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These Are All the Vitamins for Brain Health You Need in Your Diet
These Are All the Vitamins for Brain Health You Need in Your Diet “Hearst Magazines and Yahoo may earn commission or revenue on some items through these links.”
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When it comes to keeping your brain healthy as you age, your diet plays a big role. Eating a variety of foods is critical to getting the vitamins and nutrients your brain needs to keep performing at its best. But the best vitamins for brain health may help.
Research has found that “certain nutrients, flavonoids, unsaturated fats, and omega-3 fatty acids are associated with slower cognitive decline and reduced risk of dementia ,” says Puja Agarwal, Ph.D. , a nutritional epidemiologist and assistant professor in the Department of Internal Medicine at Rush Medical College in Chicago.
Meet the Experts: Puja Agarwal, Ph.D. , a nutritional epidemiologist and assistant professor in the Department of Internal Medicine at Rush Medical College in Chicago; Mirella Díaz-Santos, P.h.D., an assistant professor in the Mary S Easton Center for Alzheimer’s Disease Research; Robin Foroutan, M.S., R.D.N. , a functional dietitian; Gill Livingston, M.D. , a professor of psychiatry at University College London.
Although eating whole foods is the best way to get those brain-boosting nutrients. supplements for brain health can be a helpful option in specific circumstances. “In general, supplements aren’t often useful for brain health unless you have a deficiency in certain nutrients, which happens but is rare,” says Gill Livingston, M.D. , a professor of psychiatry at University College London whose research focuses on dementia prevention, intervention, and care.
So, which vitamins support brain health ? And how can you get more of those essential vitamins into your diet? Ahead, experts share everything you need to know. Vitamins for brain health
Omega-3 fatty acids
If you’ve ever wondered why fatty fish like salmon and tuna are always touted as part of a healthy diet, here’s one reason: They’re high in omega-3 fatty acids, a type of unsaturated fat that has a brain-protecting anti-inflammatory effect and is a building block of cell membranes in the brain. Shop Now Nordic Naturals Ultimate Omega amazon.com $32.49 Nordic Naturals More Omega-3s have also been linked to lower levels of beta-amyloid, a type of protein found in the brains of people with Alzheimer’s-related damage. “Omega-3 fatty acids easily penetrate the blood-brain barrier and are essential for the brain’s structure and functioning,” explains Dr. Agarwal.
Foroutan adds there has been some research that indicates high doses of omega-3 fatty acids after a concussion or other traumatic brain injury may have protective effects on lasting damage
Where to find it: Besides fatty fish, good sources of omega-3s include nuts and seeds and some fortified foods such as eggs and yogurt. If you’re someone who doesn’t eat seafood often, check with your doctor about taking an omega-3 supplement if bloodwork indicates you’re deficient, says Mirella Díaz-Santos, P.h.D., an assistant professor in the Mary S Easton Center for Alzheimer’s Disease Research at UCLA’s Department of Neurology and Women’s Alzheimer’s Movement partner. Vitamin E
This vitamin functions as an antioxidant in the body, and it protects cells from oxidative stress , a type of damage caused by free radicals (unstable molecules in the body), even in the brains of people with Alzheimer’s disease. The brain is particularly susceptible to oxidative stress, which increases during aging and is a major contributor to cognitive decline .
Vitamin E is also anti-inflammatory, which helps to keep DNA healthy and replicating correctly while maintaining the structure of healthy brain cell membranes, says Robin Foroutan, M.S., R.D.N. , a functional dietitian.
Where to find it: Vitamin E can be found in dark leafy greens, avocado, red bell pepper, asparagus, mango, pumpkin, and nuts and seeds. B Vitamins
When it comes to brain health, focus on the three B’s: vitamins B6, B12, and B9 ( folate ). “These three types of B vitamins are necessary for the brain’s normal functioning ,” says Dr. Agarwal, “and any deficiency in them may increase the risk of memory loss and other forms of cognitive decline.”
The reason: These vitamins help boost the production of neurotransmitters , or brain chemicals, that deliver messages between the brain and body.
Increasing your B12 by taking a supplement may also be helpful with memory loss as you age because it’s a very common nutrient for older people to develop a deficiency in, notes Díaz-Santos.
Where to find them: Beans are one of the best sources of B vitamins across the board. You can find B6 in bananas, oranges, papaya, cantaloupe, tuna, salmon, poultry, and dark leafy greens. Folate is found in broccoli, greens, whole grains, eggs, peanuts, and sunflower seeds.
Vitamin B12 is found solely in meat and fish products; for vegans and vegetarians, nutritional yeast and fortified whole grains are a good way to get your supply. People on a plant-based diet do have a much higher risk of a true B12 deficiency, so talk to your doctor or dietitian about whether or not a B12 supplement is right for you. Vitamin C
This antioxidant is known for its immunity powers, but vitamin C and other flavonoids also support the brain , potentially by taming brain-damaging inflammation.
In one study , by Rush University researchers including Dr. Agarwal, people who consumed vitamin C-rich strawberries at least once a week were less likely to develop Alzheimer’s over the course of the nearly 20-year study period.
Where to find it: Get vitamin C in abundance from kiwi, red and green bell peppers, citrus, berries, broccoli, cauliflower, brussels sprouts, and tomatoes. Supplements for brain health
There’s a lot of mixed research and feeling among experts when it comes to taking supplements for brain health. Most experts agree it’s always better to spend your money on nutritious foods, but there are exceptions.
Díaz-Santos says that if you’re someone with an allergy or aversion to a large food group (like seafood or dairy) or your doctor found a deficiency during a blood panel, you may want to consider taking a dietary supplement. Otherwise, a well-rounded diet […]
Memory Block: How Saturated Fats May Hinder Memory Formation in the Aging Brain
A new study suggests that a high-fat diet may impair memory by causing inflammatory effects and issues in cell-signaling management in the brain cells, especially as people age, but the omega-3 fatty acid DHA may help mitigate these effects. The research, focusing on microglia and hippocampal neurons, found that palmitic acid increased inflammation, while DHA protected against this effect but not against the loss of mitochondrial function induced by palmitic acid exposure. New research reveals DHA shields brain cells from fat-related inflammation.
New research suggests several mechanisms through which high-fat foods may impact brain cells, potentially elucidating the association between a high-fat diet and memory decline, particularly in aging.
A study from The Ohio State University conducted in cell cultures indicates that the omega-3 fatty acid DHA could shield the brain from the detrimental effects of an unhealthy diet by reducing fat-triggered inflammation at the cellular level.
Separate experiments using brain tissue from aging mice showed a high-fat diet may lead specific brain cells to overdo cell-signaling management in a way that interferes with the creation of new memories.
The same lab found in an earlier study in aging rats that a diet of highly processed ingredients led to a strong inflammatory response in the brain that was accompanied by behavioral signs of memory loss – and that DHA supplementation prevented those problems.
“The cool thing about this paper is that for the first time, we’re really starting to tease these things apart by cell type,” said senior author Ruth Barrientos, an investigator in Ohio State’s Institute for Behavioral Medicine Research and associate professor of psychiatry and behavioral health and neuroscience in the College of Medicine.
“Our lab and others have often looked at the whole tissue of the hippocampus to observe the brain’s memory-related response to a high-fat diet. But we’ve been curious about which cell types are more or less affected by these saturated fatty acids, and this is our first foray into determining that.”
The study was published recently in the journal Frontiers in Cellular Neuroscience .
For this work, the researchers focused on microglia, cells in the brain that promote inflammation, and hippocampal neurons, which are important for learning and memory. They used immortalized cells – copies of cells taken from animal tissue that are modified to continuously divide and respond only to lab-based stimulation, meaning their behavior may not precisely match that of primary cells of the same type.
Researchers exposed these model microglia and neurons to palmitic acid, the most abundant saturated fatty acid in high-fat foods like lard, shortening, meat, and dairy products, to observe how it affected gene activation in the cells as well as functioning of mitochondria, structures inside cells that have a primary metabolic role of generating energy.
Results showed that palmitic acid prompted gene expression changes linked to an increase in inflammation in both microglia and neurons, though microglia had a wider range of affected inflammatory genes. Pre-treatment of these cells with a dose of DHA, one of two omega-3 fatty acids in fish and other seafood and available in supplement form, had a strong protective effect against the increased inflammation in both cell types.
“Previous work has shown that DHA is protective in the brain and that palmitic acid has been detrimental to brain cells, but this is the first time we’ve looked at how DHA can directly protect against the effects of palmitic acid in those microglia, and we see that there is a strong protective effect,” said Michael Butler, first author of the study and a research scientist in Barrientos’ lab.
When it came to the mitochondria, however, DHA did not prevent the loss of function that followed exposure to palmitic acid.
“The protective effects of DHA might, in this context, be restricted to effects on gene expression related to the pro-inflammatory response as opposed to the metabolic deficits that the saturated fat also induced,” Butler said.
In another set of experiments, the researchers looked at how a diet high in saturated fat influenced signaling in the brains of aged mice by observing another microglial function called synaptic pruning. Microglia monitor signal transmission among neurons and nibble away excess synaptic spines, the connection sites between axons and dendrites, to keep communication at an ideal level.
Microglia were exposed to mouse brain tissue containing both pre- and post-synaptic material from animals that had been fed either a high-fat diet or regular chow for three days.
The microglia ate the synapses from aged mice fed a high-fat diet at a faster rate than they ate synapses from mice fed a regular diet – suggesting the high-fat diet is doing something to those synapses that gives the microglia a reason to eat them at a higher rate, Butler said.
“When we talk about the pruning, or refinement, that needs to occur, it’s like Goldilocks: It needs to be optimal – not too much and not too little,” Barrientos said. “With these microglia eating away too much too soon, it outpaces the ability for these spines to regrow and create new connections, so memories don’t solidify or become stable.”
From here, the researchers plan to expand on findings related to synaptic pruning and mitochondria function, and to see how palmitic acid and DHA effects play out in primary brain cells from young versus aged animals.
Reference: “Dietary fatty acids differentially impact phagocytosis, inflammatory gene expression, and mitochondrial respiration in microglial and neuronal cell models” by Michael J. Butler, Sabrina E. Mackey-Alfonso, Nashali Massa, Kedryn K. Baskin and Ruth M. Barrientos, 10 August 2023, Frontiers in Cellular Neuroscience .
DOI: 10.3389/fncel.2023.1227241
This work was supported by grants from the National Institute on Aging and the National Institute of Dental and Craniofacial Research. Additional co-authors, all from Ohio State, were Sabrina Mackey-Alfonso, Nashali Massa and Kedryn Baskin.
Scientists focus on glymphatic system and its role in sleep, memory consolidation, degenerative illnesses
Credit: Pixabay/CC0 Public Domain When we think of brains, we tend to think of neurons. It’s right there in our word for the study of the brain: neuroscience. But when it comes to certain mysteries of the brain—for example, the role of sleep in memory consolidation, or the genesis of traumatic brain injuries (TBIs) and degenerative neurological disorders such as Parkinson’s disease and Alzheimer’s disease—the answers we seek may lie elsewhere: the glymphatic system.
A waste clearance system for the brain and the nervous system of humans and other vertebrates, the glymphatic system derives its name from the brain’s glial cells, on which it depends, and the lymphatic system, which it resembles functionally. It consists of the pathway including channels called ventricles, the brain’s interstitial spaces—the spaces between the cells in the brain’s gray and white matter—and the perivascular spaces around veins and arteries in the brain.
