumption of fast food, fried food, butter, margarine, pastries and sweet foods such as candy.
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Sawyer said, “Among the MIND diet components are 10 brain-healthy food groups—green leafy vegetables, other vegetables, nuts, berries, whole grains, seafood, poultry, olive oil and wine—and five unhealthy food groups—red meats, butter and stick margarine, cheese pastries and sweets, and fried/fast food.”
He continued, “The good foods are rich in antioxidants while limiting intake of unhealthy foods which contribute to saturated and trans fat intakes.” The MIND diet was created to reduce dementia and a decline in brain health. It includes leafy green vegetables, other vegetables, seafood, olive oil, berries, nuts, beans, whole grains, poultry and wine. The study was published in the scientific journal Neurology and funded by the National Institute of Neurological Disorders and Stroke and the National Institute on Aging.
Sawyer and a team of scientists at the American Academy of Neurology investigated the effects of a MIND diet on 14,145 people, 70 percent white and 30 percent Black, with an average age of 64 years.
Over approximately 10 years, they found that those who ate a diet more closely aligned with MIND were less likely to experience cognitive impairment. Those whose cognition did get worse were more likely to experience a slower decline if they adhered to a MIND-adjacent style of eating.
This association was more pronounced among women and Black people than men and white people.
“Any medical intervention—diet, lifestyle or medication—should be adequately addressed in diverse populations,” Sawyer said. “Race is often a surrogate marker for genetic differences, epigenetic differences and cultural differences which can result in different outcomes.”
Participants reported their typical dietary patterns in questionnaires, were given scores for adherence to the MIND diet and were then put into three groups.
The low group had an average diet score of five out of 12, the middle group scored about seven out of 12, and the high group scored nine out of 12.
To assess cognition, thinking and memory skills were measured at the beginning and end of the study.
In the low group, 12 percent developed cognitive impairment in a decade, compared with 11 percent in the middle group and 10 percent in the high group—not stark differences.
But once the researchers adjusted these figures to take into account factors such as age, blood pressure, diabetes, obesity and income, they found that people in the high group had a 4 percent lower risk of developing cognitive impairment during the 10-year study than those in the low group.
Among female participants, the scientists found a 6 percent decreased risk of cognitive impairment if they ate a diet more closely aligned with MIND. Among male participants, no significant decrease in risk was found.
“No diet or dietary approach is perfect for everyone,” Sawyer told Newsweek . “What may be easy for one person may be very difficult for another. Many factors go into this, including personal taste, access to certain types of foods and time available for food preparation.
“The MIND diet is not about fancy ingredients that are not available but [those that] can be found in all grocery stores,” he said. “Making more informed choices is the first step to a healthier diet for the mind.”
There were several limitations in this study . It was observational, so associations can be found but not cause-and-effect relationships, and therefore this research cannot prove that the MIND diet prevents cognitive impairment.Also, the dietary data used was self-reported by participants, which is a less reliable method of data collection than some alternatives. Do you have a tip on a food story that Newsweek should be covering? Is there a nutrition concern that’s worrying you? Let us know via science@newsweek.com . We can ask experts for advice, and your story could be featured in Newsweek . Reference Sawyer, R.P., Blair, J., Shatz, R., Manly, J.J., & Judd, S.E. (2024). Association of Adherence to a MIND-Style Diet With the Risk of Cognitive Impairment and Decline in the REGARDS Cohort . Neurology, 103. https://doi.org/10.1212/WNL.0000000000209817
Brain goop that traps hunger neurons drives obesity
A mechanism for metabolic disease is traced to a defective cellular scaffolding that holds together the brain’s hunger cells. Facebook
Neurons (artist’s illustration) that affect hunger lose their ability to sense insulin when encased by a sticky scaffolding. A build-up of sticky goo that traps neurons in an appetite-control centre in the brain has been implicated in worsening diabetes and obesity , according to research on mice 1 .
The goo also prevents insulin from reaching brain neurons that control hunger. Inhibiting production of the goo led mice to lose weight, experiments found. These findings points to a new driver of metabolic disorders and could help scientists to identify targets for drugs to treat these conditions.
These results were published today in Nature . Hunger dial in the brain
Metabolic diseases such as type 2 diabetes and obesity can develop when the body’s cells become insensitive to insulin, a hormone that regulates blood-sugar levels. Scientists searching for the mechanism that causes this insulin resistance have homed in on a part of the brain called the arcuate nucleus of the hypothalamus , which senses insulin levels and, in response, adjusts energy expenditure and sensations of hunger .
As the animals develop insulin resistance, a type of cellular scaffolding , called the extracellular matrix, that holds the hunger neurons in place becomes a disorganized goo. Previously, researchers had noticed that this scaffolding changes when mice are fed a high-fat diet 2 . Milkshake neuroscience: how the brain nudges us toward fatty foods The researchers wanted to see whether these brain changes might drive insulin resistance rather than merely developing alongside it. The authors fed mice a high-fat, high-sugar diet for 12 weeks and monitored the scaffolding around the hunger neurons by taking tissue samples and monitoring gene activity.
They found that this scaffolding became thicker and stickier within weeks of the mice starting the unhealthy diet. As these animals gained weight, their hypothalamus neurons became less able to process insulin normally, even when the hormone was injected directly into their brains. This suggests that the scaffolding’s stickiness stops insulin from getting into the brain. Instead, “it gets stuck”, says co-author Garron Dodd, a neuroscientist at the University of Melbourne in Australia. Goo loss leads to weight loss
To try to reverse these changes, the researchers injected mice with either an enzyme that digests the goo or a molecule called fluorosamine that inhibits the scaffolding’s formation. Both approaches successfully got rid of the sticky logjam in the animals’ brains, allowing for increased insulin uptake. Fluorosamine even led the animals to shed weight and increase their energy expenditures. Treating insulin resistance by targeting the support structure around neurons might be safer than targeting neurons directly, Dodd says. These brain cells could influence how fast you eat — and when you stop This “high quality” study proves “again and again” that this cellular scaffolding regulates hormonal signalling in a way that directly affects the rest of the body’s metabolism and drives disease, says Kimberly Alonge, a biochemist at the University of Washington School of Pharmacy in Seattle, who was not involved with the study. It also directs the field to focus not only on individual cells and cell types, but also the “packing material the cells are sitting in”, she adds.
The team’s experiments also showed that inflammation in the hypothalamus drives disruption of the scaffolding, but the study does not address what causes the inflammation to begin with, Alonge says. Previous research has shown that brain cells called glia can affect the structural integrity of the scaffolding, and Alonge would like to know whether glial cells contribute to the inflammation observed in the study.
It’s still unclear how big a part dysfunctional scaffolding plays in causing metabolic disease compared with other well-established drivers of disease, Dodd says. He and his colleagues hope to address this question later.
Future research is needed to investigate whether this goo arises as humans develop metabolic disease. This might pose a challenge, Dodd says, because there is no non-invasive way to access the hypothalamus, which is situated deep in the brain, and it’s a difficult tissue to sample, even from donated organs.
