Want to Get Smarter? Neuroscience Says 1 Uncomfortable Habit Will Help You Learn Faster and Retain More

Want to Get Smarter? Neuroscience Says 1 Uncomfortable Habit Will Help You Learn Faster and Retain More

There are plenty of ways to get smarter . You can harness the power of interleaving by learning several things in succession. You can vary the way you study. You can test yourself. Oddly enough, simply getting more sleep can actually make you smarter .

What do you know, and what do you do with what you know ? Learning more quickly, and retaining more of what you learn?

Yep: Getting smarter is a business superpower.

Especially if you consider which type of “smart” you focus on. There’s Smart, and Then There’s Smart

While intelligence can be described in a number of ways, let’s focus on two.

The first, crystallized intelligence, is accumulated knowledge: facts, figures. In short, “educated.” Which is a good thing.

Except we all know people who are “book smart” but not necessarily smart smart.

That’s where the second form, fluid intelligence, comes into play. Fluid intelligence is the ability to learn and retain new information — but also to use that knowledge to solve a problem, to learn a new skill, to recall existing memories and modify them with new knowledge … In short, to have “applied intelligence.”

Becoming more educated? That’s not easy, but the process is reasonably simple. Improving fluid intelligence can be harder, which is one reason why “brain games” –crossword puzzles, Sudoku, brain training apps, etc. –are fairly popular.

But do they make you smarter?

More to the point, do they improve your fluid intelligence? Probably not.

A 2007 study published in Behavioral and Brain Sciences assessed the impact of brain training games on fluid intelligence. After participants played Tetris for several weeks, cortical thickness and cortical activity increased. Both are signs of an increase in neural connections and learned expertise.

In simple terms, the participants’ brains bulked up and got smarter. But after those first few weeks, cortical thickness and activity started to decrease, eventually returning to pre-Tetris mastery pursuit level, even though their skill levels remained high. They didn’t lose brain power.

Instead, their brains became so efficient at playing Tetris that those increased neural connections became unnecessary. Nor was it necessary to use more mental energy. As with most things, once they figured it out, it got easy. (Or as a friend says, “Everything is hard the first time.”)

Unfortunately, no matter how much work it takes to learn new information or gain new skills, “easy” doesn’t translate to improved fluid intelligence. Once knowledge or skill is in your pocket, you certainly benefit from the increase in crystallized intelligence, but your fluid intelligence soon returns to a more baseline level.

While the analogy sounds goofy, it’s like performing a physical task using muscle memory, although in this case, you’re using “brain memory.”

That’s the problem with, say, brain-training games. Solving Sudoku puzzles — and only solving Sudoku puzzles — won’t improve your fluid intelligence in any other areas, no matter how much of a Soduku master you become. It only makes you better at solving Sudoku puzzles.

The same is true for business skills. Learning how to use QuickBooks to keep your books will improve your fluid intelligence until you master it. Learning to use a new CRM application will improve your fluid intelligence until you master it. Once you achieve a level of (skill) comfort, your brain no longer has to work as hard, and all that new mental muscle starts to atrophy. And Then There’s Uncomfortable

Which leads us to the (literally) uncomfortable point.

To keep improving your fluid intelligence, once you master a new process, a new routine, a new skill, a new anything, you need to focus on learning something else. The key is to stay uncomfortable and keep challenging yourself.

Then you get to double-dip. You gain new knowledge, new skill, and new experience, and you keep your brain “bulked up” since it’s forced to continue forging new neural connections.

That double-dip also makes it easier to keep getting smarter at a biological and neurological level. The more you know, the more you can leverage the power of associative learning, the process of relating something new to something you already know. In simple terms, associated learning is like saying, “I get it: (This) is basically like (that).” The more you learn, the more likely you will be able to associate “old” knowledge with new things.

This means you only have to learn differences or nuances, and will be able to apply additional context — context that also helps with memory storage and retrieval — to the new information you learn.

All of this makes learning even easier, which a study published in Intelligence shows results in being able to learn even more quickly and retain a lot more. As the researchers write : The fastest learners, despite having the fewest number of study opportunities, remembered more and relearned faster. Win-win.

Keep pushing yourself to learn new things about your business, your customers, your industry, etc. In a broader sense, keep pushing yourself to learn new things about whatever interests you.

Not only will that help you become more successful, but you’ll also get to increase your crystallized intelligence and improve your fluid intelligence.Which will likely make you even more successful.

Read more at www.inc.com

Does sleep clear more toxins from the brain than when we’re awake? Latest research casts doubt on theory

Does sleep clear more toxins from the brain than when we're awake? Latest research casts doubt on theory

Credit: CC0 Public Domain Evidence also supports the notion that the brain gets rid of more toxic waste when we’re asleep than when we’re awake. This process is believed to be crucial in getting rid of potentially harmful things such as amyloid, a protein whose build-up in the brain is linked to Alzheimer’s disease .

However, a recent study in mice has come to the opposite conclusion. Its authors suggest that in mice, brain clearance is actually lower during sleep—and that previous findings could also be re-interpreted in this way. The brain’s cleaning system

Since the brain is an active tissue—with many metabolic and cellular processes happening at any moment—it produces a lot of waste. This waste is removed by our glymphatic system.

Cerebrospinal fluid is a crucial part of the glymphatic system. This fluid surrounds the brain, acting as a liquid cushion that protects it from damage and provides it nourishment, so the brain can function normally.

During the waste removal process, our cerebrospinal fluid helps transfer old and dirty brain fluid—full of toxins, metabolites and proteins—to outside the brain, and welcomes in new fluid. The waste that has been removed then ends up in the lymphatic system (a part of your immune system), where it’s ultimately eliminated from your body.

The glymphatic system was only discovered in the last decade or so . It was first observed in mice, using dyes injected into their brains to study the movement of fluids there. The existence of the glymphatic system has since been confirmed in humans with the use of MRI scans and contrast dyes .

Based on the results of animal experiments , scientists concluded the glymphatic system is more active at night, during sleep or when under anesthesia, than during the day. Other studies have shown this waste removal activity may also vary depending on different conditions—such as sleep position , the type of anesthetic used, and whether or not the subject’s circadian rhythm was interrupted. Challenging old interpretations

The recent study used male mice to examine how the movement of brain fluid differed when animals were awake, asleep and anesthetized. The researchers injected dyes into the animals’ brains to track the flow of fluid through the glymphatic system.

In particular, they examined whether an increase in dye indicated a decrease in fluid movement away from an area, rather than an increase in movement to the area as previous studies had suggested. The former would mean lower clearance via the glymphatic system—and hence less waste being removed.

More dye was found in brain areas after three hours and five hours of being asleep or anesthetized than when awake. This indicated that less dye, and therefore fluid, was being cleared from the brain when the mouse was asleep or anesthetized.

Although the findings are interesting, there are a number of limitations with the study’s design. As such, this can’t be considered absolute confirmation that the brain doesn’t flush out as much waste during the night than in the day. Limitations to this study

First, the study was conducted using mice. The results from animal studies don’t always translate to humans, so it’s difficult to say whether the same will be true for us.

The study also only looked at male mice that were kept awake for a few hours before being allowed to sleep. This may have disturbed their natural sleep-wake rhythm, which could have partially influenced the results. Studies have shown that interrupted or bad sleep is linked with an increase in stress levels—which in turn lowers brain fluid flow from the glymphatic system.

In contrast, in the first (2013) study that showed more brain toxins were removed during sleep, the mice were observed during their natural sleep time.

Different methods were also used in this study compared with previous ones—including what types of dye were injected and where. Previous studies also used both male and female mice. These differences in study methods could have influenced the results.

The glymphatic system might also behave differently depending on the brain region—with each producing different types of waste when awake or asleep. This may also explain why this study’s results were different from previous ones.

Virtually no studies looking at the glymphatic system and the effects of sleep in mice have examined the contents of the fluid excreted from the brain. So, even if the amount of fluid flowing out of the brain was lower during sleep or anesthesia, this fluid could still be removing important waste products in different amounts.

A handful of studies have found disturbances in both glymphatic system function and sleep in people with neurological conditions—including Alzheimer’s disease and Parkinson’s . A study in humans also indicates that more amyloid is found in the brain after even one night of sleep deprivation .

The glymphatic system is important when it comes to how the brain works—but it may very well function differently depending on many factors. We need more research that aims to replicate the latest study’s findings, while also examining the reasons behind its surprising conclusions. This article is republished from The Conversation under a Creative Commons license. Read the original article . Study shows that opportunity costs influence when people leave social interactions 21 minutes ago Bloody insights: Organs-on-chip ready to help snake venom research 2 hours ago Five-minute test leads to better care for people with dementia in the primary care setting 2 hours ago Researchers develop technology that may allow stroke patients to undergo rehab at home 3 hours ago Wearable brain imaging provides a precise picture of children’s developing brains 4 hours ago Researchers identify first step in allergic reactions, paving the way for preventative strategies 10 hours ago Study: High excess death rates in the West for 3 years running since start of pandemic despite containment and vaccines 12 hours ago

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How Brain Waves Influence Your Memory

How Brain Waves Influence Your Memory

Key points

Brain waves influence cognitive control and memory formation, informing how the brain manages memory.

Working memory stores and manipulates information temporarily for tasks like learning and decision-making.

Phase-amplitude coupling neurons synchronize with brain waves, aiding cognitive control and memory retrieval.

New findings have implications for therapies and cognitive enhancement strategies.

Have you ever put your keys down and then completely forgotten where to find them? The brain has to work hard to protect information in your working memory from distractions. How this process works has, until recently, been unclear. A study published in Nature looked at the interactions between the front part of the brain that controls thoughts and the hippocampus, which is important for memory. They found that individual brain cells are influenced by the theta and gamma brain waves passing between these two parts of the brain and those cells have a role in cognitive control. These findings give fresh insights into how the brain manages memory, with implications for those who wish to improve their attention , decision-making , or memory retrieval. What is working memory?

Working memory is a type of short-term memory that temporarily stores and manipulates information needed for cognitive tasks such as learning, reasoning, and comprehension. It acts as a mental workspace where information is held and processed before being encoded into long-term memory or forgotten.

Working memory is limited to holding a small amount of information (around seven items) for a brief period ranging from a few seconds to several minutes, depending on the task and the individual’s cognitive abilities. Working memory coordinates the simultaneous storage and processing of information from multiple sources and plays a crucial role in higher cognitive functions like problem-solving, decision-making, and following instructions. How does the brain make memories?