Scientists at the Johns Hopkins Applied Physics Laboratory (APL) in Laurel, Maryland, are working to advance our understanding of the glymphatic system and the role it plays in sleep, memory consolidation, degenerative illnesses and more. Reawakened interest, 150 years later
“If you go back to neuroimaging all the way back to the 1850s, scientists were primarily interested in imaging the ventricles to better understand pathologies like hydrocephalus [a neurological disorder caused by a buildup of excess cerebrospinal fluid (CSF)],” said Clara Scholl, chief scientist of the Neuroscience Group in APL’s Research and Exploratory Development Department (REDD). “And then neurons were discovered, and the focus shifted away from the ventricles and toward cellular matter in the brain for the next 150 years or so.”
In the past decade, studies with fluorescent tracers in mice led to the discovery of the glymphatic system and its role in sleep and neurodegenerative disease, among other questions. “The field has developed a solid understanding of how this system works through animal models, as well as invasive studies in humans in which they inject dyes into the CSF and then observe sleeping subjects using MRI [magnetic resonance imaging] scanners,” Scholl said.
It’s clear by now that a better understanding of the glymphatic system—how it functions, how to observe and influence its workings—could have a significant and positive impact on human health, in a variety of civilian and military applications. But before that can happen, significant technology gaps will have to be addressed.
“If you have a pathology in your glymphatic system, we have no way to determine that without injecting fluorescent tracers into your CSF or putting you in an MRI scanner while you’re sleeping,” said Scholl, “Or in some conditions, you might have a hole drilled in your skull to relieve the pressure and a sample of your CSF can be taken in the process. But there’s really no noninvasive way to observe or measure CSF flow dynamics in the brain. That’s where APL comes in.” From phantoms to humans
APL’s work in glymphatic system sensing began with an effort to use commercial off-the-shelf sensors to track its role in TBI. Sponsored by Uniformed Services University (USU) and supported by the Congressionally Directed Medical Research Programs (CDMRP), this project is a collaboration with Navy sleep physician J. Kent Werner. The potential they saw using noninvasive, near-infrared spectroscopy sensors (NIRS)—a technology traditionally used for tracking hemodynamic activity (blood flow)—inspired the APL team to extend its capabilities.
Within a relatively short period of time, Scholl and the rest of the APL team, guided by the expertise of REDD optical physicist Joseph Angelo, have applied a specialized form of NIRS, known as frequency domain functional NIRS (FD-fNIRS), to develop noninvasive sensors that can accurately track the activity of the glymphatic system.
To tune FD-fNIRS to observe the complex fluid dynamics of the glymphatic system, the APL team developed “optical phantoms” that model the optical properties of the glymphatic system—an effort described in a publication in IEEE Xplore based on a conference paper. Since that accomplishment, Will Coon, a sleep scientist and neural signals engineer in REDD, has gone on to conduct sleep studies in which glymphatic activity was measured and tracked alongside more traditional metrics associated with sleep, such as electroencephalographic (EEG) activity.
Establishing correspondence between the glymphatic system and the known dynamics of sleep is no small feat, but it’s worth the effort. “There’s good reason to believe we can interact with the glymphatic system,” Coon said. “We know the drivers. We’re starting to see that a particular kind of sleep called slow-wave sleep stimulates blood flow into the brain. And when blood flows in, CSF flows out—that seems to be the driver for much of the glymphatic system’s waste clearance activity.”
Coon continued, “Fortunately, there’s an extensive body of research around slow-wave sleep and memory consolidation —we know ways to interact with and control these slow waves, how to increase them, like using clicks and sounds to stimulate more waves. And if we can do that, it points to possible treatments for the glymphatic system—maybe treatments we can apply preventatively with TBI in order to stave off neurological decline 20 or 30 years down the road.” A cold trail revived
Recently, APL began a collaboration with Michael Smith, a sleep doctor at Johns Hopkins Medicine (JHM) in Baltimore. Smith came across a trio of research papers from the late 1980s that found that cooling delivered at specific moments during sleep could induce extended bouts of slow-wave sleep in human subjects. Those findings were replicated not long ago by several European research teams, which brought them to Smith’s attention.
“This is an exciting discovery, because using sound-based methods, you can only turn one or two slow waves into five or six waves; but this thermal effect has the potential to induce hundreds, maybe even thousands of slow waves, which adds up to significantly more restorative slow-wave sleep ,” Coon explained. “That could be a game-changer for helping aging populations achieve better glymphatic clearance, including healthy people and those with neurological disorders, including Alzheimer’s and Parkinson’s.” Reaching for the STARS: A comprehensive sleep ecosystem
Coon conducts research at APL targeted […]
Unveiling the Brain’s Secrets: Study Resolves “Paradox” in Visual Recognition Memory
A new study clarifies past conflicting observations on visual recognition memory (VRM), showing that increased visual evoked potentials (VEPs) during the recognition of familiar stimuli signal the brain’s rapid identification process, ultimately leading to decreased overall neural activity. Since determining what we observe as new or familiar is essential for prioritizing our attention, neuroscientists have dedicated years to understanding why our brains excel at this task.
During their research, they have encountered seemingly conflicting findings. However, a recent study reveals that these perplexing results are really two sides of the same coin, paving the way for a long-sought understanding of “visual recognition memory” (VRM).
VRM is the ability to quickly recognize the familiar things in scenes, which can then be de-prioritized so that we can focus on the new things that might be more important in a given moment.
Imagine you walk into your home office one evening to respond to an urgent, late email. There you see all the usual furniture and equipment—and a burglar. VRM helps ensure that you’d focus on the burglar, not your bookshelves or your desk lamp.
Data from the paper show a sharp but brief increase in neural activity — a visually evokied potential — when a stimulus pattern is shown to a mouse at about 80 milliseconds (bright orange vertical line). Notably when a stimulus is familiar, activity decreases significantly (cooler colors) after that transient increase. Credit: Bear Lab/MIT Picower Institute
“Yet we do not yet have a clear picture of how this foundational form of learning is implemented within the mammalian brain,” wrote Picower Professor Mark Bear and fellow authors of the new study in the Journal of Neuroscience .
As far back as 1991 researchers found that when animals viewed something familiar, neurons in the cortex, or the outer layer of their brain, would be less activated than if they saw something new (two of that study’s authors later became Bear’s colleagues at MIT , Picower Professor Earl K. Miller and Doris and Don Berkey Professor Bob Desimone).
But in 2003 , Bear’s lab happened to observe the opposite: Mice would actually show a sharp jump in neural activity in the primary visual region of the cortex when a familiar stimulus was flashed in front of the animal. This spike of activity is called a “visually evoked potential” (VEP), and Bear’s lab has since shown that increases in the VEPs are solid indicators of VRM.
The findings in the new study, led by former Bear Lab postdocs Dustin Hayden and Peter Finnie, explain how VEPs increase even amid an overall decline in neural response to familiar stimuli (as seen by Miller and Desimone), Bear said. They also explain more about the mechanisms underlying VRM – the momentary increase of a VEP may be excitation that recruits inhibition, thereby suppressing activity overall.
New understanding
Bear’s lab evokes VEPs by showing mice a black-and-white striped grating in which the stripes periodically switch their shade so that the pattern appears to reverse. Over several days as mice view this stimulus pattern, the VEPs increase, a reliable correlate of the mice becoming familiar with—and less interested in—the pattern. For 20 years Bear’s lab has been investigating how the synapses involved in VRM change by studying a phenomenon they’ve dubbed “stimulus-selective response plasticity” (SRP).
Early studies suggested that SRP occurs among excitatory neurons in layer 4 of the visual cortex and specifically might require the molecular activation of their NMDA receptors.
The lab had seen that knocking out the receptors across the visual cortex prevented the increase in VEPs and therefore SRP, but a follow-up in 2019 found that knocking them out just in layer 4 had no effect. So, in the new study, they decided to study VEPs, SRP, and VRM across the whole visual cortex, layer by layer, in search of how it all works.
What they found was that many of the hallmarks of VRM, including VEPs, occur in all layers of the cortex but that it seemed to depend on NMDA receptors on a population of excitatory neurons in layer 6, not layer 4. This is an intriguing finding, the authors said, because those neurons are well connected to the thalamus (a deeper brain region that relays sensory information) and to inhibitory neurons in layer 4, where they had first measured VEPs.
They also measured changes in brain waves in each layer that confirmed a previous finding that when the stimulus pattern is new, the prevailing brain wave oscillations are in a higher “gamma” frequency that depends on one kind of inhibitory neuron, but as it becomes more familiar, the oscillations shift toward a lower “beta” frequency that depends on a different inhibitory population. A short spike amid a long lull
The team’s rigorous and precise electrophysiology recordings of neural electrical activity in the different layers also revealed a potential resolution to the contradiction between VEPs and the measures of labs like that of Miller and Desimone.
“What this paper reveals is that everybody is right,” Bear quipped.
How so? The new data show that VEPs are very pronounced but transient spikes of neural electrical activity that occur amid a broader, overall lull of activity. Previous studies have reflected only the overall decrease because they have not had the temporal resolution to detect the brief spike. Bear’s team, meanwhile, has seen the VEPs for years but didn’t necessarily focus on the surrounding lull.
The new evidence suggests that what’s happening is that VEP is a sign of the activity of the brain quickly recognizing a familiar stimulus and then triggering an inhibition of activity related to it.
“What I think is exciting about this is that it suddenly sheds light on the mechanism, because it’s not that the encoding of familiarity is explained by the depression of excitatory synapses,” Bear said. “Rather, it seems to be accounted for by the potentiation of excitatory synapses on to neurons that then recruit inhibition in the cortex.”
Even as it advances that understanding of how VRM arises, the study still leaves open questions including the exact circuits involved. For instance, the […]
Aerobic plus strength training could help keep the brain young
Aerobic and strength training could help keep the brain young, a new study suggests. Image credit: Rob and Julia Campbell/Getty Images. Engaging in both aerobic exercise and strength training can improve cognitive performance in populations aged over 80 years, a new study suggests.
Participants who performed only cardio/aerobic exercise fared no better than people who were sedentary at mental acuity tests.
The study underscores the value of being physically active as long as possible as one reaches their later years.
A new study from the McKnight Brain Research Foundation , published in the journal GeroScience , finds that for people aged 80 years or older, a combination of cardio/aerobic exercise and strength training may improve cognition.
The study found that people who combined these two types of exercises exhibited higher cognitive performance than people who were sedentary and people who performed cardio exercise alone.
Individuals who engaged in cardio exercise along with strength training — regardless of duration and intensity — were more mentally agile, quicker at thinking, and also had a stronger ability to shift or adapt their thinking as necessary. What forms of exercise are best for cognitive performance?
The study involved 184 cognitively healthy individuals who were 85 to 99 years old, with a mean age of 88.49 years. Of this group, 98 were women. Their exercise regimens were self-reported, with 68.5% participating in some form of exercise.
Individuals were divided into three groups: people who were sedentary, people who did cardio exercise alone, and people who did both cardio exercise and strength training.
The cognition performance of participants was assessed according to the Montreal Cognitive Assessment battery of tests, designed to measure mild cognitive decline and early dementia signs.
The cardio plus strength training group had the highest overall cognitive performance scores.
The cardio plus strength training group scored significantly better than the sedentary group on coding and symbol search tests.
The cardio plus strength training group also scored significantly better than the cardio-alone group on symbol search, letter fluency, and Stroop Color-Word tests .