Read the related News & Views ‘ Mesh enclosing hungerneurons drives obesity’ References
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Exploring the effect of low sodium concentrations on brain microglial cells
In a new study, scientists investigated the impact of low sodium concentrations and its rapid correction on nitric oxide production dependent on expression of Nfat5 in microglial cells. Credit: Yoshihisa Sugimura from Fujita Health University Low serum sodium concentrations in the blood are called hyponatremia, a prevalent clinical electrolyte disorder. In contrast to acute hyponatremia, chronic hyponatremia has been previously considered asymptomatic because the brain can successfully adapt to hyponatremia. If not treated, chronic hyponatremia can lead to complications such as fractures, falls, memory impairment, and other mental issues.
Treating the chronic condition is, however, quite tricky as it has been observed that overly rapid correction of hyponatremia can cause ODS. It is a neurological disorder where nerve transmission is affected due to damage in the myelin sheath surrounding the neurons and is associated with neurological morbidity and mortality.
To ensure that hyponatremia is addressed without the complications associated with the treatment process, there is a need to understand the origin of ODS. In a previous study, Professor Yoshihisa Sugimura from the Department of Endocrinology, Diabetes and Metabolism, School of Medicine, Fujita Health University found that microglia, resident immune cells found in the brain and spinal cord , could play a critical role in the pathogenesis of osmotic demyelination syndrome (ODS).
Building on these findings, a team of researchers led by Prof. Sugimura, with Haruki Fujisawa as the first author, now explored the direct impact of low extracellular sodium concentrations (LS) and their rapid correction on microglia. The study was published in Free Radical Biology and Medicine and is co-authored by Haruki Fujisawa and Atsushi Suzuki from Fujita Health University, among other authors. In this study, the research team demonstrated that low sodium levels could decrease specific mRNA expression and nitric oxide (NO) production of microglia.
Microglia participates in many critical CNS functions, ranging from neurogenesis to synaptic remodeling and myelination, through movement and surveillance within the brain. They can get activated in response to external stimuli or the presence of pathogens and produce several chemicals including nitric oxide that can initiate inflammation.
“Understanding the rather elusive effect of chronic hyponatremia and its rapid correction on microglia is crucial as it may be a potential therapeutic target for ODS and hyponatremia-related neurocognitive impairment and mental manifestations,” explains Prof. Sugimura when asked the reason behind focusing on microglia for the study.
To investigate the effect of LS, the team chose microglial cell lines (BV-2 or 6–3). They found that a decrease in sodium concentrations of 36 mmol/L suppressed the mRNA expression of Nos2, an enzyme that is responsible for catalyzing and moderating the production of NO, which is essential for inflammation and regulating neurotransmission. This was further reflected in the experiments conducted in LS conditions where the researchers noticed decreased production of NO in microglial cells.
In addition, LS suppressed the expression of nuclear factor of activated T cells-5 (NFAT5), a protein responsible for regulating the expression of genes that handle osmotic stress. Furthermore, overexpression of NFAT5 significantly increased Nos2 mRNA expression and NO production in BV-2 cells.
Moreover, when these microglial cell lines were exposed to rapid correction of low sodium concentrations, the researchers observed a significant rise in NO production. This suggests that acute correction of hyponatremia contributes to the sudden increase in Nos2 mRNA expression, and therefore NO release, thus leading to ODS pathophysiology.
The team also discovered that expressions of Nos2 and Nfat5 mRNA were also suppressed in microglia isolated from the cerebral cortex in chronic hyponatremia model mice.
In summary, these findings report the impact of chronic hyponatremia and its rapid correction on the microglia , further suggesting its contribution to hyponatremia-induced neuronal dysfunctions.
“Clarifying the effect of chronic hyponatremia on brain functions can contribute to the development of new therapeutics and technology to address this condition, while also lowering the occurrence of associated complications and improving the quality of life of patients,” concludes Prof. Sugimura.
More information: Haruki Fujisawa et al, Prolonged extracellular low sodium concentrations and subsequent their rapid correction modulate nitric oxide production dependent on NFAT5 in microglia, Free Radical Biology and Medicine (2024). DOI: 10.1016/j.freeradbiomed.2024.08.019
Citation : Exploring the effect of low sodium concentrations on brain microglial cells (2024, September 18) retrieved 19 September 2024 from https://medicalxpress.com/news/2024-09-exploring-effect-sodium-brain-microglial.html
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I’m a neuroscientist — here are 4 easy ways to increase your thinking abilities
Neuroscientist and mindset coach Emily McDonald is sharing four ways to boost the birth of new brain cells, a process known as neurogenesis — exercise, meditation, polyphenol-rich foods and sunlight. She’s giving you a piece of her mind.
Emily McDonald , an Arizona neuroscientist and mindset coach, is sharing four ways to boost the birth of new brain cells — a process known as neurogenesis.
Most of our 100 billion brain cells were created before birth — the brain can still produce new cells, called neurons, as we age.
In a Tuesday TikTok , McDonald suggests supporting neuron formation with exercise, meditation, polyphenol-rich foods and sunlight exposure. Exercise regularly
McDonald suggests participating in a low-intensity workout at 60% to 70% of your maximum heart rate. Brittany Dalena Brittany Dalena An airport in Bhutan is a retching challenge for pilots. A new study finds that consuming six additional servings of flavonoid-rich foods a day can lower the risk of dementia, especially for those with high blood pressure, depression and high genetic risk. “Zone 2 exercise has been shown to boost [brain-derived neurotrophic factor levels (BDNF)] in the brain, which is a protein that can help neurons grow,” McDonald said.
Discovered in the 1980s, BDNF has been dubbed “Miracle-Gro” because it enhances learning and memory by encouraging the survival and growth of existing neurons and the development of new ones.
And Zone 2 exercise is a low-intensity workout performed at 60% to 70% of your maximum heart rate. You should be able to comfortably hold a conversation — think a brisk walk , a casual bike ride or aerobics without pushing yourself. Try meditation
Meditation may stimulate structural changes in the hippocampus, a brain region where neurogenesis occurs in adults. “Meditation can also boost BDNF levels, and it can also enhance neuroplasticity, which is the brain’s ability to rewire” in response to life experiences, McDonald explained.
Some research suggests that meditation may stimulate structural changes in the hippocampus, a region where neurogenesis occurs in adults.
One study highlighted the brain benefits of three months of intensive Vipassana meditation , an ancient mindfulness technique that encourages participants to see things as they are without judgment. Eat polyphenol-rich foods
Blueberries are a great sources of polyphenols, which are known to reduce brain inflammation. Polyphenols — found in dark chocolate, berries, pears, grapes and red wine — boast antioxidant and anti-inflammatory powers that are believed to protect against free-radical damage and help prevent neurodegenerative diseases like Alzheimer’s and Parkinson’s by reducing inflammation in the brain.
“Blueberries are a great example of this type of food,” McDonald advised. Get the latest breakthroughs in medicine, diet & nutrition tips and more.
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BDNF levels appear to be tied to seasons — one study indicated they are lower from January to May and higher from June to December.
“Sunlight can boost our BDNF levels. You’ve got to go out in the sun,” McDonald recommended.
Just don’t forget your sunscreen .
New study reveals link between cataracts and vascular dementia
Tags: Alzheimer’s disease , badhealth , badscience , brain function , brain health , cataracts , cognitive function , cognitive health , cognitive impairment , discoveries , eye health , health science , prevention , research , tips , vascular dementia , vision , visual impairment A new study has found that cataracts can increase a person’s risk of dementia , particularly vascular dementia.