The brain makes memories through a complex process involving multiple brain regions and mechanisms. Memories are initially encoded in the hippocampus region of the brain. This process involves strengthening the connections (synapses) between neurons through repeated stimulation.

The hippocampus and the prefrontal cortex are two important brain regions in memory formation. During memory formation, the hippocampus and prefrontal cortex communicate via brain waves of different frequencies (beta and theta). Beta waves reinforce correct associations, while theta waves weaken incorrect ones, guiding what the brain learns.

The coordination of interactions between the hippocampus and prefrontal cortex is called theta-gamma phase-amplitude coupling. They work together, creating a certain rhythm. Theta waves are slower while gamma waves are faster. They are synched so that when one gets stronger, so does the other. This coordination may facilitate neural dynamics for memory and cognitive processing, integrating local sensory information processing with brain-wide cognitive control. Studying working memory and memory retrieval

To understand the ways neurons involved in theta-gamma phase-amplitude coupling influence memory and thinking, a team of researchers at Cedars-Sinai Medical Center, Toronto Western Hospital, and Johns Hopkins Hospital, conducted a study on 36 epilepsy patients undergoing surgery for drug-resistant epilepsy using magnetic resonance imaging and electroencephalograms.

In the task, participants observed 140 rounds of different pictures. Each round started with a cross, and then one or three pictures appeared for the patient to remember. They had to hold them in memory when prompted, and later identify if a new picture matched any from that round by pressing a button.

Each session used new pictures from various categories like faces, animals, and cars, ensuring freshness. Harder rounds challenged patients with three pictures instead of one, maintaining consistent time limits for memory recall. Mixing categories prevented reliance on familiarity, encouraging active memory use over recognition.

Electrodes with at least eight wires recorded brain activity across various frequencies. The researchers examined how phase-amplitude coupling varied from trial to trial; they identified specific neurons that were sensitive to different categories of visual stimuli presented during the task that helped explain how individual neurons responded to specific types of images. Findings and Implications

The study reveals a direct link between theta-gamma phase-amplitude coupling and the firing patterns of single neurons. Neurons showing phase-amplitude coupling synchronize with frontal theta waves, particularly when working memory load is higher, leading to faster reaction times. This suggests that phase-amplitude coupling neurons play a role in cognitive control.

To accurately retain and access memories is the main goal of cognitive control. The study demonstrated that phase-amplitude coupling neurons contribute to this process by introducing noise correlations, which improves information content at the population level. Noise correlations enhance the decodability of working memory content, particularly when involving phase-amplitude coupling neurons.

The findings of this study support a model where frontal control processes regulate working memory maintenance in brain areas like the hippocampus. The interactions between phase-amplitude coupling neurons in the broader theta-gamma phase-amplitude coupling phenomenon represent a general mechanism for top-down control in various cognitive functions beyond working memory such as attention, decision-making, speech comprehension, and long-term memory retrieval.

Understanding the memory process can lead to the development of therapies for conditions involving memory deficits or those suffering from neurological disorders. It can also lead to strategies for enhancing cognitive performance by targeting specific neural mechanisms involved in memory and cognitive control and optimizing learning and memory retention in academic settings. In summary, the study examines the connection between brain waves, cognitive control, and memory, offering promising ways to understand the neurological basis of cognition as well as opportunities to develop innovative interventions to enhance memory and cognitive function.

Read more at www.psychologytoday.com

Does sleep clear more toxins from the brain than when we’re awake? Latest research casts doubt on this theory

Does sleep clear more toxins from the brain than when we’re awake? Latest research casts doubt on this theory

Eleftheria Kodosaki does not work for, consult, own shares in or receive funding from any company or organization that would benefit from this article, and has disclosed no relevant affiliations beyond their academic appointment. Partners

University College London provides funding as a founding partner of The Conversation UK.

View all partners Email X (Twitter) Facebook LinkedIn Print There’s no doubt sleep is good for the brain. It allows different parts to regenerate and helps memories stabilise . When we don’t get enough sleep, this can increase stress levels and exacerbate mental health issues .

Evidence also supports the notion that the brain gets rid of more toxic waste when we’re asleep than when we’re awake. This process is believed to be crucial in getting rid of potentially harmful things such as amyloid, a protein whose build-up in the brain is linked to Alzheimer’s disease .

However, a recent study in mice has come to the opposite conclusion. Its authors suggest that in mice, brain clearance is actually lower during sleep – and that previous findings could also be re-interpreted in this way. The brain’s cleaning system

Since the brain is an active tissue – with many metabolic and cellular processes happening at any moment – it produces a lot of waste. This waste is removed by our glymphatic system.

Cerebrospinal fluid is a crucial part of the glymphatic system. This fluid surrounds the brain, acting as a liquid cushion that protects it from damage and provides it nourishment, so the brain can function normally.

During the waste removal process, our cerebrospinal fluid helps transfer old and dirty brain fluid – full of toxins, metabolites and proteins – to outside the brain, and welcomes in new fluid. The waste that has been removed then ends up in the lymphatic system (a part of your immune system), where it’s ultimately eliminated from your body.

The glymphatic system was only discovered in the last decade or so . It was first observed in mice, using dyes injected into their brains to study the movement of fluids there. The existence of the glymphatic system has since been confirmed in humans with the use of MRI scans and contrast dyes .

Based on the results of animal experiments , scientists concluded the glymphatic system is more active at night, during sleep or when under anaesthesia, than during the day. Other studies have shown this waste removal activity may also vary depending on different conditions – such as sleep position , the type of anaesthetic used, and whether or not the subject’s circadian rhythm was interrupted. Challenging old interpretations

The recent study used male mice to examine how the movement of brain fluid differed when animals were awake, asleep and anaesthetised. The researchers injected dyes into the animals’ brains to track the flow of fluid through the glymphatic system.

In particular, they examined whether an increase in dye indicated a decrease in fluid movement away from an area, rather than an increase in movement to the area as previous studies had suggested. The former would mean lower clearance via the glymphatic system – and hence less waste being removed. The researchers found less dye was being cleared from the brain during sleep. More dye was found in brain areas after three hours and five hours of being asleep or anaesthetised than when awake. This indicated that less dye, and therefore fluid, was being cleared from the brain when the mouse was asleep or anaesthetised.

Although the findings are interesting, there are a number of limitations with the study’s design. As such, this can’t be considered absolute confirmation that the brain doesn’t flush out as much waste during the night than in the day. Limitations to this study

First, the study was conducted using mice. The results from animal studies don’t always translate to humans, so it’s difficult to say whether the same will be true for us.

The study also only looked at male mice that were kept awake for a few hours before being allowed to sleep. This may have disturbed their natural sleep-wake rhythm, which could have partially influenced the results. Studies have shown that interrupted or bad sleep is linked with an increase in stress levels – which in turn lowers brain fluid flow from the glymphatic system.

In contrast, in the first (2013) study that showed more brain toxins were removed during sleep, the mice were observed during their natural sleep time.

Different methods were also used in this study compared with previous ones – including what types of dye were injected and where. Previous studies also used both male and female mice. These differences in study methods could have influenced the results.

The glymphatic system might also behave differently depending on the brain region – with each producing different types of waste when awake or asleep. This may also explain why this study’s results were different from previous ones.

Virtually no studies looking at the glymphatic system and the effects of sleep in mice have examined the contents of the fluid excreted from the brain. So, even if the amount of fluid flowing out of the brain was lower during sleep or anaesthesia, this fluid could still be removing important waste products in different amounts.

A handful of studies have found disturbances in both glymphatic system function and sleep in people with neurological conditions – including Alzheimer’s disease and Parkinson’s . A study in humans also indicates that more amyloid is found in the brain after even one night of sleep deprivation .

The glymphatic system is important when it comes to how the brain works – but it may very well function differently depending on many factors. We need more research that aims to replicate the latest study’s findings, while also examining the reasons behind its surprising conclusions.

Read more at theconversation.com

Contraceptive Pills Have a Curious Effect on The Fear-Promoting Area of The Brain

Contraceptive Pills Have a Curious Effect on The Fear-Promoting Area of The Brain

(danilo.alvesd/Unsplash) Scientists have found a possible link between using oral contraceptives and changes in parts of the brain that process fear. The findings may help explain fear-related mechanisms that disproportionately affect women .

Hormonal changes during a menstrual cycle are currently understood to affect the fear circuitry in the brain . So Canadian researchers looked into the effects of combined oral contraceptive (COC) use to learn more about the relationship between sex hormones our bodies make naturally and synthetic versions of those hormones.

Over 150 million people use oral contraceptives, with COCs (containing synthetic versions of estrogens and progestogens ) being highly popular. The study found that a brain region called the ventromedial prefrontal cortex (vmPFC) was thinner in women who currently use COCs compared to men.

This effect appeared to be reversible. A comparison with those who stopped using contraceptives or those who had never used contraceptives indicated this physiological change didn’t seem to be lasting.

To be clear, these are just associations, and there are no known negative effects linked to the change in size of certain brain regions. But the authors think it could be worth exploring further.

“This part of the prefrontal cortex is thought to sustain emotion regulation, such as decreasing fear signals in the context of a safe situation,” explains Alexandra Brouillard, a physiologist at the University of Quebec in Montreal.

“Our result may represent a mechanism by which combined OCs could impair emotion regulation in women.”

Brouillard and colleagues studied healthy adults aged 23 to 35, including 139 women: 62 who were currently using COCs, 37 who had previously used only COCs, and 40 who had never used any hormonal contraceptives. The total sample also included 41 men.

Because women are more likely than men to have anxiety and stress disorders, researchers compared these groups to see if COC use was linked to short-term or long-term changes in the brain and if there are differences between sexes.

The scientists measured levels of natural and synthetic sex hormones in participants’ saliva and used magnetic resonance imaging ( MRI ) to scan their brains, specifically looking at regions involved in processing fear.

They found levels of both natural and synthetic sex hormones were linked to changes in the size and thickness of the vmPFC compared to the same anatomy in men. However, only women who were currently using oral contraceptives had a thinner vmPFC than that in men.

The researchers also found the structure in a fear-promoting brain region – the dorsal anterior cingulate cortex (dACC) – varied between men and women. This was noticeable regardless of COC use, emphasizing one way naturally-produced sex hormones can influence brain structure.

“Given our results that men have smaller dACC volume than women and thicker vmPFC than COC users, these findings may represent structural vulnerabilities to psychopathologies that predominantly affect women,” the team writes .

“Specifically, a larger dACC could represent a female predisposition to fear promotion, whereas COC use could exacerbate this vulnerability by potentially inducing a thinning of a fear-inhibiting region such as the vmPFC.”