The cardio-only group’s test results were the same as the sedentary group. Risks of a sedentary lifestyle
“Aerobic and strength training are clearly helpful for older adults, even at an advanced age,” said Dr. Eric Lenze , professor and chair of psychiatry at Washington University School of Medicine, not involved in the current research.
“It’s not unusual,” noted Dr. Lenze, “to slow down with aging, but some degree of physical activity, like regular walking, is important for maintaining function — staying out of the nursing home!”
“Strength training can add to this benefit by keeping elders able to, for example, get up off the toilet. [Such capabilities] are vital for staying independent,” Dr. Lenze pointed out.
Brain health coach and director of the FitBrain Program at Pacific Neuroscience Institute in Santa Monica, Ryan Glatt , also not involved in the research, warned of the risks associated with a sedentary lifestyle: “The risks of sedentary behavior include sarcopenia (loss of muscle mass), reduced physical functioning, an increased risk of falls and fractures, and cognitive impairment.” Why exercise may support cognitive health
A cross-sectional study such as this looks only for associations. It cannot establish a causal link, such as one between cardio plus fitness and mental acuity. As Dr. Lenze put it, “the authors themselves were careful to describe this as exploratory.”
“It’s not clear how helpful [the exercises] are for improving cognitive function like memory, though,” Dr. Lenze added.
He noted, nonetheless, that both types of exercise “would be expected to improve brain health broadly by improving insulin sensitivity, reducing risk for heart attacks and strokes, and keeping people overall more active.”
Glatt suggested it may be that the two forms of activity affect different areas of the brain, saying: “Previous research has found that exercise benefits the brain in similar ways. However, certain types of exercise have been found to affect certain brain regions.”
“For example,” said Glatt, “prior research has found that resistance training can benefit the function and structure of the frontal lobe, while aerobic exercise can benefit the function and structure of brain regions responsible for memory, such as the hippocampus.” Cardio vs strength training
Cardio and aerobic exercises are essentially the same exercises viewed from different perspectives. Both increase a person’s heart rate while increasing the amount of oxygen the body uses.
For this reason, cardio/aerobic exercises can improve heart health and lung function.
Examples of cardio/aerobic exercise include walking, running, cycling, and swimming, or the use of cardio equipment such as rowing machines, elliptical trainers, treadmills, and stair climbers.
Strength training , or resistance training, involves causing your muscles to contract against some form of external resistance. Such resistance might be weights, resistance, bands or medicine balls, for example. The goal of strength training is to increase muscle mass and power, gain joint flexibility, and strengthen bones. How to exercise safely later in life For people in their 80s or 90s, care must be taken to avoid injury when exercising. Glatt said: “Everyone, regardless of age, can have different levels of physical functioning. It is therefore important to seek out guidance from a physical therapist or qualified fitness professional.” Dr. Lenze recommended exploring The National Institute on Aging website (NIA) for ideas about exercises that are appropriate for the elderly, although it is still wise to consult a fitness professional before beginning any new exercise program.NIA suggests that older individual: begin slowly with low-intensity exercises properly warm up before and cool down after exercise remain aware of surroundings when outside hydrate — drink water — before, during, and after exercise, even when one does not feel thirsty, as older individuals can be less sensitive to sensations of thirst take care to exercise in appropriate clothes and shoes discuss an exercise plan with your healthcare provider to avoid exacerbating specific health conditions.
Lightweight system captures brain activity while mice jump
A new lightweight device with a wisplike tether can record neural activity while mice jump, run and explore their environment. The open-source recording system, which its creators call ONIX, overcomes several of the limitations of previous systems and enables the rodents to move more freely during recording.
The behavior that ONIX allows brings to mind children running around in a playground, says Jakob Voigts , a researcher at the Howard Hughes Medical Institute’s Janelia Research Campus in Ashburn, Virginia, who helped build and test the system. He and his colleagues describe their work in a preprint posted on bioRxiv earlier this month.
To understand how the brain creates complex behaviors — such as those found in social interaction , sensory processing and cognition , which are commonly affected in autism — researchers observe brain signals as these behaviors unfold.
Head-mounted devices enable researchers to eavesdrop on the electrical chatter between brain cells in mice, rats and primates. But as the smallest of these animal models, mice present some significant challenges. Current neural recording systems are bulky and heavy, making the animals carry up to a fifth of their body weight on their skulls. Predictably, this slows the mice down and tires them out.
And most neural recording systems use a tether to relay signals from the mouse’s brain to a computer. But this tether twists and tangles as the mouse turns its head and body, exerting torque that the mouse can feel. Researchers must therefore periodically replace or untangle the tether. Longer tethers allow for more time to elapse between changeouts, but the interruptions still affect natural behavior. And battery-powered, wireless systems add too much weight.
Altogether, these challenges inhibit natural behaviors and limit the amount of time that recording can take place, preventing scientists from studying, for example, the complete process of learning a new task.
ONIX features a collection of engineering improvements to address these challenges. It includes a lower-profile design for the headstage, the head-mounted platform that holds the necessary electrical components for neural recordings.
The tether that relays data, supplies power and helps to control the headstage is extremely lightweight: A typical tether may be 1.8 millimeters in diameter, but this “micro-tether” is 0.4 millimeters. Finally, a device called a commuter responds to the mouse’s movements, actively untwisting the tether during recording.
To see how mice behave with ONIX, the researchers built a 3D arena of Styrofoam in hexagonal blocks, cut to different heights, akin to a miniaturized version of the basalt columns of the Giant’s Causeway in Northern Ireland. Five cameras recording from different angles around the arena captured the animals’ head positions, running speeds and locations.
Mice outfitted with the ONIX system and lightweight micro-tether explored faster than mice equipped with a standard system. The total area these mice explored and their head movements were indistinguishable from those of completely unencumbered mice.
During more than seven hours of recording, uninterrupted by tether changes, the mice jumped up to 15 centimeters from one Styrofoam column to another while researchers captured the animals’ neural activity. Mice with the heavier system and tether did not jump at all.
Different parts of the open-access ONIX system can be swapped out for similar components, enabling other researchers to adapt the system to specific experimental needs or even improve upon it as technology advances.
Cite this article: https://doi.org/10.53053/TFKO2184
30 Best Supplements for Focus and Concentration
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In a world inundated with distractions and demands, the pursuit of enhanced focus and concentration has become a paramount endeavor for many. Astonishingly, recent studies indicate that the average attention span has plummeted to just 8 seconds, shorter than that of a goldfish. Furthermore, in a survey conducted in 2021, a staggering 75% of respondents reported struggling with maintaining concentration during daily tasks. The demand for solutions to sharpen our cognitive faculties has never been greater, and in this comprehensive guide, we present the 30 best supplements meticulously selected to help you harness your mental prowess. Whether you’re seeking to boost productivity at work or unlock your full learning potential, our curated list will serve as your roadmap to a more focused and concentrated life. 30 Best Supplements for Focus and Concentration
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One a Day Active Focus Supplements Raw Science 5-HTP Focus & Memory Supplement Life Seasons – Focus-R – Concentration and Focus Supplement Dr. Emil Nutrition 2100mg Organic Lions Mane Mushroom Supplement Roman Focus Supplement FUJI ORCHARD Citicoline 250 mg Supplements Purely Optimal Premium Brain Supplement Elm & Rye Nootropics Supplements Nootropics are supplements that can enhance various cognitive functions, including focus and concentration. As we navigate through our increasingly busy lives, our attention spans are often put to the test. That’s where Elm & Rye Nootropics Supplements come in. Their specially formulated supplements contain natural ingredients that are shown to support brain function. By taking Elm & Rye Nootropics Supplements, you’ll promote healthy brain activity that can help you stay focused on the task at hand. Whether you’re studying for an exam, working on a project at the office or simply looking to improve your cognitive abilities, Elm & Rye Nootropics Supplements may help you achieve your goals. ONNIT Alpha Brain Premium Nootropic Brain Supplement The ONNIT Alpha Brain Premium Nootropic Brain Supplement is the perfect addition to your daily routine if you’re someone who needs an extra boost of focus and concentration. This supplement is made with a unique blend of natural ingredients that work together to support mental performance and clarity. It’s specifically designed to improve memory, focus, and overall cognitive function, helping you stay alert and sharp throughout even the busiest of days. If you’re looking for a way to enhance your mental abilities without relying on caffeine or other stimulants, this is the supplement for you. Try it out for yourself and see the difference it can make in your daily life. Peak Performance Alpha Day Nootropic Energy Supplement Are you looking for a way to increase your focus and concentration throughout the day? Peak Performance Alpha Day Nootropic Energy Supplement may be just the boost you need. This energy supplement is specifically formulated to improve cognitive function, providing you with the energy and mental clarity needed to tackle even the most challenging tasks. With a unique blend of natural ingredients, such as caffeine, ginseng, and ginkgo biloba, you can trust that this supplement will deliver the results you’re looking for. Ditch the afternoon slump and achieve peak performance with Alpha Day Nootropic Energy Supplement. NEURIVA Plus Brain Supplement for Memory and Focus If you’re looking for supplements to help boost your focus and concentration, NEURIVA Plus Brain Supplement might be just what you need. This supplement is designed to support brain health, improve memory, and enhance focus and clarity. Its active ingredients, including coffee fruit extract and phosphatidylserine, work together to promote cognitive function and provide long-lasting benefits. Whether you’re a student or a busy professional, NEURIVA Plus Brain Supplement can help you stay on top of your game by providing the cognitive support you need. Try it out and experience the results for yourself! NEURIVA Destress Brain Supplement for Focus, Concentration & Accuracy Modern life can be stressful, and sometimes it can feel like our minds are working overtime just to keep up with the demands of daily life. That’s where NEURIVA Destress Brain Supplement comes in, offering a helpful aid to support focus, concentration and accuracy. This supplement is specifically designed to combat the stresses of modern living, with a carefully chosen blend of natural ingredients such as ashwagandha and phosphatidylserine to help you stay on top of your game. Whether you’re studying for exams, working on a big project, or just trying to keep up with your busy schedule, NEURIVA Destress can help you achieve your goals by enhancing your mental clarity and reducing stress impact. With this powerful brain supplement, you can feel confident and focused, no matter what life throws your way. OLLY Ultra Strength Brain Softgels If you are looking for an effective way […]
Three new projects launched to map neuronal connections in the mouse and macaque brains
A complete map of all the connections in an entire mammalian brain may be in sight. Allen Institute researchers have just launched three new projects to construct large, detailed maps of neuronal connections in sections of the mouse and macaque brains, with an eye toward creating full wiring diagrams of these animals’ brains in the future. These projects are funded by the National Institutes of Health’s Brain Research Through Advancing Innovative Neurotechnologies ® (BRAIN) Initiative.
Allen Institute research teams will use the funding to: map the fine structures and connections in a 10mm 3 piece of the mouse brain using electron microscopy;
apply new, cutting-edge techniques known as BARseq and BRICseq to trace the long-range connections of hundreds of thousands of neurons in the macaque brain; and
scale up techniques that characterize brain cell types by 3D shape, electrical properties, and gene expression to better understand connectivity between different types of cells across the whole mouse brain.