Also known as vascular cognitive impairment, vascular dementia is characterized by impaired thinking skills caused by obstructions in the blood flow to various regions of the brain. This reduced blood flow deprives brain cells of much-needed oxygen and nutrients, which eventually leads to their death. Link between visual impairment and poor cognitive function
Many ongoing studies are exploring the relationship between poor vision and cognitive decline. Scientific interest in the topic was sparked by The Lancet Commission 2020 report on dementia prevention which identified hearing impairment, specifically hearing loss, as a modifiable risk factor for dementia. Since then, researchers have begun exploring the possibility of visual impairment also increasing the risk of cognitive impairment.
In a study published in the journal Human Brain Mapping , researchers looked at how visual impairment and retinal neurodegeneration are connected to cognitive impairment. They found that decreased visual acuity and the thinning of the ganglion cell layer were associated with global brain atrophy (decrease in size) and hippocampal atrophy . The ganglion cell layer is a layer in the retina that contains the neurons responsible for transmitting information to at least 50 different areas of the midbrain.
According to the study, neurodegeneration along the visual pathway, which leads to the disintegration of intermediate visual tracts, is behind the association between visual impairment and cognitive impairment. Although the entire process is still unclear, researchers believe that changes in the visual pathway caused by retinal neurodegeneration negatively affect cognitive function by altering the structure of brain regions that are crucial to cognition.
A similar study published in the journal Aging & Mental Health investigated whether cataracts, one of the most common causes of visual impairment in older adults, is associated with the risk of developing dementia or cognitive impairment. Meta-analysis of 11 studies involving a total of 489,211 participants revealed a significant association between cataracts and an increased risk of all-cause dementia . Subgroup analyses also showed that individuals who develop cataracts have an increased risk of Alzheimer’s disease and vascular dementia.
Another study, this time by Chinese researchers, explored the relationship between cataracts and the incidence of cognitive impairment in older adults. Published in the journal Behavioral Brain Research , the meta-analysis looked at 13 studies that involved a total of 798,694 participants. The Chinese researchers found that compared to those without cataracts, participants that developed cataracts had a higher risk of all-cause dementia, Alzheimer’s disease dementia, vascular dementia and mild cognitive impairment.
Meanwhile, an earlier study published in the journal JAMA Internal Medicine reported that undergoing cataract surgery could reduce the risk of dementia by 30 percent . This lowered risk, specifically of developing Alzheimer’s disease dementia, persisted for over a decade after surgery, further cementing the link between cataracts and visual impairment and cognitive impairment.
However, much like the mechanisms underlying the link between visual impairment and cognitive decline, how cataract surgery lowers dementia risk remains unclear. Researchers, on the other hand, hypothesize that it may have to do with people receiving higher quality visual input and getting more blue light, which is specifically blocked by cataracts, after undergoing surgery. (Related: Extract from moringa trees found to prevent cataract formation .) Eye-brain connection: cataracts and vascular dementia
Cataracts are common among older adults. In fact, according to the National Eye Institute , more than half of American adults age 80 and above either have cataracts or have had surgery to remove them. Cataract refers to a cloudy area in the lens of the eye that obstructs vision, often caused by normal changes in your eyes as you age. Eye injury or damage from eye surgery, excessive sun exposure and health problems like diabetes can also raise your risk of developing cataracts.
In a new study published in the journal JAMA Network Open , American researchers sought to understand how vision and eye conditions are associated with an increased risk of Alzheimer’s disease and related dementias (ADRDs). Specifically, they wished to clarify whether this association is causal and if vision is also a modifiable risk factor for dementia. (Related: Anti-inflammatory diet helps with cardiovascular and metabolic diseases, cuts dementia risk by 31% .)
Using data from the UK Biobank and genome-wide association studies on cataract, myopia (nearsightedness) and Alzheimer’s, the researchers conducted an observational study to establish associations, followed by a 2-sample bidirectional mendelian randomization (MR) study which involved genetic analysis to determine causal relationships.
The analyzed data came from individuals aged 55 to 70 years who were dementia-free when they began to participate in the UK Biobank study. Of the 304,?953 selected participants, 14,295 had cataracts and 2,754 had worse than 20/40 vision. The researchers found that having cataracts and myopia was associated with a higher risk of ADRDs .
MR analyses further revealed that cataracts were associated with an increased risk of vascular dementia as well as lower total gray matter volume and white matter hyperintensities, which are believed to be predictive of stroke, dementia and death . MR analyses also estimated that cataracts are “associated with a 92 percent increase in the odds of vascular dementia risk.” On the other hand, while poor visual acuity was linked to increased dementia risk, myopia was not associated with dementia in the MR analyses.
The researchers also conducted genetic analysis to determine potential reverse causality. They found that Alzheimer’s disease is not associated with cataract formation. Based on their findings, the researchers concluded that “cataracts increase the risk of dementia through vascular and non-AD [Alzheimer’s disease] mechanisms,” meaning cataracts contribute to the development of Alzheimer’s through pathways not commonly linked to the disease.
Because cataracts were also associated with reduced total brain and gray matter volumes, the researchers suspect that these pathways […]
The brain’s state of attention is shaped by a handful of neurons, study shows
by University of Geneva Noradrenergic neurons in the locus coeruleus (LC) play a key role in the transition from a focused to an alert state. The image shows these neurons in a mouse brain, revealed by immunohistochemical staining. Credit: UNIGE / ETH Zurich What enables the brain to go from intense concentration to a heightened state of alertness? A study carried out by neuroscientists at the University of Geneva (UNIGE), in collaboration with ETH Zurich, shows that a brain region called locus coeruleus (LC) and the neurotransmitter noradrenaline act as conductors, reorganizing brain functions according to the mental demands of the moment.
The study, published in Nature Neuroscience , demonstrates that the way the locus coeruleus is triggered enables us to switch from one state of concentration to another. This discovery could change the way elite sportsmen and women train to achieve their goals.
How do athletes achieve the extraordinary mental clarity and precision needed to succeed in their discipline? The answer lies in the brain ‘s remarkable ability to focus, eliminating distractions to concentrate on a single task.
This phenomenon, often described as “being in the zone,” is a critical skill not just for athletes, but for anyone facing a challenging task—whether it’s taking an exam or mastering a musical instrument. At times, however, these people also need to be fully aware of their environment, especially when it comes to spotting potential dangers. A handful of neurons
In this study, neuroscientists from UNIGE and ETH investigated what allows the brain to shift between intense focus and heightened awareness. The research team focused on the locus coeruleus (LC), a small region in the brainstem that produces noradrenaline, a neurotransmitter involved in regulating arousal.
“It’s small and its location deep within the brain was a challenge from the outset, making it difficult to observe—and impossible to manipulate—in humans. For these reasons, we turned to mice where the LC consists of only about 3,000 neurons, but these neurons can still exert a significant influence over the 75 million neurons that make up the mouse brain,” explains Valerio Zerbi, assistant professor in the Department of Psychiatry and the Department of Basic Neurosciences at the UNIGE Faculty of Medicine, and initiator of the study.
To overcome this challenge, his team collaborated with Johannes Bohacek’s laboratory at ETH Zurich. Using advanced techniques such as optogenetics to artificially manipulate LC neurons and photometry to measure noradrenaline release, the researchers were able to explore LC function.