Notably, the researchers found that this effect seemed to go away when COC use stopped, though they emphasize that more research is needed to delve into the impacts. Just because a brain region changes in size doesn’t necessarily mean there are negative effects. We can’t draw firm conclusions about an individual’s emotions or behavior based on the findings about brain structure.

Ongoing exclusion of women from animal and human research contributes to the gap in our understanding of why women are more likely than men to have anxiety and stress-related disorders.

This underrepresentation of women is primarily due to a perception that changes in sex hormones would make results more variable. The bias towards studying men has led to some pretty grave consequences .

“When prescribed COCs, girls and women are informed of various physical side effects, for example that the hormones they will be taking will abolish their menstrual cycle and prevent ovulation,” Brouillard explains .

“The objective of our work is not to counter the use of COCs, but it is important to be aware that the pill can have an effect on the brain.”

The study has been published in Frontiers .

Read more at www.sciencealert.com

Naturally occurring substance in pomegranates can improve treatment of Alzheimer’s disease

A substance naturally occurring in i.a. pomegranates, strawberries and walnuts can improve memory and treatment of Alzheimer’s disease, a new study conducted at the University of Copenhagen concludes.

Forgetfulness, difficulty finding words and confusion about time and place. These are some of the most common symptoms of Alzheimer’s disease.

Now researchers at the University of Copenhagen have discovered that an ordinary fruit can help.

“Our study on mouse models with AD shows that urolithin A, which is a naturally occurring substance in i.a. pomegranates, can alleviate memory problems and other consequences of dementia,” says Vilhelm Bohr, who is Affiliate Professor at the Department of Cellular and Molecular Medicine at the University of Copenhagen and prevoiusly Department Chair at the US National Institute on Aging.

This is good news for patients with dementia — a disease that is difficult to treat.

“Even though the study was conducted on mouse models, the prospects are positive. So far, research has shown promising results for the substance in the muscles, and clinical trials on humans are being planned.”

Substance improves brain function

The researchers previously discovered that a specific molecule, nicotinamide riboside (NAD supplement) , plays a key role in neurodegenerative diseases such as Alzheimer’s and Parkinson’s, as it actively helps remove damaged mitochondria from the brain.

“Many patients with neurodegenerative diseases experience mitochondrial dysfunction, also known as mitophagy. This means that the brain has difficulties removing weak mitochondria, which thus accumulate and affect brain function. If you are able to stimulate the mitophagy process, removing weak mitochondria, you will see some very positive results,” Vilhelm Bohr explains.

The results of the new study show that a substance found in pomegranates, urolithin A, removes weak mitochondria from the brain just as effectively as NAD supplement.

Possible preventive effect

The researchers still don’t know how much urolithin A is needed to improve memory and alleviate symptoms of i.a. Alzheimer’s.

“We still cannot say anything conclusive about the dosage. But I imagine that it is more than a pomegranate a day. However, the substance is already available in pill form, and we are currently trying to find the right dosage,” Vilhelm Bohr says.

He also hopes the substance can be used for preventive purposes with no significant side effects.

“The advantage of working with a natural substance is the reduced risk of side effects. Several studies so far show that there are no serious side effects of NAD supplementation. Our knowledge of urolithin A is more limited, but as I mentioned, clinical trials with Urolithin A have been effective in muscular disease, and now we need to look at Alzheimers disease. ,” he says and adds:

“If we are going to eat something in the future to reduce the risk of Alzheimer’s, which we talk a lot about, we have to make sure there are no significant side effects.”

Read more at www.sciencedaily.com

Hitting the target with non-invasive deep brain stimulation: Potential therapy for addiction, depression and OCD

Hitting the target with non-invasive deep brain stimulation: Potential therapy for addiction, depression and OCD

by Ecole Polytechnique Federale de Lausanne A model image of the targeted deep brain zone, the striatum, a key player in reward and reinforcement mechanisms. Credit: EPFL Neurological disorders, such as addiction, depression, and obsessive-compulsive disorder (OCD), affect millions of people worldwide and are often characterized by complex pathologies involving multiple brain regions and circuits. These conditions are notoriously difficult to treat due to the intricate and poorly understood nature of brain functions and the challenge of delivering therapies to deep brain structures without invasive procedures.

In the rapidly evolving field of neuroscience, non-invasive brain stimulation is a new hope for understanding and treating a myriad of neurological and psychiatric conditions without surgical intervention or implants. Researchers, led by Friedhelm Hummel, who holds the Defitchech Chair of Clinical Neuroengineering at EPFL’s School of Life Sciences, and postdoc Pierre Vassiliadis, are pioneering a new approach in the field, opening frontiers in treating conditions like addiction and depression.

Their research, leveraging transcranial Temporal Interference Electric Stimulation (tTIS), specifically targets deep brain regions that are the control centers of several important cognitive functions and involved in different neurological and psychiatric pathologies. The research, published in Nature Human Behaviour , highlights the interdisciplinary approach that integrates medicine, neuroscience, computation, and engineering to improve our understanding of the brain and develop potentially life-changing therapies.

“Invasive deep brain stimulation (DBS) has already successfully been applied to the deeply seated neural control centers in order to curb addiction and treat Parkinson’s, OCD or depression,” says Hummel. “The key difference with our approach is that it is non-invasive, meaning that we use low-level electrical stimulation on the scalp to target these regions.”

Vassiliadis, lead author of the paper, a medical doctor with a joint Ph.D., describes tTIS as using two pairs of electrodes attached to the scalp to apply weak electrical fields inside the brain.

“Up until now, we couldn’t specifically target these regions with non-invasive techniques, as the low-level electrical fields would stimulate all the regions between the skull and the deeper zones—rendering any treatments ineffective. This approach allows us to selectively stimulate deep brain regions that are important in neuropsychiatric disorders,” he explains.

The innovative technique is based on the concept of temporal interference, initially explored in rodent models, and now successfully translated to human applications by the EPFL team. In this experiment, one pair of electrodes is set to a frequency of 2,000 Hz, while another is set to 2,080 Hz. Thanks to detailed computational models of the brain structure, the electrodes are specifically positioned on the scalp to ensure that their signals intersect in the target region. A model image of the targeted deep brain zone, the striatum, a key player in reward and reinforcement mechanisms. Credit: EPFL It is at this juncture that the magic of interference occurs: the slight frequency disparity of 80 Hz between the two currents becomes the effective stimulation frequency within the target zone. The brilliance of this method lies in its selectivity; the high base frequencies (e.g., 2,000 Hz) do not stimulate neural activity directly, leaving the intervening brain tissue unaffected and focusing the effect solely on the targeted region.

The focus of this latest research is the human striatum, a key player in reward and reinforcement mechanisms. “We’re examining how reinforcement learning , essentially how we learn through rewards, can be influenced by targeting specific brain frequencies,” says Vassiliadis. By applying stimulation of the striatum at 80 Hz, the team found they could disrupt its normal functioning, directly affecting the learning process.

The therapeutic potential of their work is immense, particularly for conditions like addiction, apathy and depression, where reward mechanisms play a crucial role. “In addiction, for example, people tend to over-approach rewards. Our method could help reduce this pathological overemphasis,” Vassiliadis, who is also a researcher at UCLouvain’s Institute of Neuroscience, points out.

Furthermore, the team is exploring how different stimulation patterns can not only disrupt but also potentially enhance brain functions. “This first step was to prove the hypothesis of 80 Hz affecting the striatum, and we did it by disrupting it’s functioning. Our research also shows promise in improving motor behavior and increasing striatum activity, particularly in older adults with reduced learning abilities,” Vassiliadis adds.

Hummel, a trained neurologist, sees this technology as the beginning of a new chapter in brain stimulation, offering personalized treatment with less invasive methods. “We’re looking at a non-invasive approach that allows us to experiment and personalize treatment for deep brain stimulation in the early stages,” he says.

Another key advantage of tTIS is its minimal side effects. Most participants in their studies reported only mild sensations on the skin, making it a highly tolerable and patient-friendly approach.

Hummel and Vassiliadis are optimistic about the impact of their research. They envision a future where non-invasive neuromodulation therapies could be readily available in hospitals, offering a cost-effective and expansive treatment scope.

More information: Non-invasive stimulation of the human striatum disrupts reinforcement learning of motor skills., Nature Human Behaviour (2024). DOI: 10.1038/s41562-024-01901-z

Provided by Ecole Polytechnique Federale de Lausanne

Read more at medicalxpress.com

Turning Back Time: Study Links Key Nutrients to Slower Brain Aging

Turning Back Time: Study Links Key Nutrients to Slower Brain Aging

A novel study highlights the critical role of specific nutrients found in the Mediterranean diet in promoting brain health and slowing cognitive decline, providing a foundation for future nutritional interventions. Participants whose brains aged more slowly had a nutrient profile that was similar to that of the Mediterranean diet.

Scientists have been extensively researching the brain to promote healthier aging. Although there is considerable knowledge about risk factors that speed up brain aging, there is less understanding of how to prevent cognitive decline.

There is evidence that nutrition matters, and a novel study published on May 21 in the journal Nature Aging , from the University of Nebraska–Lincoln’s Center for Brain, Biology and Behavior and the University of Illinois at Urbana-Champaign further signals how specific nutrients may play a pivotal role in the healthy aging of the brain.

The team of scientists, led by Aron Barbey, director of the Center for Brain, Biology, and Behavior, with Jisheng Wu, a doctoral student at Nebraska, and Christopher Zwilling, research scientist at UIUC, performed the multimodal study — combining state-of-the-art innovations in neuroscience and nutritional science — and identified a specific nutrient profile in participants who performed better cognitively. Study Design and Findings

The cross-sectional study enrolled 100 cognitively healthy participants, aged 65-75. These participants completed a questionnaire with demographic information, body measurements, and physical activity. Blood plasma was collected following a fasting period to analyze the nutrient biomarkers. Participants also underwent cognitive assessments and MRI scans. The efforts revealed two types of brain aging among the participants — accelerated and slower-than-expected. Those with slower brain aging had a distinct nutrient profile. Principal investigator Aron Barbey, psychology professor and director of the Center for Brain, Biology and Behavior at the University of Nebraska-Lincoln, with doctoral student Jisheng Wu. Credit: Craig Chandler/University Communication and Marketing/University of Nebraska–Lincoln

The beneficial nutrient blood biomarkers were a combination of fatty acids (vaccenic, gondoic, alpha-linolenic, eicosapentaenoic, eicosadienoic, and lignoceric acids); antioxidants and carotenoids including cis-lutein, trans-lutein, and zeaxanthin; two forms of vitamin E and choline. This profile is correlated with nutrients found in the Mediterranean diet, which research has previously associated with healthy brain aging.