Project 1: Enhancing transmission electron microscopy techniques to visualize brain cell shape and cell-to-cell connection networks of the mouse brain
Researchers will aim to scale and optimize a transmission electron microscopy (TEM) pipeline. The goal will be to use this pipeline to image an entire hemisphere of a mouse brain at 120 nanometer resolution and the cortical basal ganglia thalamic loop (up to 10 mm 3 ) in very fine detail to better understand how the mouse brain functions. Researchers will then assess whether this technology can be used to image an entire mouse brain-;a significant accomplishment that could provide a valuable roadmap for global neuroscience.
Transmission electron microscopy (TEM) is a technique in which a beam of electrons is shot through a tissue sample to create an extremely detailed image. “It’s become more and more clear over the last few years that most computations of the brain are actually happening, not in isolated areas, but in distributed networks that are brain wide; and so if we’re really going to understand how those kinds of computations work, we need to see the whole network, which means we need to see connections across the whole brain,” said Forrest Collman, Ph.D., Assistant Investigator at the Allen Institute.
Associate Investigator Nuno da Costa, Ph.D., notes that the potential impact for the broader scientific community is significant: “Think of it as a ‘Google Maps’ of every road, every house, and every door. If done properly, it’s a contribution that will last forever.”
Project 2: Mapping how brain cells are connected to one another using barcoded connectomics
For this project, scientists will map brain-wide connections by tracing the winding paths that axons and dendrites make as they reach out and connect to other brain cells. Think of these as the long arms and fingers of the brain cell radiating out of the cell body and reaching out to other cells across the entire brain to create networks. Researchers will trace these intricate paths using an innovative technique known as BARseq, which stands for barcoded anatomy resolved by sequencing.
It works by tagging each cell with a unique RNA barcode that makes it stand out in a cell population. By “connecting the dots” between each barcode, you can trace where and how far a brain cell-;namely its axons and dendrites-;extend.
It is much faster and more efficient than other techniques and can be combined easily with other data. We can actually map the whole macaque brain in a few years instead of 100 years. This is the main motivation.” Xiaoyin Chen, Ph.D., Assistant Investigator at the Allen Institute Project 3: Enhancing a Patch-seq pipeline to yield more data, faster results, and linking different datasets to uncover form and function in the whole mouse brain
It is critical to develop tools that link genetically defined cell types to brain-wide circuit diagrams to understand brain function. In this project, researchers will work to link genetic and circuit datasets by scaling and sharing technologies that measure features common to both datasets across the entire mouse brain.
Specifically, this project aims to enhance the Allen Institute’s ability to generate multi-dimensional data, using the Patch-seq method, and to capture the full structure of neurons from whole brain images through automation, machine vision modeling, and advanced computational techniques. Another key aim of the project is to share the tools they develop with the broader researcher community so that experts across the field can contribute to characterizing cell types and circuits across the whole mouse brain.
“We’re using more sophisticated machine learning-based approaches where you can create these deep neural networks to bring the morphological descriptions into alignment with transcriptomics, with the connectome data, and with the long-range projection data,” said Staci Sorensen, Ph.D., Associate Director of Neuroanatomy at the Allen Institute. “So far, we feel pretty excited about the results that we’re getting. I think it will work especially well at cell subclass levels.”
The Brain-Boosting MIND Diet – New Study Uncovers “Exciting” Improvement
The MIND diet study showed improvements in cognition over a three-year period, particularly during the first two years. Both the MIND diet group and the control group, focusing on calorie reduction, saw improvements, suggesting potential benefits from weight loss. The diet developed at RUSH is believed to help maintain brain health.
New research highlights the importance of a long-term commitment to the MIND diet for maximizing the benefits to brain health.
“The benefits within the new study’s three-year clinical trial weren’t as impressive as we’ve seen with the MIND diet observational studies in the past, but there were improvements in cognition in the short-term, consistent with the longer-term observational data,” said lead study author Lisa Barnes, Ph.D., associate director of the Alzheimer’s Disease Research Center at RUSH .
Results from the study, published in The New England Journal of Medicine , showed that within a three-year period, there was no significant statistical difference in change in cognition for participants in the MIND diet group compared to the usual diet control group; both groups were coached to reduce calories by 250 kilocalories per day. However, there was a significant improvement during the first two years of the study.
“What we saw was an improvement in cognition in both groups, but the MIND diet intervention group had a slightly better improvement in cognition, although not significantly better,” Barnes said. “Both groups lost approximately 5 kilograms over three years, suggesting that it could have been weight loss that benefited cognition in this trial.” ‘Exciting’ improvement
This is the first randomized clinical trial designed to test the effects of a diet thought to be protective for brain health, on the decline of cognitive abilities among a large group of individuals 65 years or older who did not have cognitive impairment. The MIND diet has been ranked among the top five diets by U.S. News & World Report annually for the last six years.
“There is established research that shows that a person’s diet affects health,” Barnes said. “The participants in this study had to have sub-optimal diets as determined by a score of 8 or less on a diet screening instrument before the study even began. It is reasonable to think that either they were going to maintain their cognition or decrease the rate of cognitive decline in the future.”
“It was exciting to see that there was an improvement in cognition over the first year or so, but it could have been due to practice effects on the cognitive tests, and we saw it for the control diet as well, which focused on just caloric restriction.”
Previous research by the late Martha Clare Morris, ScD, showed that there was a slower rate of decline among those who ate specific foods. Morris was a nutritional epidemiologist at RUSH and the original principal investigator of the MIND diet study that was funded by a $14.5 million National Institutes of Health grant and involved two clinical sites, RUSH in Chicago and Harvard School of Public Health in Boston.
In 2015, Morris and her colleagues at RUSH and Harvard University developed the MIND diet — which is short for Mediterranean-DASH Intervention for Neurodegenerative Delay — in preparation for the trial. The diet is based on the most compelling research on the foods and nutrients that affect brain health. As the name suggests, the MIND diet is a hybrid of the Mediterranean and DASH (Dietary Approaches to Stop Hypertension) diets. Both diets have been found to reduce the risk of cardiovascular conditions, such as hypertension, diabetes, heart attack, and stroke. In two studies published in 2015, Morris and colleagues found that the MIND diet could slow cognitive decline and lower a person’s risk of developing Alzheimer’s disease significantly, even if the diet was not followed meticulously. The study tracked 604 participants over three years
The latest trial of the MIND Diet for Prevention of Cognitive Decline in Older Persons, was a randomized, Phase III trial that enrolled 604 people who were overweight and had a suboptimal diet and a family history of Alzheimer’s disease. The trial compared two different diet interventions, both of which included dietary counseling with mild calorie restriction of 250 calories per day for weight loss.
Participants of both groups had individualized diet guidelines developed by dietitians, and they received regular phone and in-person consultations, as well as occasional group sessions over the three-year life of the study. Participants were seen five times during the three years to evaluate their mental abilities, blood pressure, diet, physical activity, health conditions, and medication use.
“Both groups of participants got a lot of support and accountability by trained registered dietitians,” said Jennifer Ventrelle, assistant professor in the Departments of Preventive Medicine and Clinical Nutrition and lead dietitian on the MIND diet trial at RUSH.
“The good news is that this helped all participants improve on average, but unfortunately hindered the ability to detect significant differences between the two groups in this relatively short period of time. Current and future research plans to look at people coached to follow the diet in this format compared to individuals following a usual diet in a format closer to usual care such as brief clinical encounters or a self-guided program with less support.”
“By the end of the study, the average weight loss was approximately 5.5% of initial body weight for all participants, exceeding the study target of 3%, the amount recognized as clinically significant to prevent or improve adverse health outcomes,” Ventrelle said.
“The average MIND score at the end of three years for the MIND group was 11.0 and 8.3 for the control group, placing both groups in a therapeutic range to slow cognitive decline and lower the risk for Alzheimer’s disease, according to previous studies. The significant weight loss and improved MIND scores suggest that the control group also improved their diet and may suggest that following the MIND diet at a score of at least 8.3, coupled with at least a 250-calorie reduction to produce weight loss, may improve cognition. More research is needed to confirm this.” Fish, chicken, […]
Musk’s Neuralink to test brain-chip in humans after FDA nod. How it’s meant to work & key concerns
Bengaluru: The US Food and Drug Administration (FDA) has given the green light to Neuralink, a company founded by Elon Musk, to conduct human trials in brain-computer interface (BCI) technology. This technology involves implanting a tiny chip in the brain that can read and interpret neural signals.
Founded in 2016, the company aims to treat brain diseases and eventually perform human enhancement and augmentation, where biological implants theoretically alter the body to improve physical and mental capabilities. It has been conducting trials in animals like monkeys and pigs since 2018.
However, the company has also faced criticism and scrutiny for its treatment of animals and its management practices. The US Department of Agriculture (USDA) even has the company under investigation for violating animal welfare laws through careless testing without safety.
Engineers and researchers have reportedly expressed concerns and criticisms over the Neuralink BCI project, stating that Musk’s demonstrated technology has been in existence since 2002 with other BCI projects and have criticised its ability to enhance brain functions without enough scientific knowledge about it.
His ideas for human enhancement, they said, could create more division in society by increasing inequality.
Last year, the FDA rejected Neuralink’s application for human testing, citing safety concerns over the device’s design and functionality. It raised doubts about the device’s ability to move in the brain without causing damage, to be removed safely, if needed, without brain tissue damage, and to operate with a lithium battery.
This month, the FDA approved human clinical trials for Neuralink.
Neuralink has been very secretive about its work and research, revealing only a few details to the public. In 2021, the company showed a video of a monkey playing a video game called Pong by using only its brain signals to control the cursor.
Neuralink is not the only player in the field of BCI. There are many other researchers and institutions that have been developing and using BCI for various purposes, including restoring vision, movement, and speech in people who have lost these abilities due to injury or disease.
ThePrint explains what BCI is, how it works, and what Neuralink plans to do with it.
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BCI is a technology that connects the brain with external devices, such as computers or robots, using electrical signals. The human brain produces oscillating patterns of activity, called brainwaves, that reflect different mental states. These brainwaves can be measured by an electroencephalogram or EEG.
BCIs — the development work of which began in the 1960s and 70s — can be invasive or non-invasive, depending on the objective.
Non-invasive BCI uses external equipment that can sense brain signals through an EEG without penetrating the skull, and then use those signals to control external objects. The first non-invasive EEG control of a physical object was performed in 1988.
Two years later, bidirectional control was established, where an external source could modify the brain signal as well. Devices were able to induce a state of expectation in the brain, thus modifying brainwaves as well.
Invasive BCI, which became popular in the 2000s, involves surgically implanting a chip or a fibre into the brain that can directly read and write neural signals.
Many labs and universities have shown monkeys and rats with implants being able to perform tasks on external objects with their neural signals alone, or by just thinking about it.
These neural signals have also been captured by computers, which then decode them and transmit them to motor or movement neurons, recovering mobility in impaired animals and people.
A similar process is used to restore vision, as well as recording typed language output in people without arms and/or spinal cord injuries. Concerns and limitations
BCI is a very expensive and complex technology and has many limitations and dangers.
For example, volunteers in experiments with BCIs have to remain very still, and there are unknown long-term effects of having a chip in the brain. There is also a high risk of misuse or abuse of the technology.
For the future, there are already many ethical and social issues related to BCI. There are concerns around mind reading and lack of privacy, as well as the ability to track an individual and use technology to gain information. It could also lead to greater discord in society through abuse or selective use of the technology.
There are also ethical concerns around informed consent from those who are impaired in communication or are in ‘vegetative states’ (brain dysfunction) or coma, and worries about equitable access.