Functional Magnetic Resonance Imaging (fMRI) provided the first empirical evidence into how LC stimulation affects brain activity across different regions, shedding light on the LC’s role in dynamically modulating attention and focus. A question of rhythm
Neuroscientists discovered that triggering the LC three times a second in a continuous manner—so-called “tonic” activity—had different consequences than triggering the same frequency over a short period of time—so-called “burst” activity.
“When the LC is triggered in bursts, more noradrenaline is released, and the brain’s sensory functions are prioritized. This sensory brain mode enables mice to be more alert to the environment around them,” explains Zerbi.
Conversely, when the LC is triggered in a moderate tonic mode, less noradrenaline is released by the LC and brain regions such as the prefrontal cortex and hippocampus are activated. These two structures are known for processing information and are conducive to reflection and intense attention. Controlling the locus coeruleus for performance
“While cutting-edge equipment and meticulous training are certainly part of the equation, the secret of top athletes may well lie in their mastery over their LC. By finely tuning its activity, they can switch between states of intense focus and broad awareness, performing at their peak when it matters most,” concludes Zerbi.
Also, thanks to the findings of this study, brain imaging could help sportsmen and women to make better use of their LC, notably by using neurofeedback approaches, a technique that uses devices to monitor brain activity in real time to enable a person to regulate it based on visual feedback.
More information: Christina Grimm et al, Tonic and burst-like locus coeruleus stimulation distinctly shift network activity across the cortical hierarchy, Nature Neuroscience (2024). DOI: 10.1038/s41593-024-01755-8 . www.nature.com/articles/s41593-024-01755-8
Provided by University of Geneva
How novelty positively impacts your brain
[Source Illustration: Pixabay ] Sticking to your routine can help you get more things done. It also means the brain doesn’t have to work as hard, reinventing the wheel every time you get ready for work in the morning or schedule your day . Sticking to a “same-old, same-old” approach, however, can turn into a fast track to boredom and discontent.
Instead, it’s important to introduce some novelty to your life , says Dr. Lorraine Besser, author of The Art of the Interesting: What We Miss in Our Pursuit of the Good Life and How to Cultivate It and professor of philosophy at Middlebury College.
“Our mind likes to stay safe and play with routines,” she says. “When something new happens, it forces the brain out of its routine thought patterns. It challenges it to have a new thought. Anytime you have a new thought, it’ll lead to other new thoughts. Novelty and sources of newness stimulate your mind to think.” 3 Ways to Train Your Brain to Look for Novelty
Novelty is anything that you experience as new, explains Besser. Fortunately, it exists all around you—if you’re open to it. The key is to train your mind to get out of your routines.
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Besser recommends intentionally finding points during the day for newness. For example, take a lunch break away from your desk, stepping outside of your routine to notice something new in the world. “Give your mind the opportunity to wander,” she says. “Be intentional, pausing and giving yourself some space to have this kind of experience.”
Next, make sure you aren’t overly focused on goals . When you strive for something, you only see things through the lens of how it impacts your plans and what you want, says Besser.
“When you look at the world like that, you narrow your focus,” she says. “If you can give your mind space to step outside of your evaluating, pursuing mode and give it space to have a new cognitive experience, it will take off.”
Finally, avoid the temptation to check out and go on autopilot during monotonous tasks . “When you’re on autopilot, you’re not really experiencing anything of value,” says Besser. “You’re just going through the motions. If you can better engage with what you’re doing, you will enhance your workplace experience.”
Pay attention and respond to the details, suggests Besser. You can also tap your senses , using them to deliver stimulation and connection with what you’re doing. Why Novelty is Important
While novelty doesn’t necessarily enhance happiness, Besser says it contributes to psychological richness. “ Research shows that this is an important part of people’s lives overall,” she says. “It’s an experience in the mind where you are engaging in new frames of thinking, stimulating interest and arousing and engaging your thoughts.”
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Novelty can also combat boredom. “We know that boredom in the workplace inhibits productivity and lowers employee satisfaction ,” says Besser. “One of the things that resolves boredom is to engage more with what you’re doing.”
Novel experiences also enhance small moments in your day-to-day life. Since you’re more likely to remember them, Besser says they can shape and improve how you experience other events, helping to change your perspective, potentially generating more interesting ideas .
Novelty can affect self-expansion, too. “Psychologically rich experiences lead towards a greater sense of self,” says Besser. “My gut tells me that this is happening because we are tapping into different kinds of cognitive reactions and emotions. These are the kinds of things that can get squeezed away when you’re too focused on your plans or agendas. When you allow your brain to operate fully and engage in interesting experiences, you expand your very notion of yourself, seeing yourself as more robust and tapping into a greater sense of identity through it.”
A life without challenge also shrinks your potential and what you may be capable of experiencing. “Interesting experiences offer a distinctive and unique aspect of this dimension of the ‘good life,’” explains Besser. “It’s simply engaging in what we’re doing in a different way.”
While clinging to your routines may feel safe and productive, a life without novelty can be boring and impoverished, says Besser. “If you don’t seek out something new, you get stuck in cycles of comfort and stability,” she says. “Comfort and stability are important—and there are times in our lives where that’s what we need—but if you stay within your circles of comfort and safety, you’re going to live a very one-dimensional life.”
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ABOUT THE AUTHOR
Stephanie Vozza is a freelance writer who covers productivity, careers, and leadership. She’s written for Fast Company since 2014 and has penned nearly 1,000 articles for the site’s Work Life vertical More
Research suggests neurons protect and preserve certain information through a dedicated zone of stable synapses
A layer 5 pyramidal neuron imaged in vivo with two-photon microscopy. The oblique dendritic domain (pink) contains stable synapses, and the basal dendritic domain (blue) contains plastic synapses. The cell body and part of the dendritic trunk are white. Credit: Courtney Yaeger and Mark Harnett One of the brain’s most celebrated qualities is its adaptability. Changes to neural circuits, whose connections are continually adjusted as we experience and interact with the world, are key to how we learn. But to keep knowledge and memories intact, some parts of the circuitry must be resistant to this constant change.
“Brains have figured out how to navigate this landscape of balancing between stability and flexibility, so that you can have new learning and you can have lifelong memory,” says neuroscientist Mark Harnett, an investigator at MIT’s McGovern Institute for Brain Research.
In research published in Cell Reports , Harnett and his team show how individual neurons can contribute to both parts of this vital duality. By studying the synapses through which pyramidal neurons in the brain’s sensory cortex communicate, they have learned how the cells preserve their understanding of some of the world’s most fundamental features, while also maintaining the flexibility they need to adapt to a changing world. Visual connections
Pyramidal neurons receive input from other neurons via thousands of connection points. Early in life, these synapses are extremely malleable; their strength can shift as a young animal takes in visual information and learns to interpret it. Most remain adaptable into adulthood, but Harnett’s team discovered that some of the cells’ synapses lose their flexibility when the animals are less than a month old. Having both stable and flexible synapses means these neurons can combine input from different sources to use visual information in flexible ways.
Postdoc Courtney Yaeger took a close look at these unusually stable synapses, which cluster together along a narrow region of the elaborately branched pyramidal cells. She was interested in the connections through which the cells receive primary visual information, so she traced their connections with neurons in a vision-processing center of the brain’s thalamus called the dorsal lateral geniculate nucleus (dLGN).