“We investigated specific nutrient biomarkers, such as fatty acid profiles, known in nutritional science to potentially offer health benefits. This aligns with the extensive body of research in the field demonstrating the positive health effects of the Mediterranean Diet, which emphasizes foods rich in these beneficial nutrients,” Barbey, Mildred Francis Thompson Professor of Psychology, said. “The present study identifies particular nutrient biomarker patterns that are promising and have favorable associations with measures of cognitive performance and brain health.” Christopher Zwilling is a research scientist at the University of Illinois at Urbana-Champaign. Credit: University of Nebraska-Lincoln

Barbey noted that previous research on nutrition and brain aging has mostly relied on food frequency questionnaires, which are dependent on participants’ own recall. This study is one of the first and the largest to combine brain imaging, blood biomarkers, and validated cognitive assessments.

“The unique aspect of our study lies in its comprehensive approach, integrating data on nutrition, cognitive function, and brain imaging,” Barbey said. “This allows us to build a more robust understanding of the relationship between these factors. We move beyond simply measuring cognitive performance with traditional neuropsychological tests. Instead, we simultaneously examine brain structure, function, and metabolism, demonstrating a direct link between these brain properties and cognitive abilities. Furthermore, we show that these brain properties are directly linked to diet and nutrition, as revealed by the patterns observed in nutrient biomarkers.” Future Research and Implications

The researchers will continue to explore this nutrient profile as it relates to healthy brain aging. Barbey said it’s possible, in the future, that the findings will aid in developing therapies and interventions to promote brain health.

“An important next step involves conducting randomized controlled trials. In these trials, we will isolate specific nutrients with favorable associations with cognitive function and brain health, and administer them in the form of nutraceuticals,” Barbey said. “This will allow us to definitively assess whether increasing the levels of these specific nutrient profiles reliably leads to improvements in cognitive test performance and measures of brain structure, function, and metabolism.”

Barbey is also co-editing an upcoming special collection for the Journal of Nutrition, “Nutrition and the Brain — Exploring Pathways to Optimal Brain Health Through Nutrition,” which is currently inviting submissions for consideration, and articles will begin publishing next year.

“There’s immense scientific and medical interest in understanding the profound impact of nutrition on brain health,” Barbey said. “Recognizing this, the National Institutes of Health recently launched a ten-year strategic plan to significantly accelerate nutrition research. Our work directly aligns with this critical initiative, aiming to contribute valuable insights into how dietary patterns influence brain health and cognitive function.”

Reference: “Investigating nutrient biomarkers of healthy brain aging: a multimodal brain imaging study” by Christopher E. Zwilling, Jisheng Wu and Aron K. Barbey, 21 May 2024, npj Aging .
DOI: 10.1038/s41514-024-00150-8

The study was funded by Abbott Nutrition.

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Serotonin Affects Behavior and Motivation

Serotonin Affects Behavior and Motivation

Summary: A new study reveals how activating the brain’s serotonin center affects behavior and motivation in awake mice. Using optogenetics and high-field MRI, researchers found that stimulating serotonin neurons in the dorsal raphe nucleus (DRN) activates the cerebral cortex and basal ganglia, critical areas for cognitive functions.

This study highlights the intricate role of serotonin in brain-wide activation and its impact on behavior and mood. These findings could enhance our understanding of mood therapy medications and behavioral adaptation.

Key Facts: Innovative Techniques : Researchers used optogenetics and high-field MRI to study serotonin activation in awake mice.

Brain Activation : DRN serotonin stimulation activates the cerebral cortex and basal ganglia, affecting motivation and behavior.

Therapeutic Insights : Understanding serotonin’s role in brain activation could improve mood therapy and behavioral adaptation strategies.

Source: OIST

Our brains are made of tens of billions of nerve cells called neurons. These cells communicate with each other through biomolecules called neurotransmitters.

Serotonin, a type of neurotransmitter, is produced by serotonin neurons in our brains and influences many of our behavioral and cognitive functions such as memory, sleep, and mood.

Using mice, scientists at the Okinawa Institute of Science and Technology (OIST) and their collaborators from Keio University School of Medicine have studied the main source of serotonin in the brain—the dorsal raphe nucleus (DRN). Activation of DNR serotonin neurons can therefore lead to changes in motivation and behavior. Credit: Neuroscience News By studying how activating the brain’s ‘serotonin center’ affects awake animals for the first time, they found that serotonin from the DRN activates brain areas that affect behavior and motivation.

“Learning about the brain’s serotonin system can help us understand how we adapt our behaviors and how mood therapy medication works. But it was hard to study how serotonin from the DRN affects the entire brain.

First, because electric stimulation of the DRN can also activate neurons that don’t use serotonin to communicate with each other, and second, using drugs can affect other serotonin in the brain,” explained Dr. Hiroaki Hamada, a former Ph.D. student at OIST’s Neural Computation Unit.

Dr. Hamada is lead author of a paper on this study published in the journal Nature Communications .

Previous studies by researchers at the Neural Computation Unit have shown that serotonin neurons in the DRN promote adaptive behaviors in mice associated with future rewards. Dr. Hamada and his collaborators wanted to understand the mechanisms in the brain that cause these adaptive behaviors.

“We knew that DRN serotonin activation has strong effects on behavior, but we didn’t know how this serotonin activation affects different parts of the brain,” stated Prof. Kenji Doya, leader of the Neural Computation Unit. Observing the entire brain’s response to DRN serotonin activation

The researchers used a novel technique called opto-functional MRI to address this question. They used a method called optogenetics to selectively activate serotonin neurons in the DRN with light and observed the entire brain’s response using functional MRI (Magnetic Resonance Imaging).

They utilized the latest MRI scanner with a strong magnetic field to achieve the high resolution needed to study the small brains of mice. The mice were put in the MRI scanner and serotonin neurons were stimulated at regular intervals to see how this affected the whole brain.

They found that DRN serotonin stimulation causes activation of the cerebral cortex and the basal ganglia, brain areas involved in many cognitive functions. This result was very different from a previous study performed under anesthesia.

Additionally, the brain’s response to serotonin stimulation is strongly linked to the distribution of serotonin receptors (proteins activated by serotonin) and the connection patterns of DRN serotonin neurons.

“We clearly see from the high-field MRI images which areas in the brain are activated and deactivated during the awake state and under anesthesia when we activate serotonin neurons in the DRN,” Dr. Hamada said.

“A previous study showed that the cerebral cortex and the basal ganglia were mostly deactivated under anesthesia, which we also observed. However, in awake states, these areas are significantly activated.”

The cerebral cortex and the basal ganglia are parts of the brain critical for many cognitive processes, including motor activity and behaviors to gain rewards like food and water. Activation of DNR serotonin neurons can therefore lead to changes in motivation and behavior. Patience and stimulating your own serotonin

Combining the new technique of high field MRI and optogenetics presented many obstacles that Dr. Hamada had to overcome.

“We introduced and adapted a method previously used by our collaborators and established many new procedures at OIST. For me, the main challenge was using the new MRI machine at the time, so I needed to have patience and stimulate my own serotonin. I started doing a lot of exercise after that,” he said.

Seeing activations in the DRN for the first time was a standout moment for Dr. Hamada. In the beginning, he used the same light intensity that his collaborators used, but this was too weak to see the brain responses in the MRI. He then used bigger optical fibers and increased the intensity to stimulate the DRNs.

Prof. Doya noted that the next important milestone to achieve is understanding exactly how this brain-wide activation of serotonin occurs.

“It’s important to find out what is the actual molecular mechanism allowing this activation in our brain.“People who would like to get better at adjusting their behavior and thinking in different situations could also find it helpful to learn more about how serotonin helps control our moods.” About this serotonin, motivation, and behavior research news Author: Hiroaki Hamada Source: OIST Contact: Hiroaki Hamada – OIST Image: The image is credited to Neuroscience News Original Research: Open access. “ Optogenetic activation of dorsal raphe serotonin neurons induces brain-wide activation ” by Hiroaki Hamada et al. Nature Communications Abstract Optogenetic activation of dorsal raphe serotonin neurons induces brain-wide activation Serotonin is a neuromodulator that affects multiple behavioral and cognitive functions. Nonetheless, how serotonin causes such a variety of effects via brain-wide projections and various receptors remains unclear.Here we measured brain-wide responses to optogenetic stimulation of serotonin neurons in […]

Read more at neurosciencenews.com

Eating more ultra-processed foods tied to cognitive decline, stroke, according to study

People who eat more ultra-processed foods like soft drinks, chips and cookies may have a higher risk of having memory and thinking problems and having a stroke than those who eat fewer processed foods, according to a new study published in the May 22, 2024, online issue of Neurology ® , the medical journal of the American Academy of Neurology. The study does not prove that eating ultra-processed foods causes memory and thinking problems and stroke. It only shows an association.

Ultra-processed foods are high in added sugar, fat and salt, and low in protein and fiber. They include soft drinks, salty and sugary snacks, ice cream, hamburger, canned baked beans, ketchup, mayonnaise, packaged breads and flavored cereals. Unprocessed or minimally processed foods include meats such as simple cuts of beef, pork and chicken, and vegetables and fruits.

“While a healthy diet is important in maintaining brain health among older adults, the most important dietary choices for your brain remain unclear,” said study author W. Taylor Kimberly, MD, PhD, of Massachusetts General Hospital in Boston. “We found that increased consumption of ultra-processed foods was associated with a higher risk of both stroke and cognitive impairment, and the association between ultra-processed foods and stroke was greater among Black participants.”

For the study, researchers looked at 30,239 people age 45 or older who self-identified as Black or white. They were followed an average of eleven years.

Participants filled out questionnaires about what they ate and drank. Researchers determined how much ultra-processed food people ate by calculating the grams per day and comparing it to the grams per day of other foods to create a percentage of their daily diet. That percentage was calculated into four groups, ranging from the least processed foods to the most processed foods.

Of the total participants, researchers looked at 14,175 participants for cognitive decline and 20,243 participants for stroke. Both groups had no history of cognitive impairment or stroke.

By the end of the study, 768 people were diagnosed with cognitive impairment and 1,108 people had a stroke.

For those in the cognitive group, people who developed memory and thinking problems consumed 25.8% of their diet in ultra-processed foods, compared to 24.6% for those who did not develop cognitive problems.