While today the technology is limited to very basic and experimental benefits, Musk has reportedly stated that he founded Neuralink because he believes artificial intelligence to be a “threat to humanity”. For the future, he envisions the device to be similar to a video game where the brain reverts to the last saved state.
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The company, which is headquartered in California, was founded in 2016 by a team of eight members, including Musk and seven other scientists and engineers. It conducts research in partnership with the University of California Davis.As of 2023, only two of the original team of the eight remain with the company.In January last year, the company was reportedly criticised for its work culture of “blame and fear” and mismanagement.In February last year, Neuralink was hit with accusations that the company along with UC Davis had mistreated several monkeys and subjected them to physical and psychological distress as well as chronic and painful infections from surgeries, which was reported widely.Among 23 macaque monkeys involved in research, the complaints by the Physicians Committee for Responsible Medicine, an animal-welfare-in-research advocacy group, reportedly stated that 15 died or were euthanised, and that evidence for this was withheld.Neuralink, according to a Reuters report, stated that macaque monkeys died and were euthanised after experimentation and not during experiments. It also denied that animal abuse had […]
Brain’s Dual-Chemical Switch for Attention Revealed
Summary: Researchers have unveiled the brain’s chemical mechanism behind our attention span.
Historically, the neurotransmitter acetylcholine was considered the sole regulator of attention. Yet, this study shows that gamma-aminobutyric acid (GABA) collaborates with acetylcholine, toggling like a ‘switch’ in the brain’s claustrum region to filter essential information from noise.
This breakthrough can aid in therapies for concentration-related disorders.
Key Facts:
> Besides the known neurotransmitter acetylcholine, GABA also plays a crucial role in attention span regulation.
The claustrum acts as an attention-regulating hub where acetylcholine and GABA toggle the transfer of brain information.
This discovery might lead to enhanced treatments for attention disorders like ADHD and depression.
Source: NTU
A team of researchers from Nanyang Technological University, Singapore (NTU Singapore) has uncovered new clues about how chemicals released by brain cells regulate our attention span.
Findings from the study could pave the way for new therapies to treat neurological conditions associated with concentration difficulties, such as depression and attention-deficit hyperactivity disorder (ADHD). The opposing actions of the neurotransmitters (acetylcholine and GABA) on neurons in the claustrum enable brain signals to be encoded efficiently, allowing the brain to pay attention and ignore noise. Credit: Neuroscience News To communicate with one another, neurons in the brain and nervous system release chemicals called neurotransmitters that relay messages from one cell to another. Neurotransmitters are crucial for brain function and regulating all bodily functions, ranging from breathing and heart rate to reproduction.
These chemicals also coordinate cognitive processes that enable us to focus on important information within the constant barrage of stimuli the brain receives from the external environment, otherwise known as our attention span.
Researchers have long thought that our attention span was directed by only one neurotransmitter, acetylcholine, which excites neurons and causes them to fire electrical signals. However, recent work suggests that attention could require another neurotransmitter, gamma-aminobutyric acid (GABA), which inhibits neurons from receiving and sending messages.
In their study published in the Proceedings of the National Academy of Sciences (PNAS), the team demonstrated for the first time that GABA works together with acetylcholine in a precise sequence to regulate the transmission of signals from a part of the brain’s information processing network, called the claustrum.
Hidden deep in the brain, the claustrum is a thin sheet-like structure that receives and processes information from different parts of it. The claustrum helps to regulate concentration, but its exact role remains unknown.
Neurotransmitters toggle ‘like a switch’ to relay information
In lab experiments, the NTU scientists investigated how neurons in the claustrum in mice respond to acetylcholine and GABA produced by a part of the brain called the forebrain, that plays a central role in several brain functions.
The key technological advance that allowed the researchers to make this discovery is called optogenetics . Optogenetics uses light-sensitive proteins to selectively control the activity of specific types of neurons within the brain. In this case, the neurons within the forebrain that release acetylcholine and GABA were activated by light, allowing the team to measure the response of the claustrum to such a stimulus.
They discovered that two types of neurons in the claustrum, which send output signals to different parts of the brain, respond in opposing ways to acetylcholine and GABA. Neurons that extend to structures deep in the brain were excited by acetylcholine while neurons that extend to structures on the surface of the brain were inhibited by GABA.
Through this coordinated sequence of opposing actions, the two neurotransmitters toggle the transfer of information between the claustrum and the rest of the brain, like a switch. The study provides evidence that the neurotransmitters regulate a “microcircuit” in the brain, that allows the organ to differentiate important information from noise, helping a person pay attention.
The opposing actions of the neurotransmitters ( acetylcholine and GABA) on neurons in the claustrum enable brain signals to be encoded efficiently, allowing the brain to pay attention and ignore noise.
First author Mr Aditya Nair, former researcher at LKCMedicine and a current Ph.D. student at Caltech, said, “Our study advances our understanding of the claustrum’s role in directing attention span. Understanding how the claustrum regulates attention span at the cellular level also provides a window into other areas regulated by similar signalling pathways, such as arousal and learning.”
Lead investigator and neuroscientist Professor George Augustine from NTU’s Lee Kong Chian School of Medicine (LKCMedicine) said, “By understanding how acetylcholine and GABA work together to direct our attention, new and more effective therapies may be developed in the future to improve the attention span of patients with conditions such as ADHD and depression.”
Commenting as an independent expert, Dr Geoffrey Tan, Consultant (Psychiatry) Clinician-Scientist at the Institute of Mental Health Singapore, said, “Directing attention and multi-tasking are crucial cognitive processes for everyday functioning that require toggling between networks or circuits in the brain.
This study identifies a ‘switch’ in the claustrum that provides a mechanism by which acetylcholine may drive computations such as these. It is timely as we increasingly incorporate brain networks into how we think about cognition, psychiatric conditions and even interventions like mindfulness.”
The next steps for this project will be to determine how altering the dual-transmitter switch alters attention and brain disorders that affect attention, such as ADHD. It will also be important to determine whether the switch mechanism applies to other brain processes, such as arousal and learning. About this neuroscience research news
Author: Junn Loh Source: NTU Contact: Junn Loh – NTU Image: The image is credited to Neuroscience News Original Research: Open access. “ A functional logic for neurotransmitter corelease in the cholinergic forebrain pathway ” by Aditya Nair et al. PNAS Abstract A functional logic for neurotransmitter corelease in the cholinergic forebrain pathway The cholinergic system of the basal forebrain plays an integral part in behaviors ranging from attention to learning, partly by altering the impact of noise in neural populations.The circuit computations underlying cholinergic actions are confounded by recent findings that forebrain cholinergic neurons corelease both acetylcholine (ACh) and GABA.We have identified that corelease of ACh and GABA by […]
New brain biomarker predicts recovery from treatment-resistant depression
Using a novel deep brain stimulation (DBS) device capable of recording brain signals, researchers have identified a pattern of brain activity or “biomarker” related to clinical signs of recovery from treatment-resistant depression. The findings from this small study are an important step towards using brain data to understand a patient’s response to DBS treatment. The study was published in Nature and supported by the National Institutes of Health’s Brain Research Through Advancing Innovative Neurotechnologies ® Initiative, or The BRAIN Initiative ® .
Although the approach is still experimental, clinical research shows that DBS can be used safely and effectively to treat cases of depression in which symptoms have not improved with antidepressant medications, referred to as treatment-resistant depression. People receiving DBS undergo surgery to have a thin metal electrode implanted into specific brain areas to deliver electrical impulses that modulate brain activity. How exactly DBS improves symptoms in people with depression is not well-understood, which has made it difficult for researchers to objectively track patients’ response to treatment and adjust as needed.
The small study enrolled 10 adults with treatment-resistant depression, all of whom underwent DBS therapy for six months. Each participant received the same stimulation dose to begin and then stimulation levels were increased once or twice. Later, researchers used artificial intelligence (AI) tools to analyze collected brain data from six patients and observed a common brain activity signature or biomarker that correlated with patients self-reporting feeling symptoms of depression or stable as they recovered. In one patient, researchers identified the biomarker and were retrospectively able to predict that a patient would fall back into a major depressive episode four weeks before clinical interviews showed they were at risk of a relapse occurring. This study demonstrates how new technology and a data-driven approach can refine DBS therapy for severe depression, which can be debilitating. It’s this type of collaborative work made possible by the BRAIN Initiative that moves promising therapies closer to clinical use.” John Ngai, Ph.D., Director of the BRAIN Initiative In the study, patients received DBS targeting the subcallosal cingulate cortex (SCC), a brain region that regulates emotional behavior and is involved in feelings of sadness. DBS of the SCC is an emerging therapy that can provide stable, long-term relief from depressive symptoms for years. However, using DBS to treat depression remains challenging because each patient’s path to stable recovery looks different. Clinicians also must rely on subjective self-reports from patient interviews and psychiatric rating scales to track symptoms, which can fluctuate over time. This makes it hard to distinguish between normal mood variations and more serious situations requiring a tweak in stimulation. In addition, changes in symptoms in response to DBS can take weeks or months to occur, making it difficult to tell how well the therapy is working.
“This biomarker suggests that brain signals can be used to help understand a patient’s response to DBS treatment and adjust the treatment accordingly,” said Joshua A. Gordon, M.D., Ph.D., director of NIH’s National Institute of Mental Health. “The findings mark a major advance in translating a therapy into practice.”
The patients in the study responded well to DBS therapy; after six months, 90% showed a significant improvement in depression symptoms, and 70% were in remission or no longer depressed. This high response rate was a unique opportunity to look back and examine how each patient’s brain responded differently to the stimulation during treatment.
Christopher Rozell, Ph.D., Julian T. Hightower Chair and professor of electrical and computer engineering at Georgia Tech in Atlanta, and his colleagues used a technique called explainable artificial intelligence to understand these subtle changes in brain activity. The algorithm used brain data to distinguish between depressive versus stable recovery states and was able to explain what activity changes in the brain were the main drivers of this transition. Importantly, the biomarker also distinguished between normal day-to-day transient mood changes and sustained worsening symptoms. This algorithm could provide clinicians with an early warning signal that a patient is moving toward a highly depressive state and requires a DBS adjustment and extra clinical care.
“Nine out of 10 patients in the study got better, providing a perfect opportunity to use a novel technology to track the trajectory of their recovery,” said Helen Mayberg, M.D., director of the Nash Family Center for Advanced Circuit Therapeutics at Icahn Mount Sinai in New York City and co-senior author of the study. “Our goal is to identify an objective, neurological signal to help clinicians decide when, or when not, to make a DBS adjustment.”
“We showed that by using a scalable procedure with single electrodes in the same brain region and informed clinical management, we can get people better,” said Dr. Rozell, co-senior author of the study. “This study also gives us an amazing scientific platform to understand the variation between patients, which is key to treating complex psychiatric disorders like treatment-resistant depression.”
Next, the team analyzed data from MRI brain scans collected from patients before surgery. The results revealed structural and functional abnormalities in the specific brain network targeted by the DBS therapy. More severe white matter deficits were related to longer recovery times.
Researchers also used AI tools to analyze changes in facial expression extracted from videos of participant interviews. In a clinical setting, a patient’s facial expression can reflect the severity of their depression symptoms, a change that psychiatrists likely pick up on in routine clinical evaluations. They found patterns in individual patient expressions that coincided with their transition from illness to stable recovery. This could serve as an additional tool and new behavioral marker to track recovery in DBS therapy. More research is needed to determine whether the video analysis can reliably predict current and future disease states.