The long extensions through which a neuron receives signals from other cells are called dendrites, and they branch of from the main body of the cell into a tree-like structure. Spiny protrusions along the dendrites form the synapses that connect pyramidal neurons to other cells. Yaeger’s experiments showed that connections from the dLGN all led to a defined region of the pyramidal cells—a tight band within what she describes as the trunk of the dendritic tree.
Yaeger found several ways in which synapses in this region—formally known as the apical oblique dendrite domain—differ from other synapses on the same cells. “They’re not actually that far away from each other, but they have completely different properties,” she says. Stable synapses
In one set of experiments, Yaeger activated synapses on the pyramidal neurons and measured the effect on the cells’ electrical potential. Changes to a neuron’s electrical potential generate the impulses the cells use to communicate with one another. It is common for a synapse’s electrical effects to amplify when synapses nearby are also activated. But when signals were delivered to the apical oblique dendrite domain, each one had the same effect, no matter how many synapses were stimulated.
Synapses there don’t interact with one another at all, Harnett says. “They just do what they do. No matter what their neighbors are doing, they all just do kind of the same thing.”
The team was also able to visualize the molecular contents of individual synapses. This revealed a surprising lack of a certain kind of neurotransmitter receptor, called NMDA receptors, in the apical oblique dendrites. That was notable because of NMDA receptors’ role in mediating changes in the brain.
“Generally when we think about any kind of learning and memory and plasticity, it’s NMDA receptors that do it,” Harnett says. “That is the by far most common substrate of learning and memory in all brains.”
When Yaeger stimulated the apical oblique synapses with electricity, generating patterns of activity that would strengthen most synapses, the team discovered a consequence of the limited presence of NMDA receptors. The synapses’ strength did not change. “There’s no activity-dependent plasticity going on there, as far as we have tested,” Yaeger says.
That makes sense, the researchers say, because the cells’ connections from the thalamus relay primary visual information detected by the eyes. It is through these connections that the brain learns to recognize basic visual features like shapes and lines.
“These synapses are basically a robust, high-fidelity readout of this visual information,” Harnett explains. “That’s what they’re conveying, and it’s not context-sensitive. So it doesn’t matter how many other synapses are active, they just do exactly what they’re going to do, and you can’t modify them up and down based on activity. So they’re very, very stable.”
“You actually don’t want those to be plastic,” adds Yaeger. “Can you imagine going to sleep and then forgetting what a vertical line looks like? That would be disastrous.”
By conducting the same experiments in mice of different ages, the researchers determined that the synapses that connect pyramidal neurons to the thalamus become stable a few weeks after young mice first open their eyes. By that point, Harnett says, they have learned everything they need to learn. On the other hand, if mice spend the first weeks of their lives in the dark, the synapses never stabilize—further evidence that the transition depends on visual experience.
The team’s findings not only help explain how the brain balances flexibility and stability; they could help researchers teach artificial intelligence how to do the same thing. Harnett says artificial neural networks are notoriously bad at this: When an artificial neural network that does something well is trained to do something new, it almost always experiences “catastrophic forgetting” and can no longer perform its original task. Harnett’s team is exploring how they can use what they’ve learned about real brains to overcome this problem in artificial networks.
More information: Courtney E. Yaeger et […]
Feeling anxious or unhappy? Here’s how to pump up your serotonin and dopamine naturally
From exercising to changing your diet, you can naturally increase your serotonin and dopamine levels.
Enjoying sunlight outdoors can help boost your serotonin and dopamine levels. (Getty Images) If you’ve been lacking the motivation to clean your house, get a workout in or just can’t get out of bed, it could be that your serotonin and dopamine levels are out of whack. When you’re deficient in one or both, it can wreak havoc on your mental health, causing anxiety and depression. The good news is that many people can naturally raise the levels of both of those hormones.
While it’s always a good idea to talk with a health provider about supplements and treatment options if you’re feeling anxious or down, simple activities like spending time outdoors, adjusting your diet, and exercising regularly can help boost both serotonin and dopamine.
We spoke to expert Dr. Ramaswamy Viswanathan , president of the American Psychiatric Association, to find out how to up your dopamine and serotonin levels to get your life back on track. For more on mental health, here’s how to reduce cortisol and lower your early-morning anxiety and tips to boost your mood when you’re feeling depressed .
Content concerning mental health is for informational purposes only and is not intended as professional medical or health advice. Consult a medical professional for questions about your health. How to boost serotonin naturally
How to boost dopamine naturally
What is serotonin?
What is dopamine?
How to boost serotonin naturally
If you’re looking to increase serotonin levels without medication, you’ll need to make some lifestyle changes, Viswanathan tells Yahoo. We’ll break them down below. Exercise: Regular physical activity is an effective way to increase serotonin levels. Exercise can be as effective as taking medication for people with moderate depression, in some cases, Viswanathan says. And Georgeann Freimuth , a registered dietitian at Nourish , agrees. She says aerobic exercise increases tryptophan , which is an important amino acid that helps boost serotonin. You should aim for at least 30 minutes of moderate exercise at least five days a week.
Eat a healthy diet: Eating foods rich in tryptophan, like eggs, tofu, dairy, turkey and spinach, can positively impact serotonin levels , Freimuth says. Viswanathan adds that some foods, like blueberries and nuts, may actually help increase that feel-good chemical. He says some nuts can help contribute to a better mood because they can help improve the brain-derived neurotrophic factor in people who are depressed.
Practice mindfulness activities: While some stress in life is unavoidable, Viswanathan notes that mitigating stress can be a huge way to increase your happiness, focus and calm. Much like the foods mentioned above, activities like meditation and yoga can give you a boost because, Freimuth says, they also help release tryptophan.
Be social: Having positive social interactions, like engaging in social activities, volunteering and spending time with friends and family are all ways to improve your mood and boost your happy hormones, according to Harvard Medical School .
Avoid using harmful substances: Things like smoking cigarettes and drinking alcohol can cause a drop in serotonin, Viswanathan says. Avoiding them entirely would be the most beneficial, but otherwise, try cutting back your daily dose a little at a time.
Get outside: Sunlight can increase serotonin production, and helps regulate your body’s internal clock, which can improve mood and sleep patterns. The Cleveland Clinic recommends going outside for at least 10 minutes a day.
Supplements: Freimuth says that making sure you’re getting enough B vitamins is essential. You can also talk to your doctor about supplements that contain tryptophan.
How to boost dopamine naturally
You can also raise your dopamine levels naturally without medication by following similar steps to increasing serotonin. Exercise: Getting regular physical activity can alter your dopamine levels, Freimuth says, because it changes how your neurons work. Viswanathan says taking new routes on your daily walk, or even trying other types of workout activities like dancing, can also help keep these levels on track.
Get some sleep: For your body to have enough dopamine, you need enough sleep, Freimuth says. “Dopamine plays a big part in how you feel when you wake up, and if you get adequate sleep, you end up feeling more awake.” Try to aim for seven to nine hours of sleep each night.
Good nutrition: Eating foods high in magnesium and tyrosine , such as chicken, oatmeal, apples, bananas and avocados, can help support dopamine production.