After adjusting for age, sex, high blood pressure and other factors that could affect risk of dementia, researchers found that a 10% increase in the amount of ultra-processed foods eaten was associated with a 16% higher risk of cognitive impairment.

They also found that eating more unprocessed or minimally processed foods was linked with a 12% lower risk of cognitive impairment.

For those in the stroke group, people who had a stroke during the study consumed 25.4% of their diet in ultra-processed foods, compared to 25.1% for those who did not have a stroke.

After adjustments, researchers found greater intake of ultra-processed foods was linked to an 8% increase in risk of stroke, while greater intake of unprocessed or minimally processed foods was linked to a 9% decreased risk of stroke.

The effect of ultra-processed food consumption on stroke risk was greater among Black participants, with a 15% relative increase in risk of stroke.

“Our findings show that the degree of food processing plays an important role in overall brain health,” Kimberly said. “More research is needed to confirm these results and to better understand which food or processing components contribute most to these effects.”

A limitation of the study was that only participants who self-identified as Black or white were included in the study, so results may not be generalizable to people from other populations.

The study was funded by the National Institute of Neurological Disorders and Stroke, the National Institute on Aging, National Institutes of Health and Department of Health and Human Services.

Read more at www.sciencedaily.com

Unlocking Memory: Neuroscientists Reveal How the Brain Decides What To Remember

Unlocking Memory: Neuroscientists Reveal How the Brain Decides What To Remember

Human Brain Memories Neuroscientists have determined that some daily experiences are transformed into permanent memories during sleep through a process facilitated by the brain. A recent study led by NYU Grossman School of Medicine has identified “sharp wave-ripples” in the hippocampus as the key mechanism that selects which memories to retain permanently. These ripples occur during idle moments and play a crucial role in determining which experiences, followed closely by multiple ripples, are consolidated into long-lasting memories during sleep.

Recent research identifies “sharp wave-ripples” in the hippocampus as a brain mechanism that determines which daily experiences become permanent memories, with significant ripples during idle moments leading to memory consolidation during sleep.

Neuroscientists have discovered over the past few decades that the brain converts some of daily experiences into lasting memories during sleep that same night. A recent study introduces a mechanism that decides which memories are important enough to be preserved in the brain until sleep solidifies them permanently.

Led by researchers from NYU Grossman School of Medicine , the study revolves around brain cells called neurons that “fire” – or bring about swings in the balance of their positive and negative charges – to transmit electrical signals that encode memories. Large groups of neurons in a brain region called the hippocampus fire together in rhythmic cycles, creating sequences of signals within milliseconds of each other that can encode complex information.

Called “sharp wave-ripples,” these “shouts” to the rest of the brain represent the near-simultaneous firing of 15 percent of hippocampal neurons, and are named for the shape they take when their activity is captured by electrodes and recorded on a graph.

While past studies had linked ripples with memory formation during sleep, the new study, published recently in the journal Science , found that daytime events followed immediately by five to 20 sharp wave-ripples are replayed more during sleep and so consolidated into permanent memories. Events followed by very few or no sharp wave-ripples failed to form lasting memories.

“Our study finds that sharp wave-ripples are the physiological mechanism used by the brain to ‘decide’ what to keep and what to discard,” said senior study author György Buzsáki, MD, PhD, the Biggs Professor of Neuroscience in the Department of Neuroscience and Physiology at NYU Langone Health. Walk and Pause

The new study is based on a known pattern: mammals including humans experience the world for a few moments, then pause, then experience a little more, then pause again. After we pay attention to something, say the study authors, brain computation often switches into an “idle” re-assessment mode. Such momentary pauses occur throughout the day, but the longest idling periods occur during sleep.

Buzsaki and colleagues had previously established that no sharp wave-ripples occur as we actively explore sensory information or move, but only during the idle pauses before or after. The current study found that sharp wave-ripples represent the natural tagging mechanism during such pauses after waking experiences, with the tagged neuronal patterns reactivated during post-task sleep.

Importantly, sharp wave-ripples are known to be made up the firing of hippocampal “place cells” in a specific order that encodes every room we enter, and each arm of a maze entered by a mouse. For memories that are remembered, those same cells fire at high speed, as we sleep, “playing back the recorded event thousands of times per night.” The process strengthens the connections between the cells involved.

For the current study, successive maze runs by study mice were tracked via electrodes by populations of hippocampal cells that constantly changed over time despite recording very similar experiences. This revealed for the first time the maze runs during which ripples occurred during waking pauses, and then were replayed during sleep.

Sharp wave-ripples were typically recorded when a mouse paused to enjoy a sugary treat after each maze run. The consumption of the reward, say the authors, prepared the brain to switch from an exploratory to an idle pattern so that sharp wave-ripples could occur.

Using dual-sided silicon probes, the research team was able to record up to 500 neurons simultaneously in the hippocampus of animals during maze runs. This in turn created a challenge because data becomes exceedingly complex the more neurons are independently recorded. To gain an intuitive understanding of the data, visualize neuronal activity, and form hypotheses, the team successfully reduced the number of dimensions in the data, in some ways like converting a three-dimensional image into a flat one, and without losing the data’s integrity.

“We worked to take the external world out of the equation, and looked at the mechanisms by which the mammalian brain innately and subconsciously tags some memories to become permanent,” said first author Wannan (Winnie) Yang, PhD, a graduate student in Buzsáki’s lab. “Why such a system evolved is still a mystery, but future research may reveal devices or therapies that can adjust sharp wave-ripples to improve memory, or even lessen recall of traumatic events.”

Reference: “Selection of experience for memory by hippocampal sharp wave ripples” by Wannan Yang, Chen Sun, Roman Huszár, Thomas Hainmueller, Kirill Kiselev and György Buzsáki, 28 March 2024, Science .
DOI: 10.1126/science.adk8261
New research indicates that unlike flu vaccines, previous COVID-19 immunizations may enhance the efficacy of subsequent vaccines by fostering broad-spectrum neutralizing antibodies, suggesting annual updates could help combat emerging variants and related viruses. The response to an updated vaccine is influenced by previous vaccinations but also produces broadly neutralizing antibodies.

The COVID-19 pandemic has ended, yet the virus responsible continues to circulate, hospitalizing thousands weekly and frequently producing new variants. Due to the virus’s remarkable capacity for mutation and immune evasion, the World Health Organization (WHO) advises yearly updates to COVID-19 vaccines.

But some scientists worry that the remarkable success of the first COVID-19 vaccines may work against updated versions, undermining the utility of an annual vaccination program. A similar problem plagues the annual flu vaccine campaign; immunity elicited by one year’s flu shots can interfere with immune responses in subsequent years, reducing the vaccines’ effectiveness.

A new study by researchers at Washington University School of Medicine in […]

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Ultra-Processed Foods Could Lead to Strokes and Dementia, Says Harvard Study

Ultra-Processed Foods Could Lead to Strokes and Dementia, Says Harvard Study

A picture of a meal from a fast food restaurant . A Harvard study has found that eating ultra-processed foods could damage a person’s brain.

According to The Times , the study – which was published in the journal Neurology – concluded that consuming large amounts of the foods could be linked to strokes and dementia.

Memory problems were reported by middle-aged people if they consumed mostly cakes, sweets, burgers and fizzy drinks. The study also found that a higher rate of consumption of the products resulted in a higher risk of stroke.

This resulted in the conclusion that “food processing plays an important role in overall brain health.”

Never miss a story — sign up for PEOPLE’s free daily newsletter to stay up-to-date on the best of what PEOPLE has to offer, from juicy celebrity news to compelling human interest stories. A picture of a shopping cart with groceries. Getty Images Nestlé Announces a Line of Food Specifically for People on Weight Loss Medications

According to the outlet, the study claimed that the manufacturing of the foods caused the products to be harmful, not just their high-calorie content. They also found that gut bacteria could be disrupted thanks to industrially produced foods containing high levels of additives.

This could lead to chronic illnesses caused by the inflammation produced in the body from the additives.

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“The vast majority of [ultra-processed foods] are unhealthy, and the more of them you eat, the higher your risk of various diseases,” Frank Hu , Fredrick J. Stare Professor of Nutrition and Epidemiology and chair of the Department of Nutrition at Harvard T.H. Chan School of Public Health, said per Harvard T.H CHAN . Ultra-processed foods could damage your brain, Harvard study says Is the Paleo Diet a Myth? Cavemen Likely Ate a Plant-Based Diet

According to The Times , data from over 30,000 adults aged 45 and over were examined by Harvard Medical School for 11 years. The data collection method included questionnaires about the foods the adults consumed.

This was then divided into four groups that compared the people who had eaten more processed foods to the ones who had the least processed foods.

Meanwhile, the study concluded that by the end of the research, 1,108 participants had had a stroke and 768 were diagnosed with cognitive impairment.

“Our findings show that the degree of food processing plays an important role in overall brain health,” Lead author of the study, Dr William Taylor Kimberly said, per the outlet. More research is needed to confirm these results and to better understand which food or processing components contribute most to these effects.”

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Ultra-processed foods may raise risk of stroke, dementia

Ultra-processed foods may raise risk of stroke, dementia

A 10% increase in the amount of ultra-processed foods a person eats is associated with a 16% higher risk of cognitive problems, researchers found. Photo by Adobe Stock/HealthDay News Ultra-processed foods are bad for more than your waistline: New research shows they seem to raise the risk of stroke and dementia -related memory or thinking problems.

Likewise, greater intake of ultra-processed foods is linked to an 8% increased risk of stroke, results show.

“Our findings show that the degree of food processing plays an important role in overall brain health,” said researcher Dr. W. Taylor Kimberly , a critical care neurologist with Massachusetts General Hospital in Boston.

Ultra-processed foods typically are factory-made fare containing high levels of sugar, fat and salt. They’re a patchwork of ingredients, additives and preservatives engineered for flavor and shelf-life.

Examples include chicken nuggets, frozen meals, hot dogs, canned soups, potato chips, soft drinks, sugary breakfast cereals, ice cream, packaged breads, and condiments like ketchup and mayonnaise.

Ultra-processed foods already have been linked to an increased risk of heart disease, obesity and type 2 diabetes, the Cleveland Clinic says.

For this study, published Wednesday in the journal Neurology , researchers compared intake of ultra-processed foods to that of unprocessed or minimally processed foods like vegetables, fruits and simple cuts of beef, pork and chicken.

“While a healthy diet is important in maintaining brain health among older adults, the most important dietary choices for your brain remain unclear,” Kimberly said.