Both the observed facial expression changes and anatomical deficits correlated with cognitive states captured by the biomarker, supporting the use of this biomarker in managing DBS therapy for depression.
The research team, including Drs. Mayberg and Rozell, and Patricio Riva-Posse, M.D., at Emory University School of Medicine in Atlanta, is now confirming their findings in a second cohort […]
Brain stimulation could boost maths ability – study
Using electrodes to ‘excite’ certain areas of the brain could help people who struggle with maths enjoy the subject more, a study has suggested (Alamy/PA) Using electrodes to “excite” certain areas of the brain could help people who struggle with maths enjoy the subject more, a study has suggested.
A team spanning the universities of Surrey and Oxford , Loughborough University , and Radboud University in the Netherlands investigated the impact of neurostimulation on learning.
High-frequency random noise stimulation, also known as tRNS, works by sending a mild electrical current to the brain through two electrodes on the scalp. Previously, we have shown that a person’s ability to learn is associated with neuronal excitation in their brains
Roi Cohen Kadosh, a professor of cognitive neuroscience and head of the School of Psychology at the University of Surrey led the project. Recommended
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He said: “ Learning is key to everything we do in life – from developing new skills, such as driving a car, to learning how to code. Our brains are constantly absorbing and acquiring new knowledge.
“Previously, we have shown that a person’s ability to learn is associated with neuronal excitation in their brains. What we wanted to discover in this case is if our novel stimulation protocol could boost, in other words excite, this activity and improve mathematical skills.”
Some 102 people were recruited for the study – published in the journal Plos Biology – with their mathematical skills assessed beforehand.
They were split into four groups, including a learning group and an ‘overlearning’ group – in which people practised sums “beyond the point of mastery” – while being exposed to high-frequency random electrical noise stimulation.
The other two groups were exposed to a placebo, which researchers said was similar to real stimulation but without significant electrical currents.
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Brain activity was measured via an electroencephalogram (EEG) recording at the beginning and end of the stimulation. This discovery could not only pave the way for a more tailored approach in a person’s learning journey but also shed light on the optimal timing and duration of its application
The team found the ability of those whose brains were less “excited” by maths during the assessment had improved post-stimulation.
There was no change in those who performed well in the initial assessment, nor in those included in the placebo groups.
Prof Cohen Kadosh added: “What we have found is how this promising neurostimulation works and under which conditions the stimulation protocol is most effective. Recommended
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“This discovery could not only pave the way for a more tailored approach in a person’s learning journey but also shed light on the optimal timing and duration of its application.”
Dr Nienke van Bueren from Radboud University, who led the study under Prof Cohen Kadosh’s supervision, said: “These findings highlight that individuals with lower brain excitability may be more receptive to electrical noise stimulation, leading to enhanced learning outcomes, while those with high brain excitability might not experience the same benefits in their mathematical abilities.”
A mouse with 100,000 human neurons in its brain illuminates the enigma of Alzheimer’s
When a person gets older and begins to lose his or her memory, even to forget the names of their loved ones, it is already too late. Alzheimer’s has been quietly destroying the brain for years. If you could open the skull, you would see dead neurons and accumulations of two characteristic proteins: amyloid and tau. The disease threatens to wipe out civilization in the coming decades — there are 10 million new cases of dementia every year — but the scientific community still has no idea what causes it. An international team, including Spanish neuroscientist Amaia Arranz, has introduced 100,000 human neurons into the brains of mice to try to investigate in vivo what happens during the advance of Alzheimer’s disease. The authors have observed how the cells perish and have managed to avoid this neuronal death with a simple oral treatment. Their breakthrough was published Thursday in the journal Science .
Mice are not susceptible to Alzheimer’s, but the researchers genetically modified them to suffer from an accumulation of the amyloid protein. By introducing human neurons into the brains of these rodents, the scientists were able to identify the exact mechanism of neuronal destruction: activation of the MEG3 gene induces necroptosis, a genetically programmed cell death, which is also present in cancer. A drug approved for the treatment of leukemia, ponatinib, and another for melanoma, dabrafenib, prevented neuronal death in these mice. The anti-inflammatory necrosulfonamide achieves the same effect. “There are still no drugs that cure or help alleviate the symptoms of Alzheimer’s disease. This study could help to find therapies that prevent the loss of neuronal cells,” says Arranz of the Achúcarro Basque Center for Neuroscience in Bilbao.
The work was carried out in the laboratory of Belgian biologist Bart De Strooper, of the VIB-KU Leuven Center for Brain & Disease Research (CBD). Arranz and fellow scientist Ira Espuny participated at the CBD in 2017 in the development of the first mouse with human neurons that recreated something similar to Alzheimer’s. The new study has gone a step further by implanting both human and mouse neurons in the rodents. The human neurons immediately showed the hallmarks of the disease: tau and amyloid proteins and cell death. The mouse neurons, on the other hand, remained intact. In the authors’ opinion, these results reveal “a human-specific vulnerability to Alzheimer’s disease .”
The brain of a mouse is the size of a pea, weighs half a gram and contains about 70 million neurons. Arranz explains that the 100,000 implanted human neurons remain in a very specific region. “The mouse brain is still a mouse brain, with a little piece where there are human cells. We are not going to create monsters or Frankensteins,” says the neuroscientist. Her research center is named after Nicolás Achúcarro, a Spanish physician who was working in Munich in Alois Alzheimer’s laboratory when the German neurologist described a new disease in 1906, based on the case of a 50-year-old woman with memory loss issues. More than a century later, mankind continues to ignore the causes of Alzheimer’s disease.
Biologist Estela Area Gómez won last year’s Oskar Fischer Prize for postulating a hypothesis that links neuronal death in Alzheimer’s disease to failures in cholesterol metabolism. In her opinion, the scientific community has been stuck for decades on a false premise: that deposits of amyloid and tau proteins are responsible for dementia. The researcher recalls that the Colombian neurologist Francisco Lopera found two people with an aggressive genetic mutation that condemned them to suffer early Alzheimer’s , but they remained healthy for years due to other protective mutations. “Those patients had a lot of amyloid plaques. In other words, it has been shown that it is not the amyloid plaques that lead to the disease,” says Gómez, of the Margarita Salas Center for Biological Research in Madrid.
Gómez is skeptical about the conclusions of the new study, in which she did not participate. “These mice, at a technical level, are wonderful, but I have serious doubts as to whether they really reflect what happens in humans,” she says. “It’s like if you want to make a mouse that models a covid infection and, instead of infecting it with the cause — the coronavirus — you decide you’re just going to induce an increase in fever. What you’re doing is mirroring the symptoms of the disease in the mouse, but not the disease per se.”
Two years ago, the United States authorized aducanumab , touted as the first drug to attack the presumed causes of Alzheimer’s disease. The drug — developed by the U.S. pharmaceutical company Biogen and priced at about $42,500 euros per patient per year — eliminates the amyloid proteins that accumulate between neurons. The European Medicines Agency, however, has refused to approve aducanumab because it found no evidence of its efficacy.
“My question is how long are we going to continue investing all our efforts in eliminating amyloid plaques, when we are seeing that there are people with three, four or five times more amyloid plaques than an Alzheimer’s patient and they have no cognitive defects,” says Gómez. The biologist recalls that carrying the APOE4 gene multiplies the risk of suffering from Alzheimer’s and is related to cholesterol metabolism. “Nature is shouting at us that the failure of cholesterol metabolism in neurons is one of the causes, if not the main cause, of Alzheimer’s.”
De Strooper founded the prestigious Dementia Research Institute in the UK in 2016, where he directed the work of over 800 scientists until last year. The Belgian is one of the world’s leading experts on Alzheimer’s. His study suggests that understanding the molecular intricacies of neuronal resistance in mice to the disease will illuminate the path to protecting the human brain.
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Brain inspires more robust AI
image: To our eyes the input images x1 and x2 look the same, but hidden features nudge a typical neural network to classify this bird image as a monkey by mistake. It’s said the images are distant at the input space, but close in the hidden-layer space. The researchers aimed to close this exploit. view more Credit: ©2023 Ohki & Ukita CC-BY Most artificially intelligent systems are based on neural networks, algorithms inspired by biological neurons found in the brain. These networks can consist of multiple layers, with inputs coming in one side and outputs going out of the other. The outputs can be used to make automatic decisions, for example, in driverless cars. Attacks to mislead a neural network can involve exploiting vulnerabilities in the input layers, but typically only the initial input layer is considered when engineering a defense. For the first time, researchers augmented a neural network’s inner layers with a process involving random noise to improve its resilience.
Artificial intelligence (AI) has become a relatively common thing; chances are you have a smartphone with an AI assistant or you use a search engine powered by AI. While it’s a broad term that can include many different ways to essentially process information and sometimes make decisions, AI systems are often built using artificial neural networks (ANN) analogous to those of the brain. And like the brain, ANNs can sometimes get confused, either by accident or by the deliberate actions of a third party. Think of something like an optical illusion — it might make you feel like you are looking at one thing when you are really looking at another.
The difference between things that confuse an ANN and things that might confuse us, however, is that some visual input could appear perfectly normal, or at least might be understandable to us, but may nevertheless be interpreted as something completely different by an ANN.
A trivial example might be an image-classifying system mistaking a cat for a dog, but a more serious example could be a driverless car mistaking a stop signal for a right-of-way sign. And it’s not just the already controversial example of driverless cars; there are medical diagnostic systems, and many other sensitive applications that take inputs and inform, or even make, decisions that can affect people.
As inputs aren’t necessarily visual, it’s not always easy to analyze why a system might have made a mistake at a glance. Attackers trying to disrupt a system based on ANNs can take advantage of this, subtly altering an anticipated input pattern so that it will be misinterpreted, and the system will behave wrongly, perhaps even problematically. There are some defense techniques for attacks like these, but they have limitations. Recent graduate Jumpei Ukita and Professor Kenichi Ohki from the Department of Physiology at the University of Tokyo Graduate School of Medicine devised and tested a new way to improve ANN defense.
“Neural networks typically comprise layers of virtual neurons. The first layers will often be responsible for analyzing inputs by identifying the elements that correspond to a certain input,” said Ohki. “An attacker might supply an image with artifacts that trick the network into misclassifying it. A typical defense for such an attack might be to deliberately introduce some noise into this first layer. This sounds counterintuitive that it might help, but by doing so, it allows for greater adaptations to a visual scene or other set of inputs. However, this method is not always so effective and we thought we could improve the matter by looking beyond the input layer to further inside the network.”
Ukita and Ohki aren’t just computer scientists. They have also studied the human brain, and this inspired them to use a phenomenon they knew about there in an ANN. This was to add noise not only to the input layer, but to deeper layers as well. This is typically avoided as it’s feared that it will impact the effectiveness of the network under normal conditions. But the duo found this not to be the case, and instead the noise promoted greater adaptability in their test ANN, which reduced its susceptibility to simulated adversarial attacks.
“Our first step was to devise a hypothetical method of attack that strikes deeper than the input layer. Such an attack would need to withstand the resilience of a network with a standard noise defense on its input layer. We call these feature-space adversarial examples,” said Ukita. “These attacks work by supplying an input intentionally far from, rather than near to, the input that an ANN can correctly classify. But the trick is to present subtly misleading artifacts to the deeper layers instead. Once we demonstrated the danger from such an attack, we injected random noise into the deeper hidden layers of the network to boost their adaptability and therefore defensive capability. We are happy to report it works.”