Engage in new activities: While routines are good to have, getting involved in new hobbies or activities can help produce dopamine, Viswanathan explains, because of the reward factor. Some examples include meeting new people, joining a new yoga class and trying your hand at pottery making.
Get some sunlight: Exposure to sunlight also helps with your dopamine levels, according to Baptist Health .
Reduce stress: If you’re stressed out, it can deplete your dopamine. Try some techniques to minimize your stress, like meditation, to help keep your dopamine levels stable.
Supplements: If you have low levels of zinc, iron, folate, B6, Vitamin C, tyrosine and Vitamin D, Freimuth says taking supplements can help elevate your dopamine levels.
Getting a good night’s rest regularly can help maintain dopamine levels. (Getty Images) What is serotonin
Serotonin is often referred to as the “feel-good” neurotransmitter, Freimuth says. When levels are normal, you’re more likely to feel happy and emotionally stable. But when those levels drop, you may start to feel anxious, depressed and even experience panic disorders .”In terms of mental health, serotonin is important for having a sense of calmness. It’s often low in people with depression and people with impulsivity,” Viswanathan says.Freimuth notes that roughly 95% of serotonin is produced in your gastrointestinal tract, so eating the foods mentioned above can have a major impact on your serotonin levels.If you’re experiencing things like mood swings, digestion issues, nausea or trouble sleeping, it […]
7 Types of medications that can damage your kidneys
The kidneys are two bean-shaped organs located in the abdomen just below your rib cage. They are part of your urinary system and are tasked with filtering your blood, among other things. Your kidneys help clean your blood by removing toxins and waste and secreting them out into your urine .
As one of the body’s detoxification organs, your kidneys play a major role in processing toxic molecules and chemicals that enter your body, including medications. As such, they are just as susceptible as the liver – the body’s main detoxification organ – to damage (nephrotoxicity) caused by drug toxicity.
The detoxification process is a series of events that starts in the liver. The liver first breaks down substances present in your blood into their chemical components. While the beneficial ones are returned to circulation to be distributed throughout your body, the harmful molecules/toxins are further broken down by the liver, making them ready for the next stage of processing which happens in the kidneys. (Related: Help your liver detoxify: 4 Tips to remove toxins from the body .)
The kidneys work like a sieve, removing waste, other unwanted substances and excess fluid from your blood so they can be flushed out of your body via your urine. Because your kidneys need water to clear out all the harmful chemicals from your bloodstream, sufficient water intake is vital to the success of your body’s detoxification process. Your kidneys normally filter your entire blood supply between 20 and 25 times each day. How medications can harm your kidneys
Although not discussed as often as it should be, many commonly used medications do in fact harm the kidneys even when taken in small doses or only occasionally. In fact, research suggests that about 20 percent of community- and hospital-acquired cases of acute kidney failure are caused by medications.
There are many ways harmful prescriptions can cause kidney injury and impair kidney function. According to research, drug-induced nephrotoxicity occurs through the following mechanisms: Altered intraglomerular hemodynamics – This occurs when medications that affect blood pressure interfere with the activity of the glomerulus – the kidney’s filtering unit – and decrease glomerular filtration rate. Under normal conditions and sustained intraglomerular pressure, the glomerulus filters about 120 milliliters (mL) of blood plasma per minute.
Tubular cell toxicity – This occurs when medications impair mitochondrial function and increase oxidative stress in renal tubular cells. These kidney cells, specifically the proximal tubule cells, are highly exposed to toxic chemicals because they are directly involved in concentrating and reabsorbing glomerular filtrate.
Inflammation (glomerulonephritis) – Severe or prolonged inflammation, which can be triggered by oxidative stress or an allergic response to medications, can injure the glomerulus and renal tubular cells, leading to fibrosis and kidney scarring. The scarring process is said to cause loss of nephrons — kidney structures composed of the glomerulus and renal tubules — hyperfiltration and progressive decline of kidney function.
Crystal nephropathy – Some medications produce crystals that are insoluble in urine. When these crystals precipitate, they can obstruct the flow of urine and cause an interstitial reaction that leads to fibrosis. Crystal nephropathy can impair kidney function or cause kidney failure.
Rhabdomyolysis – This syndrome is characterized by the rupturing (lysis) of myocytes, or muscle cells. Certain medications, most notably statins, and commonly abused drugs, have been reported to predispose myocytes to injury, resulting in lysis of myocytes and the release of cellular contents like myoglobin. Myoglobin breaks down into chemicals that can harm the kidneys.
Thrombotic microangiopathy (TMA) – A life-threatening complication commonly associated with chemotherapeutic and antiplatelet agents, TMA can damage organs like the kidneys due to the formation of microscopic blood clots in small blood vessels .
7 Categories of prescription medications that can harm your kidneys
Despite their intended use, modern pharmaceuticals have the potential to cause more health problems, especially with prolonged or incorrect use. In fact, many commonly prescribed medications are notorious for causing side effects that reduce quality of life for their users.
While prescription drugs may help resolve certain issues, this does not change the fact that they are still made of synthetic chemicals that can cause toxicity to healthy cells and organs. Besides the liver, your kidneys are among the most susceptible to the toxic effects of certain medications.
Here are seven categories of medications that are known to harm the kidneys: (h/t to TheEpochTimes.com ) Anti-inflammatory and analgesic medications
Non-steroidal anti-inflammatory drugs (NSAIDs) like ibuprofen and naproxen are said to help reduce pain, fever and inflammation by blocking the production of prostaglandins . While the analgesic acetaminophen is thought to work in a similar way, it does not treat inflammation .
According to studies, NSAIDs cause kidney injury via altered intraglomerular hemodynamics and glomerulonephritis. Acetaminophen and aspirin are linked to chronic interstitial nephritis, which impairs your kidneys’ ability to filter blood and make urine . Blood pressure and heart medications
Excessive use of diuretics, which help bring down blood pressure and get rid of extra fluid at the same time, can decrease blood flow to your kidneys, resulting in kidney damage. Meanwhile, angiotensin-converting enzyme inhibitors and angiotensin receptor blockers, which are used to manage hypertension, have been associated with altered intraglomerular hemodynamics.
The antiplatelet (anti-blood clot) medications, clopidogrel and ticlopidine, have been found to cause TMA, while statins, which are used to lower blood cholesterol levels, are reported to cause rhabdomyolysis. (Related: Statins are the most prescribed drug with over-hyped benefits and downplayed side effects .) Antibiotics and antifungals
Excessive use of antibiotics is linked to the development of antibiotic-resistant strains of bacteria. Certain antibiotics are also known to cause kidney damage. For example, aminoglycosides, which are known as broad-spectrum antibiotics, are associated with tubular cell toxicity.
Meanwhile, beta-lactams, which include penicillin derivatives and cephalosporins, have been found to cause acute interstitial nephritis and glomerulonephritis. Quinolones, a type of antibiotics that directly kill bacterial cells, have been reported to cause acute interstitial nephritis and crystal nephropathy.
Amphotericin B, which is used to treat serious fungal infections, and pentamidine, an antifungal agent […]
The CONNECTION between AUTISM and COVID JABS could boil down to destruction of good gut bacteria
There is no question that gut microbiota influences neurological disorders such as autism, where normal brain development is affected. This is well-documented, as most autistic people suffer from gastrointestinal symptoms . Many comprehensive and in-depth studies of the gut microbiome-brain axis help researchers and those privy to that research understand the mechanism that leads to the onset of neurological dysfunctions and disorders and may be the key to finding treatments for autism.