Researchers recruited more than 30,000 white or Black people ages 45 or older, and had them fill out questionnaires about what they typically eat or drink.

Researchers used the responses to calculate how much ultra-processed foods were in each person’s daily diet, compared to healthier options.

About 14,000 participants were then tracked over an average 11 years for cognitive decline, and more than 20,000 for stroke.

“We found that increased consumption of ultra-processed foods was associated with a higher risk of both stroke and cognitive impairment,” Kimberly said in a journal news release.

On the other hand, eating unprocessed or minimally processed foods was linked with a 12% lower risk of brain problems and a 9% decreased risk of stroke.

Ultra-processed foods had an even greater effect on Black participants, increasing their risk of stroke by 15%.

“More research is needed to confirm these results and to better understand which food or processing components contribute most to these effects,” Kimberly said.

More information

The Cleveland Clinic has more on ultra-processed foods .

Copyright © 2024 HealthDay. All rights reserved.

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Upgrading brain storage: Quantifying how much information our synapses can hold

Upgrading brain storage: Quantifying how much information our synapses can hold

Two neurons, one in full (left, light purple) and one partially out of frame (right, light blue) on top of a background of zeros and ones to symbolize the unit of bits used to quantify information storage in synapses. The neuron on the left is sending messages to the neuron on the right. The electrical pulse of synapses processing and sending information is represented by flashes of yellow where the two neurons meet. Credit: Salk Institute With each flip you make through a deck of vocabulary word flashcards, their definitions come more quickly, more easily. This process of learning and remembering new information strengthens important connections in your brain. Recalling those new words and definitions more easily with practice is evidence that those neural connections, called synapses, can grow stronger or weaker over time—a feature known as synaptic plasticity.

Quantifying the dynamics of individual synapses can be a challenge for neuroscientists, but recent computational innovations from the Salk Institute may be changing that—and revealing new insights about the brain along the way.

To understand how the brain learns and retains information, scientists try to quantify how much stronger a synapse has gotten through learning, and how much stronger it can get. Synaptic strength can be measured by looking at the physical characteristics of synapses, but it’s much more difficult to measure the precision of plasticity (whether synapses grow weaker or stronger by a consistent amount) and the amount of information a synapse can store.

Salk scientists have established a new method to explore synaptic strength, precision of plasticity, and amount of information storage. Quantifying these three synaptic features can improve scientific understanding of how humans learn and remember, as well as how those processes evolve over time or deteriorate with age or disease. The findings were published in Neural Computation on April 23, 2024.

“We’re getting better at identifying exactly where and how individual neurons are connected to each other, but we still have a lot to learn about the dynamics of those connections,” says Professor Terrence Sejnowski, senior author of the study and holder of the Francis Crick Chair at Salk.

“We have now created a technique for studying the strength of synapses, the precision with which neurons modulate that strength, and the amount of information synapses are capable of storing—leading us to find that our brain can store 10 times more information than we previously thought.”

When a message travels through the brain, it hops from neuron to neuron, flowing from the end of one neuron into the outstretched tendrils, called dendrites, of another. Each dendrite on a neuron is covered with tiny bulbous appendages, called dendritic spines , and at the end of each dendritic spine is the synapse—a tiny space where the two cells meet, and an electrochemical signal is transmitted. Different synapses are activated to send different messages.

Some messages activate pairs of synapses, which live near one another on the same dendrite. These synapse pairs are a fantastic research tool—if two synapses have identical activation histories, scientists can compare the strength of those synapses to draw conclusions about the precision of plasticity.

Since the same type and amount of information has passed through these two synapses, did they each change in strength by the same amount? If so, their precision of plasticity is high. White arrows pointing at two synapses (red) on the same dendrite (yellow), sharing the same axon (spotted black tube). Credit: Salk Institute The Salk team applied concepts from information theory to analyze synapse pairs from a rat hippocampus—a part of the brain involved in learning and memory—for strength, plasticity, and precision of plasticity.

Information theory is a sophisticated mathematical way of understanding information processing as an input traveling through a noisy channel and being reconstructed on the other end.

Crucially, unlike methods used in the past, information theory accounts for the noisiness of the brain’s many signals and cells, in addition to offering a discrete unit of information—a bit—to measure the amount of information stored at a synapse.

“We divided up synapses by strength, of which there were 24 possible categories, then compared special synapse pairs to determine how precisely each synapses’ strength is modulated,” says Mohammad Samavat, first author of the study and a postdoctoral researcher in Sejnowski’s lab.

“We were excited to find that the pairs had very similar dendritic spine sizes and synaptic strengths, meaning the brain is highly precise when it makes synapses weaker or stronger over time.”

In addition to noting the similarities in synapse strength within these pairs, which translates to a high level of precision of plasticity, the team also measured the amount of information held in each of the 24 strength categories. Despite differences in the size of each dendritic spine, each of the 24 synaptic strength categories held a similar amount (between 4.1 and 4.6 bits) of information.

Compared to older techniques, this new approach using information theory is (1) more thorough, accounting for 10 times more information storage in the brain than was previously assumed, and (2) scalable, meaning it can be applied to diverse and large datasets to gather information about other synapses.

“This technique is going to be a tremendous help for neuroscientists,” says Kristen Harris, a professor at the University of Texas at Austin and an author of the study. “Having this detailed look into synaptic strength and plasticity could really propel research on learning and memory, and we can use it to explore these processes in all different parts of human brains, animal brains, young brains, and old brains.”

Sejnowski says future work by projects like the National Institutes of Health’s BRAIN Initiative, which established a human brain cell atlas in October 2023, will benefit from this new tool.

In addition to scientists who catalog brain cell types and behaviors, the technique is exciting for those studying when information storage goes awry—like in Alzheimer’s disease.

In years to come, researchers around the world could use this technique to make exciting discoveries about the human brain’s ability to learn new skills, remember day-to-day actions, and store information short- and long-term.

More information: Mohammad Samavat […]

Read more at medicalxpress.com

More Research Links Ultra-Processed Foods to Increased Risk of Cognitive Decline, Stroke

More Research Links Ultra-Processed Foods to Increased Risk of Cognitive Decline, Stroke

New research on the risks associated with consuming ultra-processed foods, shows a correlation rather than causation between the consumption of ultra-processed foods and these health issues. The findings are published in the current issue of the journal Neurology .

Ultra-processed foods, which are characterized by high levels of added sugar, fat, and salt, but low in protein and fiber , include items like soft drinks, salty and sugary snacks, ice cream, hamburgers, canned baked beans, ketchup, mayonnaise, packaged breads, and flavored cereals. Conversely, unprocessed or minimally processed foods include simple proteins, as well as vegetables and fruits. “While a healthy diet is important in maintaining brain health among older adults, the most important dietary choices for your brain remain unclear,” said study author W. Taylor Kimberly, MD, PhD, of Massachusetts General Hospital in Boston. “We found that increased consumption of ultra-processed foods was associated with a higher risk of both stroke and cognitive impairment, and the association between ultra-processed foods and stroke was greater among Black participants.” Researchers analyzed data from 30,239 individuals aged 45 or older who identified as Black or white. These participants were monitored for an average of eleven years. Participants completed questionnaires detailing their dietary habits. Researchers measured the daily intake of ultra-processed foods in grams and calculated what percentage of each participant’s diet was made up of these foods. Participants were then divided into four groups, ranging from those who consumed the least to those who consumed the most ultra-processed foods. Pixabay

RELATED: Long-Term Study Links Ultra-Processed Meat, Dairy to Higher Mortality Risk

The study focused on two groups: 14,175 participants for cognitive decline and 20,243 participants for stroke, with both groups having no prior history of these conditions. By the conclusion of the study, 768 participants were diagnosed with cognitive impairment, and 1,108 had experienced a stroke.

In the cognitive group, those who developed memory and thinking problems had an average of 25.8 percent of their diet composed of ultra-processed foods, compared to 24.6 percent among those without cognitive issues.

Adjustments for age, sex, high blood pressure, and other dementia risk factors revealed that a 10 percent increase in the intake of ultra-processed foods corresponded to a 16 percent higher risk of cognitive impairment. Conversely, a higher consumption of unprocessed or minimally processed foods was linked to a 12 percent lower risk of cognitive decline.

For the stroke group, those who experienced a stroke consumed an average of 25.4 percent of their diet in ultra-processed foods, slightly higher than the 25.1 percent among those who did not suffer a stroke. After adjustments, a greater intake of ultra-processed foods was associated with an 8 percent increased risk of stroke, whereas a higher intake of unprocessed or minimally processed foods was associated with a 9 percent reduced stroke risk. The impact of ultra-processed food consumption on stroke risk was notably greater among Black participants, with a 15 percent relative increase in stroke risk.

“Our findings show that the degree of food processing plays an important role in overall brain health,” Kimberly stated. “More research is needed to confirm these results and to better understand which food or processing components contribute most to these effects.” For the latest plant-based news, read:

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Ultra-Processed Foods an Independent Risk Factor for Poor Brain Health

Ultra-Processed Foods an Independent Risk Factor for Poor Brain Health

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Consuming highly processed foods may be harmful to the aging brain, independent of other risk factors for adverse neurologic outcomes and adherence to recommended dietary patterns, new research suggests.

Observations from a large cohort of adults followed for more than 10 years suggested that eating more ultra-processed foods (UPFs) may increase the risk for cognitive decline and stroke, while eating more unprocessed or minimally processed foods may lower the risk.

“The first key takeaway is that the type of food that we eat matters for brain health, but it’s equally important to think about how it’s made and handled when thinking about brain health,” study investigator W. Taylor Kimberly, MD, PhD, with Massachusetts General Hospital in Boston, told Medscape Medical News .

“The second is that it’s not just all a bad news story because while increased consumption of ultra-processed foods is associated with a higher risk of cognitive impairment and stroke, unprocessed foods appear to be protective,” Kimberly added.

The study was published online on May 22 in Neurology . Food Processing Matters

UPFs are highly manipulated, low in protein and fiber, and packed with added ingredients, including sugar, fat, and salt. Examples of UPFs are soft drinks, chips, chocolate, candy, ice cream, sweetened breakfast cereals, packaged soups, chicken nuggets, hotdogs, and fries.

Unprocessed or minimally processed foods include meats such as simple cuts of beef, pork and chicken, and vegetables and fruits.

Research has shown associations between high UPF consumption and increased risk for metabolic and neurologic disorders.