While the new idea does prove robust, the team wishes to develop it further to make it even more effective against anticipated attacks, as well as other kinds of attacks they have not yet tested it against. At present, the defense only works on this specific kind of attack.
“Future attackers might try to consider attacks that can escape the feature-space noise we considered in this research,” said Ukita. “Indeed, attack and defense are two sides of the same coin; it’s an arms race that neither side will back down from, so we need to continually iterate, improve and innovate new ideas in order to protect the systems we use every day.”
###
Journal article: Jumpei Ukita and Kenichi Ohki. “Adversarial attacks and defenses using feature-space stochasticity ”, Neural Networks , DOI: 10.1016/j.neunet.2023.08.022
Funding:
This work was supported by Brain Mapping by Integrated Neurotechnologies for Disease Studies (Brain/MINDS) from Japan Agency for Medical Research and Development (AMED) (14533320, JP16dm0207034, JP20dm0207048 to K.O.); CREST-JST (JPMJCR22P1 to K.O.); Institute for AI and Beyond (to K.O.); JSPS KAKENHI (25221001, 19H05642, 20H05917, to K.O.); Takeda Science Foundation (to J.U.); and Masayoshi Son Foundation (to J.U.).
Departmental links:
Ohki Lab – https://physiol1.m.u-tokyo.ac.jp/ern24596/en/
[…]
France suspends iPhone 12 sales over concerns of high electromagnetic radiation emissions
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France’s National Frequency Agency (ANFR) has ordered Apple to halt sales of the iPhone 12 on the French market following recent tests showing that the phone model is emitting electromagnetic waves exceeding levels acceptable to the country’s regulatory limits .
The move gives Apple 15 days to correct the issue and bring the iPhone 12’s specific absorption rate (SAR) within acceptable levels. The ANFR has urged the tech giant to implement all available means quickly to remedy the malfunction before a full recall of the copies already sold begins. (Related: Apple warns users with medical devices to keep iPhones away from body because they emit EMF .)
The ANFR monitors public exposure to electromagnetic waves using SAR – the measurement that determines electromagnetic waves transported and absorbed by the human body when a phone is in a pocket or in the hand – with the limit placed at four watts per kilogram (w/kg).
The agency recently tested 141 phones, including the iPhone 12, and found that the iPhone 12 exceeded the limit with a reading of 5.74 w/kg and ordered Apple to quickly fix the issue, which could possibly be achieved through a simple software update.
” The rule is the same for everyone , including the digital giants,” said French Minister of Digital and Telecommunications Jean-Noel Barrot. French newspaper Le Parisien even noted that French officials are willing to recall every single iPhone 12 in France, including units that have already been sold.
Barrot said a software update would be sufficient to fix the radiation issues linked to the iPhone model , which the company has been selling since 2020. “Apple is expected to respond within two weeks. If they fail to do so, I am prepared to order a recall of all iPhone 12s in circulation,” he added.
The European Union (EU) has set safety limits for SAR values linked to exposure to mobile phones, which could increase the risk of some forms of cancer according to scientific studies. In 2020, France widened regulations requiring retailers to display the radiation value of products on packaging beyond cellphones, including tablets and other electronic devices.
Barrot assured users that the European standard for electromagnetic emissions is 10 times lower than the levels that scientific studies have established as consequential for users.
The French watchdog ANFR will now pass on its data findings to regulators in other EU member countries
“In practical terms, this decision could ‘snowball’ the restrictive measures,” Barrot said.
ANFR agents have been instructed to ensure that the iPhone 12 is no longer offered for sale through any distribution channel in France. EMFs in radio frequency range pose danger to human health
The International Agency for Research on Cancer (IARC) has classified non-ionizing EMFs in the radio frequency range as Group 2B – a possible human carcinogen . These fields are produced by electronic products, like Bluetooth devices, cellphones, computers, smart devices, smart meters, tablets and wireless routers.
The current IARC evaluation from 2011 pointed to a possible link between RF radiation and cancer in people – particularly glioma, a malignant type of brain cancer. This conclusion means that there could be some risk.
Some researchers feel there’s already enough evidence of harm from long-term, low-level exposure to non-ionizing radiation that the IARC should upgrade the classification to a Group 1 – a known carcinogen.
In a multicenter study published in the International Journal of Epidemiology , researchers followed cancer rates and cellphone use in more than 5,000 people in 13 countries and found a “loose connection” between the highest rate of exposure and glioma – which were more often found on the same side of the head people used to speak on the cellphone.
Another review of more than two dozen studies on low-frequency EMFs published in the Journal of Chemical Neuroanatomy suggested that these energy fields may cause neurological and psychiatric problems in people.
That being said, the best approach is to be aware that EMFs exist and be smart about your exposure. Experts say this is a developing field of research that will undoubtedly expand as the use of wireless devices and labor-saving machines increases.
Radiation.news has more on the dangers of smartphones.
Watch the following video on the dangers of smartphone radiation . Screen radiation Combined with Cell phone radiation is like morphine and Marijuana ararwana
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This video is from the EMF Safety Co channel on Brighteon.com . More related stories:
Radio signals from mobile phone towers could lead ALIENS to Earth .
SGT Report: 5G towers, smart phones and mRNA injections are inextricably connected .
“Substantial scientific evidence” shows that RF radiation from mobile phones causes cancer . Sources include: Barrons.com TheMessenger.com Reuters.com IARC.WHO.int PubMed.NCBI.NLM.NIH.gov 1 PubMed.NCBI.NLM.NIH.gov 2 Brighteon.com
Unhealthy pathobiome in the brain could cause some forms of Alzheimer’s and related dementias
The human microbiome includes the genetic material of more than 100 trillion tiny microorganisms – fungi, yeast, bacteria, and even viruses, most of which hang out in our gastrointestinal tract to serve as guardians of our health. But when a healthy microbiome gives way to an imbalance -; a “pathobiome” -; any number of health problems can occur -; from rheumatoid arthritis, to bacterial vaginosis. New data published this month in the journal Frontiers in Cellular and Infection Microbiology , from researchers at Drexel’s College of Medicine, gives more evidence to the possibility that developing a pathobiome in the brain could cause some forms of Alzheimer’s and related dementias.
When biomes turn unhealthy, either by invasion of outside pathogens, or a major change in the relative numbers of the microbial species present, a dysbiosis, or imbalance in the microbiota, occurs. This dysbiosis can alter human metabolism and cause inflammation, which has been linked to the tissue damage seen in ulcerative colitis, rheumatoid arthritis and many other chronic inflammatory diseases.
Studying 130 samples from the donated brains of 32 people – 16 with Alzheimer’s and 16 age-matched controls without the disease, the Drexel researchers found bacterial flora in all the brains-; but the Alzheimer’s brains showed profoundly different bacterial profiles compared to their age-matched controls.
The group used full-length 16s ribosomal RNA gene sequencing, a technique that can detect any and all bacterial species present in a sample. In this process, the researchers pinpointed disease-specific sets of bacteria in almost all of the Alzheimer’s-affected brains, suggesting these groups of bacteria are strong predictors of the disease.
The authors detected five brain microbiomes, four that are hypothesized to be present at different times in the evolution of the Alzheimer’s-afflicted brains. The authors said it is likely that the observed Alzheimer’s microbiomes evolve to become more pathogenic as the disease progresses with the later stages characterized as a pathobiome. The authors hypothesize that the brain begins with a healthy biome, but as the disease develops, the healthy biome is supplanted as a new set of microbes replace the original healthy ones with the eventual emergence of the Alzheimer’s pathobiome.
Samples from both sets of brain samples were drawn from the frontal and temporal lobes and entorhinal cortex. Based on the random distribution of microbiomes requiring delivery all over the brain, the results were consistent with failure in one or more of the brain’s networks; however it too soon to tell if the observed distribution patterns result from a leaky blood-brain barrier, the brain’s glymphatic system, or synaptonemal transmission that allowed bacteria, including Cutibacterium acnes (formerly called Proprionibacterium acnes ), Methylobacterium, Bacillus, Caulobacter, Delftia, and Variovora to enter the brain. In Alzheimer’s brain samples, the researchers noted, these pathogenic bacteria appeared to have overpowered and replaced Comamonas sp. bacteria, which are associated with a dementia-free brain. Perhaps destruction of the Comamonas bacteria, part of a healthy brain microbiome, is the first sign of impending dementia. We’re now coming up with the questions to guide future studies, but the hypotheses are many. The culprit could be bacteria or something else – like fungi, parasites, or viruses – at the same time.” Garth D. Ehrlich, PhD, professor in the College of Medicine, senior author of the paper When a patient has Alzheimer’s, they experience inflammation in the brain characterized by deposits of amyloid beta which are formed by an increase in the production of the Aβ peptide (an antimicrobial peptide, which is part of the innate immune response) resulting in amyloid plaques in the brain. Similarly, Alzheimer’s is characterized by tau protein tangles found with the cells which are characterized by abnormal phosphorylation which ultimately lead to the destruction of synapses and neurons, but which have also been demonstrated to help stop the spread of pathogens in the brain.
These protein-oriented pathologies – known as the “amyloid cascade hypothesis”-; have been the main focus of Alzheimer’s research for decades. Recently, studies are challenging that model by suggesting a role for bacteria, fungi and viruses, and immune system and brain inflammation, which some researchers call the “pathogen hypothesis.”
“Multiple studies have now shown the presence of bacteria in Alzheimer’s-afflicted brains,” said Jeffrey Lapides, PhD, an adjunct associate professor in the College of Medicine, and a senior author of the study. “Perhaps plaques, whose constituents have anti-microbial properties in vitro, aren’t the direct cause of Alzheimer’s, but instead are a response to bacteria in the brain – some benign, some pathogenic, perhaps causing damage that has not yet resulted in cognitive deficits, making them part of the pathobiome.”
This unique set of bacteria found in the Alzheimer’s-afflicted brains are also commonly found in brains afflicted with the neurodegenerative disease amyotrophic lateral sclerosis, or ALS — suggesting that this set of bacteria may contribute to more than one neurological illness.
The next step for this research, according to the authors, is to study the possible contributions of other microbes and figure out what happened, physiologically, in the brain to make this microbiome change over time.
“The development of Alzheimer’s and other dementias is complex and likely involves the interaction of many systems,” said Ehrlich. “I’m a believer in the more infections you get in the brain, the higher your risk of Alzheimer’s. There are many pathogens that likely increase the risk. This pathobiome is not the whole answer, but it’s a piece of the puzzle.”
The exact location of the problematic bacteria within the brain is also an open question, according to the team. Researchers need to know more precisely where the bacteria are to better understand the role they are playing. The authors found that when an unhealthy pathobiome is located in the frontal lobe, the likelihood of Alzheimer’s disease being present is very high. It’s less likely to develop in the temporal lobe.
Despite the many unknowns, the authors said this is a significant step forward for studying the microbiome. The strength of our work is also to combine a breakthrough sequencing technology and the most advanced and innovative statistical approaches. Microbiome data analysis is notoriously challenging without […]
Here’s how essential oils help relieve depression symptoms
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Aromatherapy is the practice of using essential oils – potent plant extracts that possess beneficial properties – to promote well-being and treat various health issues. This holistic treatment has been around for centuries and can be traced back to the time of the ancient Egyptians .