Big Pharma and the Vaccine Industrial Complex (VIC) do not want anyone studying this, reading about it, or talking about it. Autism is one of the biggest cash cows for the VIC, and now it’s come to light that the Covid-19 mRNA jabs are contributing to the further spike in autism cases. Surprised? Big Pharma’s cash cow autism now “injected” with new major cause – Fauci Flu mRNA “vaccines”
One of the most insidious ways Big Pharma bankrolls off human health detriment is via vaccines, and now there’s a new secret biological weapon for bankrolling off kids during their developmental years. Realize that babies are not born with autism . This should be parents’ first red flag that something external is influencing the child’s inability to experience normal brain development, good communication skills, proper reasoning abilities and typical behavioral patterns from about 2 years of age through elementary school.
Medical doctors are either puzzled by the Autism Spectrum Disorder (ASD) “pandemic” or they know the main culprit and simply can’t talk about it, and don’t know how to “fix it” or at least minimize future damage (tell parents to stop administering most vaccines to the child). Families spend a fortune on doctors who try to alleviate autistic conditions with drugs, including antidepressants which are quite dangerous and interfere with serotonin uptake (SSRIs).
Now research is revealing that the Covid “clot shots” that trick human cells into creating billions of microscopic virus-mimicking prions are contributing to the autism nightmare. Pile this onto all the other dirty vaccines infants and toddlers get injected with during their developmental years, and you’ve got a compounded, persistent issue with the biological seat of immunity – the gut. Now the CDC has ADDED the deadly, autism-causing Covid stabs to the recommended childhood vaccine schedule. It’s just medical insanity, and more profits for Big Pharma from their autism and vaccine cash cows. Clot shots are a cash cow for the Big Pharma autism scamdemic, driving ASD rates even higher over the past 3 years than they already were
According to the CDC, the average lifetime cost for an individual with autism is around $1.4 million. For U.S. cases identified over the past three decades, families have spent over $7 trillion. Think about that for a minute.
Here’s how the Covid jabs are contributing to the autism rates. The spike proteins travel throughout the vascular system to the entire body, including the gut, destroying beneficial gut bacteria, such as Bifidobacterium infantis , that convert tryptophan into serotonin, regulating behavior and emotions. This is also destroying the proper production of antioxidants and neuro-protectant molecules in the gut.
See what’s happening? The child’s immune system then believes that the gut is being invading by foreign intruders and pathogenic microbes (because it is, even though its own cells are creating them), and attacks them, leading to auto-immune disorders also. It gets worse. Then the infant or toddler’s gut is susceptible to being invaded by various pathogens, leading to the development of GI issues from the presence of bacteria called Clostridium bolteae ( Tsai et al., 2012 ; Rosenfeld, 2015 ).
This would indicate a much higher risk and severity of Autism Spectrum Disorder, as this bacteria produces a neurotoxin (TeNT) that passes through the Vagus nerve to the central nervous system and blocks neurotransmitters in the brain. And that’s the low-down on clot shots and why all parents should question the safety of all vaccines, especially the mRNA “gene therapy” injections. Bookmark Vaccines.news to your favorite independent websites for updates on Long-Vax-Syndrome that’s contributing to autism, heart disorders and dementia.
Sources for this article include:
NaturalNews.com
Expose-news.com
NCBI.nlm.nih.gov
Study reveals how, when and where non-invasive brain stimulation influences neuronal activity and cognition
Overall response time modulations in humans and in monkeys. Credit: Brain (2024). DOI: 10.1093/brain/awae273 Brain stimulation using electrodes placed on the head has a great potential to be used in clinical practice to treat depression, anxiety and even addiction. Yet despite its widespread use in clinics and online availability for home use to improve mood and performance in various tasks, it is not clear how the therapy actually works to exert its modulatory effects on various cognitive functions.
Now, Monash researchers have studied what happens in the brain when it is being treated with Transcranial Direct Current Stimulation (tDCS), a non-invasive brain stimulation technique in which low-intensity direct currents are delivered through electrodes positioned on a person’s scalp. The tDCS has a low intensity which is equivalent to the power provided by small batteries.
Associate Professor Farshad Mansouri from Monash University’s Biomedicine Discovery Institute (BDI), the lead author of the study, published in the journal Brain , highlighted the significant potential of tDCS to improve cognitive and behavioral deficits in patients suffering from stroke, depression, schizophrenia and substance addiction.
Associate Professor Mansouri noted that tDCS is becoming commercially available, with growing public interest in using it for improving mood, boosting learning, and managing conditions such as overeating, gambling, and age-related cognitive decline.
“This widespread use—without truly understanding what is happening within the brain—has provoked concerns regarding the safety and efficacy of this technique, particularly because our understanding of how it affects the brain is very limited,” he said.
“Our findings show how tDCS modulates both prefrontal cell activity and behavior and provide mechanistic evidence to address where, when, and how tDCS influences neuronal activity and cognitive functions.”
In collaboration with Dr. Daniel Fehring and other researchers at the RIKEN Center for Brain Science in Japan and Monash BDI’s Professor Marcello Rosa, the team conducted a five-year study that has finally addressed fundamental questions regarding the neuronal basis of tDCS effects on cognitive functions.
The researchers recorded the activity of individual neurons in the prefrontal cortex before, during, and after using tDCS while participants performed cognitive tasks. They found that tDCS, when applied to the prefrontal cortex , significantly influences how neurons respond to specific tasks and situations, affecting behavior as a result.
According to Associate Professor Mansouri, unlike the common belief that tDCS simply increases or decreases overall neuronal activity , “Our study showed that tDCS specifically enhances the neurons’ response to certain events without altering their baseline activity.
“Additionally, tDCS reduced the variability in neuron activity while boosting task-related brain activities. Importantly, multiple tDCS sessions did not lead to any seizure-like activity,” he said.
“This study marks a significant advancement in understanding the mechanistic basis of tDCS and bridges the gap between cellular-level modulations and cognitive-behavioral outcomes, paving the way for a safer and more effective application of brain stimulation techniques in research and clinical settings.”
More information: Daniel J Fehring et al, Direct current stimulation modulates prefrontal cell activity and behaviour without inducing seizure-like firing, Brain (2024). DOI: 10.1093/brain/awae273
Provided by Monash University
Study finds Alzheimer’s drugs might boost healthy protein in brain
Researchers have discovered that Alzheimer’s drugs Leqembi and Kisunla boost levels of a healthy form of protein in the brain, even as they reduce its more toxic form. Photo by Adobe Stock/HealthDay News Two monoclonal antibody treatments to slow Alzheimer’s disease , lecanemab (Leqembi) and donanemab (Kisunla), have been approved by the U.S. Food and Drug Administration over the past two years.
It’s thought the drugs curb Alzheimer’s by reducing levels of toxic amyloid protein plaques in the brain.
But what if another neurological effect could explain the benefit?