As reported previously by Medscape Medical News , in the ELSA-Brasil, higher intake of UPFs was significantly associated with a faster rate of decline in executive and global cognitive function.

Yet, it’s unclear whether the extent of food processing contributes to the risk of adverse neurologic outcomes independent of dietary patterns.

Kimberly and colleagues examined the association of food processing levels with the risk for cognitive impairment and stroke in the long-running REGARDS study, a large prospective US cohort of Black and White adults aged 45 years and older.

Food processing levels were defined by the NOVA food classification system, which ranges from unprocessed or minimally processed foods (NOVA1) to UPFs (NOVA4). Dietary patterns were characterized based on food frequency questionnaires.

In the cognitive impairment cohort, 768 of 14,175 adults without evidence of impairment at baseline who underwent follow-up testing developed cognitive impairment. Diet an Opportunity to Protect Brain Health

In multivariable Cox proportional hazards models adjusting for age, sex, high blood pressure, and other factors, a 10% increase in relative intake of UPFs was associated with a 16% higher risk for cognitive impairment (hazard ratio [HR], 1.16). Conversely, a higher intake of unprocessed or minimally processed foods correlated with a 12% lower risk for cognitive impairment (HR, 0.88).

In the stroke cohort, 1108 of 20,243 adults without a history of stroke had a stroke during the follow-up.

In multivariable Cox models, greater intake of UPFs was associated with an 8% increased risk for stroke (HR, 1.08), while greater intake of unprocessed or minimally processed foods correlated with a 9% lower risk for stroke (HR, 0.91).

The effect of UPFs on stroke risk was greater among Black than among White adults (UPF-by-race interaction HR, 1.15).

The associations between UPFs and both cognitive impairment and stroke were independent of adherence to the Mediterranean diet, the Dietary Approaches to Stop Hypertension (DASH) diet, and the Mediterranean-DASH Intervention for Neurodegenerative Delay diet.

These results “highlight the possibility that we have the capacity to maintain our brain health and prevent poor brain health outcomes by focusing on unprocessed foods in the long term,” Kimberly said.

He cautioned that this was “an observational study and not an interventional study, so we can’t say with certainty that substituting ultra-processed foods with unprocessed foods will definitively improve brain health,” Kimberly said. “That’s a clinical trial question that has not been done but our results certainly are provocative.” Consider UPFs in National Guidelines?

The coauthors of an accompanying editorial said the “robust” results from Kimberly and colleagues highlight the “significant role of food processing levels and their relationship with adverse neurologic outcomes, independent of conventional dietary patterns.”

Peipei Gao, MS, with Harvard T.H. Chan School of Public Health, and Zhendong Mei, PhD, with Harvard Medical School, both in Boston, noted that the mechanisms underlying the impact of UPFs on adverse neurologic outcomes “can be attributed not only to their nutritional profiles,” including poor nutrient composition and high glycemic load, “but also to the presence of additives including emulsifiers, colorants, sweeteners, and nitrates/nitrites, which have been associated with disruptions in the gut microbial ecosystem and inflammation.”

“Understanding how food processing levels are associated with human health offers a fresh take on the saying ‘you are what you eat,'” wrote Gao and Mei.

This new study, they noted, adds to the evidence by highlighting the link between UPFs and brain health, independent of traditional dietary patterns and “raises questions about whether considerations of UPFs should be included in dietary guidelines, as well as national and global public health policies for improving brain health.”

The editorialists called for large prospective population studies and randomized controlled trials to better understand the link between UPF consumption and brain health. “In addition, mechanistic studies are warranted to identify specific foods, detrimental processes, and additives that play a role in UPFs and their association with neurologic disorders,” the editorialists concluded. Funding for the study was provided by the National Institute of Neurological Disorders and Stroke, the National Institute on Aging, National Institutes of Health, and Department of Health and Human Services. The authors and editorial writers had no relevant disclosures. 0

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Study shows exercise spurs neuron growth and rewires the brain, helping mice forget traumatic and addictive memories

Study shows exercise spurs neuron growth and rewires the brain, helping mice forget traumatic and addictive memories

Exercise-induced formation of neurons and genetically-inducted neuron growth rewired neural circuits in the hippocampus, helping mice forget traumatic memories and reducing their PTSD-like symptoms. Credit: Risako Fujikawa, Kyushu University and Hospital for Sick Children Researchers from the University of Toronto, Canada, and Kyushu University, Japan, have found that increased neuron formation and the subsequent rewiring of neural circuits in the hippocampus through exercise or genetic manipulation helps mice forget traumatic or drug-associated memories. The findings, reported on May 8 in Molecular Psychiatry , could offer a new approach to treating mental health conditions like post-traumatic stress disorder (PTSD) or drug addiction.

PTSD is a mental health condition that can be triggered by experiencing or seeing a traumatic event, such as a natural disaster, serious accident, or attack. Worldwide, around 3.9% of the general population has PTSD, with symptoms including vivid flashbacks and avoidance behaviors, such as staying away from places or pushing away people that remind them of the traumatic event. Currently, PTSD is often treated through therapy or medications such as anti-depressants, but as many people do not respond effectively, researchers are still looking for different treatments.

In this study on mice, Assistant Professor Risako Fujikawa from Kyushu University’s Faculty of Pharmaceutical Sciences, her former supervisor Professor Paul Frankland from the University of Toronto, and their team members including Adam Ramsaran focused on how neurogenesis—the process of forming new neurons—in the hippocampus impacts the ability to forget fear memories. The hippocampus, a brain region important for forming memories linked to specific places and contexts, produces new neurons daily in an area called the dentate gyrus.

“Neurogenesis is important for forming new memories but also for forgetting memories. We think this happens because when new neurons integrate into neural circuits, new connections are forged and older connections are lost, disrupting the ability to recall memories,” explains Fujikawa. “We wanted to see if this process could help mice forget stronger, traumatic memories too.”

The researchers gave mice two strong shocks in different settings. First, the mice were shocked after leaving a brightly-lit, white box and entering a dark, ethanol-scented compartment. After the second shock in another distinct environment, the mice showed PTSD-like behaviors.

Over a month later, the mice were still fearful and hesitant to enter the original dark compartment, indicating they couldn’t forget the traumatic memory. This fear extended to other dark compartments, showing generalized fear. Additionally, the mice explored less in open spaces and avoided the center, suggesting anxiety.

The researchers then explored whether these PTSD-like behaviors could be alleviated through exercise , which studies have shown boosted neurogenesis. The double-shocked mice were split into two groups and one group was provided with a running wheel.

Four weeks later, these mice showed increased numbers of newly-formed neurons in their hippocampi, and importantly, the PTSD-like behaviors were less severe, compared to the double-shocked mice without wheel access.

Furthermore, when the mice were free to exercise before the second shock, it also prevented some PTSD-like behaviors from developing.

However, since exercise impacts the brain and body in many different ways, it wasn’t clear whether the effect of exercise was due to hippocampal circuit rewiring by neurogenesis, or other factors. The researchers therefore used two different genetic approaches to assess the impact of newborn neuron integration into the hippocampus, exclusively. When activated with light, newly-formed neurons in the hippocampus grew faster and showed more branching. Credit: Paul Frankland; University of Toronto First, the researchers used a technique called optogenetics, where they added light-sensitive proteins to newly formed neurons in the dentate gyrus, allowing the neurons to be activated by light. When they shone blue light on these cells, the new neurons matured faster. After 14 days, the neurons had grown longer, had more branches, and integrated more quickly into the neural circuits of the hippocampus.

In the second approach, the research team used genetic engineering to remove a protein in the newly formed neurons that slows down neuron growth. This also resulted in the neurons growing faster and increased incorporation into neural circuits.

Both these genetic approaches reduced PTSD-like symptoms in mice after double-shocking and shortened the time taken for the mice to forget the fear memory. However, the researchers found that the effect was weaker than they saw with exercise, and did not reduce the level of the mice’s anxiety.

“It could be that the neurogenesis and the re-modeling of the hippocampus circuits disrupt fear memory, but have less effect on mood or emotions,” suggests Fujikawa. “Exercise also has broader physiological effects, which may contribute to the stronger outcomes seen.”

Finally, the research team explored whether increased neurogenesis and hippocampus re-modeling could also help in other mental disorders where memory plays an important role, such as substance use disorders . For people battling drug dependency, relapse often happens when reminders, like being in a similar environment where the drug was used, trigger powerful cravings.

The researchers placed the mice in a cage with two rooms. In one room, the mice were given a saline solution and in the other room, they were given cocaine. Afterward, when given free access to both rooms, the mice spent more time in the room in which they had received cocaine.

However, when the researchers used exercise and genetic methods to boost neurogenesis and hippocampus re-modeling, they found that the mice stopped showing a preference for the room where they had taken cocaine, suggesting the mice had forgotten the link between the room and the drug.

For future research, Risako is planning to find a drug that can boost neurogenesis or hippocampus re-modeling, in the hopes that it could be tested as a potential treatment for PTSD and drug dependence. However, she also stressed the importance of exercise.

“In our experiments, exercise had the most powerful impact on reducing symptoms of PTSD and drug dependence in mice, and clinical studies in humans also show it is effective,” says Risako. “I think this is the most important takeaway.”

Provided by Kyushu University

Read more at medicalxpress.com

Exercise spurs neuron growth and rewires the brain, helping mice forget traumatic and addictive memories

Researchers from the University of Toronto, Canada, and Kyushu University, Japan, have found that increased neuron formation and the subsequent rewiring of neural circuits in the hippocampus through exercise or genetic manipulation helps mice forget traumatic or drug-associated memories. The findings, reported on May 8 in Molecular Psychiatry , could offer a new approach to treating mental health conditions like post-traumatic stress disorder (PTSD) or drug addiction.

PTSD is a mental health condition that can be triggered by experiencing or seeing a traumatic event, such as a natural disaster, serious accident, or attack. Worldwide, around 3.9% of the general population has PTSD, with symptoms including vivid flashbacks and avoidance behaviors, such as staying away from places or pushing away people that remind them of the traumatic event. Currently, PTSD is often treated through therapy or medications such as anti-depressants, but as many people do not respond effectively, researchers are still looking for different treatments.

In this study on mice, Assistant Professor Risako Fujikawa from Kyushu University’s Faculty of Pharmaceutical Sciences, her former supervisor Professor Paul Frankland from the University of Toronto, and their team members including Adam Ramsaran focused on how neurogenesis — the process of forming new neurons — in the hippocampus impacts the ability to forget fear memories. The hippocampus, a brain region important for forming memories linked to specific places and contexts, produces new neurons daily in an area called the dentate gyrus.

“Neurogenesis is important for forming new memories but also for forgetting memories. We think this happens because when new neurons integrate into neural circuits, new connections are forged and older connections are lost, disrupting the ability to recall memories,” explains Fujikawa. “We wanted to see if this process could help mice forget stronger, traumatic memories too.”

The researchers gave mice two strong shocks in different settings. First, the mice were shocked after leaving a brightly-lit, white box and entering a dark, ethanol-scented compartment. After the second shock in another distinct environment, the mice showed PTSD-like behaviors. Over a month later, the mice were still fearful and hesitant to enter the original dark compartment, indicating they couldn’t forget the traumatic memory. This fear extended to other dark compartments, showing generalized fear. Additionally, the mice explored less in open spaces and avoided the center, suggesting anxiety.

The researchers then explored whether these PTSD-like behaviors could be alleviated through exercise, which studies had shown boosted neurogenesis. The double-shocked mice were split into two groups and one group was provided with a running wheel. Four weeks later, these mice showed increased numbers of newly-formed neurons in their hippocampi, and importantly, the PTSD-like behaviors were less severe, compared to the double-shocked mice without wheel access.

Furthermore, when the mice were free to exercise before the second shock, it also prevented some PTSD-like behaviors from developing.

However, since exercise impacts the brain and body in many different ways, it wasn’t clear whether the effect of exercise was due to hippocampal circuit rewiring by neurogenesis, or other factors. The researchers therefore used two different genetic approaches to assess the impact of newborn neuron integration into the hippocampus, exclusively.

Firstly, the researchers used a technique called optogenetics, where they added light-sensitive proteins to newly-formed neurons in the dentate gyrus, allowing the neurons to be activated by light. When they shone blue light on these cells, the new neurons matured faster. After 14 days, the neurons had grown longer, had more branches, and integrated more quickly into the neural circuits of the hippocampus.

In the second approach, the research team used genetic engineering to remove a protein in the newly-formed neurons that slows down neuron growth. This also resulted in the neurons growing faster and increased incorporation into neural circuits.

Both these genetic approaches reduced PTSD-like symptoms in mice after double-shocking and shortened the time taken for the mice to forget the fear memory. However, the researchers found that the effect was weaker than they saw with exercise, and did not reduce the level of the mice’s anxiety.

“It could be that the neurogenesis and the re-modeling of the hippocampus circuits disrupt fear memory, but have less effect on mood or emotions,” suggests Fujikawa. “Exercise also has broader physiological effects, which may contribute to the stronger outcomes seen.”

Finally, the research team explored whether increased neurogenesis and hippocampus re-modeling could also help in other mental disorders where memory plays an important role, such as substance use disorders. For people battling drug dependency, relapse often happens when reminders, like being in a similar environment where the drug was used, trigger powerful cravings.

The researchers placed mice in a cage with two rooms. In one room, the mice were given a saline solution and in the other room, they were given cocaine. Afterward, when given free access to both rooms, the mice spent more time in the room in which they had received cocaine.

However, when the researchers used exercise and genetic methods to boost neurogenesis and hippocampus re-modeling, they found that the mice stopped showing a preference for the room where they had taken cocaine, suggesting the mice had forgotten the link between the room and the drug.

For future research, Risako is planning to find a drug that can boost neurogenesis or hippocampus re-modeling, in the hopes that it could be tested as a potential treatment for PTSD and drug dependence. However, she also stressed the importance of exercise.

“In our experiments, exercise had the most powerful impact on reducing symptoms of PTSD and drug dependence in mice, and clinical studies in humans also show it is effective,” says Risako. “I think this is the most important takeaway.”

Read more at www.sciencedaily.com

Study: Certain nutrients may slow brain aging

Study: Certain nutrients may slow brain aging

Chronological versus brain age. Credit: npj Aging (2024). DOI: 10.1038/s41514-024-00150-8 Scientists have long been studying the brain with the goal of aiding healthier aging. While much is known about risk factors for accelerated brain aging, less has been uncovered to identify ways to prevent cognitive decline.

There is evidence that nutrition matters, and a novel study published in npj Aging , from the University of Nebraska–Lincoln’s Center for Brain, Biology and Behavior and the University of Illinois at Urbana-Champaign further signals how specific nutrients may play a pivotal role in the healthy aging of the brain.

The team of scientists, led by Aron Barbey, director of the Center for Brain, Biology and Behavior, with Jisheng Wu, a doctoral student at Nebraska, and Christopher Zwilling, research scientist at UIUC, performed the multimodal study—combining state-of-the-art innovations in neuroscience and nutritional science—and identified a specific nutrient profile in participants who performed better cognitively.

The cross-sectional study enrolled 100 cognitively healthy participants, aged 65–75. These participants completed a questionnaire with demographic information, body measurements and physical activity.

Blood plasma was collected following a fasting period to analyze the nutrient biomarkers. Participants also underwent cognitive assessments and MRI scans. The efforts revealed two types of brain aging among the participants—accelerated and slower-than-expected. Those with slower brain aging had a distinct nutrient profile.

The beneficial nutrient blood biomarkers were a combination of fatty acids (vaccenic, gondoic, alpha linolenic, elcosapentaenoic, eicosadienoic and lignoceric acids); antioxidants and carotenoids including cis-lutein, trans-lutein and zeaxanthin; two forms of vitamin E and choline. This profile is correlated with nutrients found in the Mediterranean diet, which research has previously associated with healthy brain aging.

“We investigated specific nutrient biomarkers, such as fatty acid profiles, known in nutritional science to potentially offer health benefits. This aligns with the extensive body of research in the field demonstrating the positive health effects of the Mediterranean Diet, which emphasizes foods rich in these beneficial nutrients,” Barbey, Mildred Francis Thompson Professor of Psychology, said.

“The present study identifies particular nutrient biomarker patterns that are promising and have favorable associations with measures of cognitive performance and brain health.”

Barbey noted that previous research on nutrition and brain aging has mostly relied on food frequency questionnaires, which are dependent on participants’ own recall. This study is one of the first and the largest to combine brain imaging, blood biomarkers and validated cognitive assessments.

“The unique aspect of our study lies in its comprehensive approach, integrating data on nutrition, cognitive function, and brain imaging,” Barbey said. “This allows us to build a more robust understanding of the relationship between these factors. We move beyond simply measuring cognitive performance with traditional neuropsychological tests.

“Instead, we simultaneously examine brain structure, function, and metabolism, demonstrating a direct link between these brain properties and cognitive abilities. Furthermore, we show that these brain properties are directly linked to diet and nutrition , as revealed by the patterns observed in nutrient biomarkers.”

The researchers will continue to explore this nutrient profile as it relates to healthy brain aging. Barbey said it’s possible, in the future, that the findings will aid in developing therapies and interventions to promote brain health.

“An important next step involves conducting randomized controlled trials. In these trials, we will isolate specific nutrients with favorable associations with cognitive function and brain health, and administer them in the form of nutraceuticals,” Barbey said.

“This will allow us to definitively assess whether increasing the levels of these specific nutrient profiles reliably leads to improvements in cognitive test performance and measures of brain structure, function, and metabolism.”

More information: Christopher E. Zwilling et al, Investigating nutrient biomarkers of healthy brain aging: a multimodal brain imaging study, npj Aging (2024). DOI: 10.1038/s41514-024-00150-8

Provided by University of Nebraska-Lincoln

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Unique brain circuit is linked to Body Mass Index

Why can some people easily stop eating when they are full and others can’t, which can lead to obesity?

A Northwestern Medicine study has found one reason may be a newly discovered structural connection between two regions in the brain that appears to be involved in regulating feeding behavior. These regions involve the sense of smell and behavior motivation.

The weaker the connection between these two brain regions, the higher a person’s Body Mass Index (BMI), the Northwestern scientists report.

The investigators discovered this connection between the olfactory tubercle, an olfactory cortical region, which is part of the brain’s reward system, and a midbrain region called the periaqueductal gray (PAG), involved in motivated behavior in response to negative feelings like pain and threat and potentially in suppression of eating.

The study will be published May 16 in the Journal of Neuroscience.

Previous research at Northwestern by co-author Thorsten Kahnt, now at the National Institutes of Health, has shown the smell of food is appetizing when you’re hungry. But the smell is less appealing when you eat that food until you are full.

Odors play an important role in guiding motivated behaviors such as food intake, and — in turn — olfactory perception is modulated by how hungry we are.

Scientists have not fully understood the neural underpinnings of how the sense of smell contributes to how much we eat.

“The desire to eat is related to how appealing the smell of food is — food smells better when you are hungry than when you are full,” said corresponding author Guangyu Zhou, research assistant professor of neurology at Northwestern University Feinberg School of Medicine. “But if the brain circuits that help guide this behavior are disrupted, these signals may get confused, leading to food being rewarding even when you are full. If this happens, a person’s BMI could increase. And that is what we found. When the structural connection between these two brain regions is weaker, a person’s BMI is higher, on average.”

Though this study does not directly show it, the study authors hypothesize that healthy brain networks connecting reward areas with behavior areas could regulate eating behavior by sending messages telling the individual that eating doesn’t feel good anymore when they’re full. In fact, it feels bad to overeat. It’s like a switch in the brain that turns off the desire to eat.

But people with weak or disrupted circuits connecting these areas may not get these stop signals, and may keep eating even when they aren’t hungry, the scientists said.

“Understanding how these basic processes work in the brain is an important prerequisite to future work that can lead to treatments for overeating,” said senior author Christina Zelano, associate professor of neurology at Feinberg.

How the study worked

This study used MRI brain data — neurological imaging — from the Human Connectome Project, a large multi-center NIH project designed to build a network map of the human brain.

Northwestern’s Zhou found correlations to BMI in the circuit between the olfactory tubercle and the midbrain region, the periaqueductal gray. For the first time in humans, Zhou also mapped the strength of the circuit across the olfactory tubercle, then replicated these findings in a smaller MRI brain dataset that scientists collected in their lab at Northwestern.

“Future studies will be needed to uncover the exact mechanisms in the brain that regulate eating behavior,” Zelano said.

The research reported in this press release was supported by the National Institute on Deafness and Other Communication Diseases grants R01-DC-016364, R01-DC-018539, R01-DC-015426 and the Intramural Research Program at the National Institute on Drug Abuse grant ZIA DA000642, all of the National Institutes of Health. The content is solely the responsibility of the authors and does not necessarily represent the official views of the National Institutes of Health.

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Nature Knows Nootropics