Researchers at the University of Cincinnati have discovered that Leqembi and Kisunla boost levels of a healthy form of amyloid beta (Aβ42) protein in the brain, even as they reduce its more toxic form in amyloid plaques. Related
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New cancer drugs might also help treat Alzheimer’s
“If the problem with Alzheimer’s is the loss of the normal protein, then increasing it should be beneficial, and this study showed that it is,” explained study lead author Dr. Alberto Espay , a professor of neurology at Cincinnati.
“The story makes sense: Increasing Aβ42 levels to within the normal range is desirable,” he said in a university news release.
Aβ42 is a complex protein made up of 42 amino acids, giving it its name.
Sometimes these proteins can harden and clump together to form the brain tissue plaques that have long been associated with Alzheimer’s disease.
However, Aβ42 in its natural state should not do that. It is normally soluble, and when in a soluble state Aβ42 plays a crucial role in maintaining the health of brain cells, the Cincinnati team explained.
Espay’s team theorized that perhaps it is the loss of soluble Aβ42 that drives Alzheimer’s, not its later clumping into plaques.
Stressors, such as inflammation or infection, might drive amyloid to clump into plaques instead of roaming free to help maintain brain health.
“Most of us will accrue amyloid plaques in our brains as we age, and yet very few of us with plaques go on to develop dementia,” Espay noted.
His theory: “Amyloid plaques don’t cause Alzheimer’s, but if the brain makes too much of it while defending against infections, toxins or biological changes, it can’t produce enough Aβ42, causing its levels to drop below a critical threshold. That’s when dementia symptoms emerge.”
In the new study, Espay’s team analyzed data from nearly 26,000 patients enrolled in 24 randomized clinical trials involving the new antibody treatments.
They found that when use of Leqembi or Kinsunla (or their now-discontinued predecessor, Aduhelm) was associated with a rise in brain levels of soluble Aβ42, Alzheimer’s progression slowed.
“All stories have two sides — even the one we have told ourselves about how anti-amyloid treatments work: by lowering amyloid,” Espay said. “In fact, they also raise the levels of Aβ42. Even if this is unintended, it is why there may be a benefit.”
However, according to Espay, monoclonal antibody drugs may be boosting Aβ42 in an inefficient and perhaps (in the long term) unsafe way. He believes that the steady removal of amyloid plaques from the brain could prove to be toxic in the long run.
“Do we give patients an anti-protein treatment to increase their protein levels? I think the end, increasing Aβ42, doesn’t justify the means, decreasing amyloid,” Espay said.
He said his team are currently working on alternative therapies, ones that focus on boosting soluble Aβ42 levels without targeting amyloid plaques.
The findings were published Wednesday in the journal Brain .
More information
Find out more about Alzheimer’s disease at the U.S. Centers for Disease Control and Prevention .
Copyright © 2024 HealthDay. All rights reserved.
Neuroscientists map how the brain transforms sensation into action
Researchers map how the brain transforms sensation into action. Credit: Sainsbury Wellcome Centre Neuroscientists have revealed how sensory input is transformed into motor action across multiple brain regions in mice. The research, conducted at the Sainsbury Wellcome Center at UCL, shows that decision-making is a global process across the brain that is coordinated by learning. The findings could aid artificial intelligence research by providing insights into how to design more distributed neural networks.
“This work unifies concepts previously described for individual brain areas into a coherent view that maps onto brain-wide neural dynamics. We now have a complete picture of what is happening in the brain as sensory input is transformed through a decision process into an action,” explained Professor Tom Mrsic-Flogel, Director of the Sainsbury Wellcome Center at UCL and corresponding author on the paper.
The study, published in Nature , outlines how the researchers used Neuropixels probes, a state-of-the-art technology enabling simultaneous recordings across hundreds of neurons in multiple brain regions , to study mice taking part in a decision-making task .
The task, developed by Dr. Ivana Orsolic at SWC, allowed the team to distinguish between sensory processing and motor control. The researchers also revealed the contribution of learning through studying animals trained in the task and comparing them to naive animals. Each circle is a neuron, only those that are significantly active are shown at each point of time and the size of the circle is scaled with the amount of activity of that neuron. Credit: Sainsbury Wellcome Centre “We often make decisions based on ambiguous evidence. For example, when it starts to rain, you have to decide how frequent the raindrops need to be before you open your umbrella. We studied this same ambiguous evidence integration in mice to understand how the brain processes perceptual decisions,” explained Dr. Michael Lohse, Sir Henry Wellcome Postdoctoral Fellow at SWC and joint first author on the paper.
Mice were trained to stand still while they watched a visual pattern moving on a screen. To receive a reward, the mice had to lick a spout when they detected a sustained increase in the speed of movement of the visual pattern. The task was designed so that the speed of the movement was never constant, instead it continuously fluctuated.
The timing of the increase in the average speed also changed from trial to trial so that the mice could not simply remember when the sustained increase occurred. Thus, the mice had to constantly pay attention to the stimulus and integrate information to work out whether the increase in the speed had happened.
“By training the mice to stand still, the data analysis we could perform was much cleaner and the task allowed us to look at how neurons track random fluctuations in speed before the mice made an action,” explained Dr. Andrei Khilkevich, Senior Research Fellow in the Mrsic-Flogel lab and joint first author on the paper.
“In trained mice, we found that there is no single brain region that integrates sensory evidence or orchestrates the process. Instead, we found neurons that are sparsely but broadly distributed across the brain link sensory evidence and action initiation.”
The researchers recorded from each mouse multiple times and collected data from over 15,000 cells across 52 brain regions in 15 trained mice. To look at learning, the team also compared the results to recordings from naïve mice.
“We found that when mice don’t know what the visual stimulus means, they only represent the information in the visual system in the brain and a few midbrain regions. After they have learned the task, cells integrate the evidence all over the brain,” explained Dr. Lohse. Each circle is a neuron, only those that are significantly active are shown at each point of time and the size of the circle is scaled with the amount of activity of that neuron. Credit: Sainsbury Wellcome Centre In this study, the team only looked at naive animals and those that had fully learned the task, but in future work they hope to uncover how the learning process occurs by tracking neurons over time to see how they change as mice begin to understand the task.
The researchers are also looking to explore whether specific areas in the brain act as causal hubs in establishing these links between sensations and actions.
A number of additional questions raised by the study include how the brain incorporates an expectation of when the speed of visual pattern will increase such that animals only react to the stimulus when the information is relevant. The team plan to study these questions further using the dataset they have collected.
More information: Thomas Mrsic-Flogel, Brain-wide dynamics linking sensation to action during decision-making, Nature (2024). DOI: 10.1038/s41586-024-07908-w . www.nature.com/articles/s41586-024-07908-w
Provided by Sainsbury Wellcome Centre
The Power Within by Corey Daniels book available for only $2.99
Mind has both conscious and subconscious halves. These are likened to a driver and the truck he drives. The driver plans the destination and observes road conditions, while the truck provides motive power. Your subconscious mind is like the truck and it only goes in the direction in which is a steered. This can be the road or off a cliff. Likewise, the consciousness paints a picture of what the world is and what your goals are and the subconscious acts on them through emotion, physical response and energy, whether these are correct, rational images or false negative ones. The subconscious is also like an emotional reservoir which your body and mind draw responses from to external stimuli.
The Power Within lays out a method of programming your subconscious and tapping into the Holy Spirit, God voice or what the Greeks called the daimon (godman).