Today, aromatherapy is still used as an adjunct therapy in clinical practice . Clinical trials have shown that certain essential oils can be used as natural remedies for minor complaints like insomnia, nausea, loss of appetite, headaches and post-operative pain, as well as mental health-related issues like anxiety, stress and depression. (Related: Natural remedies: Treating headaches with essential oils .) Physical and cognitive symptoms of depression
Depression is a mood disorder characterized by a persistent feeling of sadness that could last for weeks or months . This condition manifests itself as a combination of cognitive and physical symptoms that greatly impact a person’s quality of life and ability to perform everyday tasks. Depression is said to affect more than 300 million people around the world and, if left untreated, could be life-threatening.
According to the National Institute of Mental Health, over 18 million American adults suffer from a depressive illness in any given year. Major depression (clinical depression), the most common and severe form of depression , is the psychiatric diagnosis most commonly associated with suicide. Research suggests that the risk of suicide among people with major depression is about 20 times that of the general population.
Common physical symptoms of depression include: Tiredness or fatigue
Insomnia or sleeping more than usual
Increased or decreased appetite
Slow speech or movements
Unexplained pain or headaches
Low libido
Constipation or diarrhea
Cognitive decline is also common among people who suffer from depression. This decline usually affects executive functioning, which encompasses a person’s ability to plan, solve problems and make decisions. Aside from executive dysfunction, other cognitive symptoms of depression include reduced attention and concentration, lower processing speed, impaired learning and poor memory. The science behind aromatherapy
Today, the first-line treatment for depression is antidepressants. Pharmaceutical companies have developed a wide variety of antidepressants to address the different symptoms of depression. However, many patients end up looking for alternatives because of the suboptimal effectiveness of these medications and the unpleasant side effects they can cause .
One of the alternatives people with depression often turn to is aromatherapy. This complementary and alternative medicine (CAM) has been shown to help alleviate symptoms of depression. In a systematic review published in the journal Evidence-Based Complementary and Alternative Medicine , researchers looked at the results of 12 randomized controlled trials and concluded that aromatherapy is an effective treatment option for relieving depression symptoms .
According to the review, aromatherapy can be administered in two ways: Individuals suffering from depression can either inhale essential oils directly or have the oils massaged on their skin. When essential oils are inhaled, their beneficial components can easily enter the bloodstream through the blood capillary network in the nose and the bronchi in the lungs.
One of the main organs targeted by essential oils is the brain. Research shows that the active components of essential oils can stimulate parts of the brain through the olfactory epithelium. Located behind the nostrils, this thin tissue is composed of neurons and supporting cells that line about half of your nasal cavity. The most important cells in the olfactory epithelium are the olfactory receptor neurons, which help transmit olfactory information to the brain.
When you inhale essential oils, their chemical components stimulate olfactory receptor neurons, which then transmit signals to your limbic system and hypothalamus. The limbic system is the part of your brain involved in emotional and behavioral responses , while the hypothalamus is the part of your brain that produces hormones responsible for controlling your body temperature, heart rate, hunger, mood, sleep and thirst.
Once the signals reach your olfactory cortex — the part of your brain concerned with the sense of smell — they trigger the release of specific brain chemicals, or neurotransmitters, like serotonin. Serotonin is a natural mood booster that is linked to feelings of happiness. Research shows that serotonin acts on different brain regions and affects a range of functions and behaviors , such as memory, fear, digestion, sleep, breathing, body temperature and stress response. Treating depression with aromatherapy
Studies at the Monell Chemical Senses Center in Philadelphia suggest that specific odors can change your mood and emotions , and these changes correlate to measurable physiological variations such as changes to your blood pressure, heart rate and body temperature. Studies also reveal that odors provide cues that trigger memory, and these memories are “more evocative and emotionally intense” than any memory triggered by other types of sensory cues.
By triggering memory associations and influencing specific parts of your brain that regulate physiological and emotional changes, aromatherapy can help relieve cognitive and physical symptoms of depression .
Here are four of the best essential oils for relieving depression symptoms , according to science: Lavender essential oil
In a study published in the journal Phytomedicine , researchers found that lavender oil in capsule form (Silexan) is just as effective at relieving generalized anxiety disorder — a common trigger of depression — as Ativan, an anti-anxiety drug. They also noted that lavender oil showed no sedative effects and was well-tolerated by participants, making it a safe natural alternative to commonly prescribed depressant medications.
Aside from anxiety, lavender oil can also help with panic attacks and general nervousness and is particularly helpful for postpartum depression . It is also a good natural remedy for restlessness, depression, anxiety and sleep disturbances that accompany post-traumatic stress disorder . Bergamot essential oil
According to a study published in the journal Neuroimmunomodulation , citrus fragrance not only helps restore homeostatic balance to the body, it could also normalize neuroendocrine hormone levels and immune function in people suffering from depression. These effects are extremely beneficial for the treatment of depression as dysregulation of neuroendocrine and immune function is associated with psychosomatic or psychiatric disorders like depression.
Among citrus oils, bergamot essential […]
Could a breakdown in the brain’s networks allow infections to contribute to Alzheimer’s disease?
Cartoon of the LDA algorithm. Credit: Frontiers in Cellular and Infection Microbiology (2023). DOI: 10.3389/fcimb.2023.1123228 The human microbiome includes the genetic material of more than 100 trillion tiny microorganisms—fungi, yeast, bacteria, and even viruses, most of which hang out in our gastrointestinal tract to serve as guardians of our health. But when a healthy microbiome gives way to an imbalance—a “pathobiome”—any number of health problems can occur—from rheumatoid arthritis, to bacterial vaginosis.
New data published this month in the journal Frontiers in Cellular and Infection Microbiology , from researchers at Drexel’s College of Medicine, gives more evidence to the possibility that developing a pathobiome in the brain could cause some forms of Alzheimer’s and related dementias.
When biomes turn unhealthy, either by invasion of outside pathogens, or a major change in the relative numbers of the microbial species present, a dysbiosis, or imbalance in the microbiota, occurs. This dysbiosis can alter human metabolism and cause inflammation, which has been linked to the tissue damage seen in ulcerative colitis, rheumatoid arthritis and many other chronic inflammatory diseases .
Studying 130 samples from the donated brains of 32 people—16 with Alzheimer’s and 16 age-matched controls without the disease—the Drexel researchers found bacterial flora in all the brains, but the Alzheimer’s brains showed profoundly different bacterial profiles compared to their age-matched controls.
The group used full-length 16s ribosomal RNA gene sequencing, a technique that can detect any and all bacterial species present in a sample. In this process, the researchers pinpointed disease-specific sets of bacteria in almost all of the Alzheimer’s-affected brains, suggesting these groups of bacteria are strong predictors of the disease.
The authors detected five brain microbiomes, four that are hypothesized to be present at different times in the evolution of the Alzheimer’s-afflicted brains. The authors said it is likely that the observed Alzheimer’s microbiomes evolve to become more pathogenic as the disease progresses with the later stages characterized as a pathobiome.
The authors hypothesize that the brain begins with a healthy biome, but as the disease develops, the healthy biome is supplanted as a new set of microbes replace the original healthy ones with the eventual emergence of the Alzheimer’s pathobiome.
Samples from both sets of brain samples were drawn from the frontal and temporal lobes and entorhinal cortex. Based on the random distribution of microbiomes requiring delivery all over the brain, the results were consistent with failure in one or more of the brain’s networks; however it is too soon to tell if the observed distribution patterns result from a leaky blood-brain barrier, the brain’s glymphatic system, or synaptonemal transmission that allowed bacteria, including Cutibacterium acnes (formerly called Proprionibacterium acnes), Methylobacterium, Bacillus, Caulobacter, Delftia, and Variovora to enter the brain.
In Alzheimer’s brain samples, the researchers noted, these pathogenic bacteria appeared to have overpowered and replaced Comamonas sp. bacteria, which are associated with a dementia-free brain.
“Perhaps destruction of the Comamonas bacteria, part of a healthy brain microbiome, is the first sign of impending dementia,” said Garth D. Ehrlich, Ph.D., a professor in the College of Medicine, who was a senior author of the paper. “We’re now coming up with the questions to guide future studies, but the hypotheses are many. The culprit could be bacteria or something else—like fungi, parasites, or viruses—at the same time.”
When a patient has Alzheimer’s, they experience inflammation in the brain characterized by deposits of amyloid beta which are formed by an increase in the production of the Aβ peptide (an antimicrobial peptide, which is part of the innate immune response) resulting in amyloid plaques in the brain.
Similarly, Alzheimer’s is characterized by tau protein tangles found with the cells which are characterized by abnormal phosphorylation which ultimately lead to the destruction of synapses and neurons, but which have also been demonstrated to help stop the spread of pathogens in the brain.
These protein-oriented pathologies—known as the “amyloid cascade hypothesis”— have been the main focus of Alzheimer’s research for decades. Recently, studies are challenging that model by suggesting a role for bacteria, fungi and viruses, and immune system and brain inflammation, which some researchers call the “pathogen hypothesis.”
“Multiple studies have now shown the presence of bacteria in Alzheimer’s-afflicted brains,” said Jeffrey Lapides, Ph.D., an adjunct associate professor in the College of Medicine, and a senior author of the study. “Perhaps plaques, whose constituents have anti-microbial properties in vitro, aren’t the direct cause of Alzheimer’s, but instead are a response to bacteria in the brain—some benign, some pathogenic, perhaps causing damage that has not yet resulted in cognitive deficits, making them part of the pathobiome.”
This unique set of bacteria found in the Alzheimer’s-afflicted brains are also commonly found in brains afflicted with the neurodegenerative disease amyotrophic lateral sclerosis , or ALS—suggesting that this set of bacteria may contribute to more than one neurological illness.
The next step for this research, according to the authors, is to study the possible contributions of other microbes and figure out what happened, physiologically, in the brain to make this microbiome change over time.
“The development of Alzheimer’s and other dementias is complex and likely involves the interaction of many systems,” said Ehrlich. “I’m a believer in the more infections you get in the brain, the higher your risk of Alzheimer’s. There are many pathogens that likely increase the risk. This pathobiome is not the whole answer, but it’s a piece of the puzzle.”
The exact location of the problematic bacteria within the brain is also an open question, according to the team. Researchers need to know more precisely where the bacteria are to better understand the role they are playing. The authors found that when an unhealthy pathobiome is located in the frontal lobe, the likelihood of Alzheimer’s disease being present is very high. It’s less likely to develop in the temporal lobe.
Despite the many unknowns, the authors said this is a significant step forward for studying the microbiome.
“The strength of our work is also to combine a breakthrough sequencing technology and the most advanced and innovative statistical approaches,” said lead author Yves Moné, Ph.D., a research associate in the College […]
Aromatherapy May Lead to a 226% Boost in Cognition
Certain aromas can help build better brains—and memories—during sleep.
Smell is directly linked to memory.
Scents may offer a safe and possibly beneficial option to boost brain health.
Source: Palo Cech/ Pexels You know those small vials of fragrant oils sometimes placed on a hotel pillow to calm a guest and improve sleep? Well, science says they work, even suggesting certain aromas can help build better brains—and memories—during sleep.
Researchers writing in a July 2023 issue of Frontiers in Neuroscience contend “ olfactory enrichment”—inhaling pleasant fragrances during sleep—influences brain function in ways that significantly improve cognition and boost memory . How Scientists Conducted the Study
Of 43 study participants—all healthy men and women between the ages of 60 and 85—20 underwent two hours of aromatherapy nightly. Seven different fragrant oils were dispersed through a room diffuser on a rotating basis—a different one each night—for a period of six months. When compared to the control group, the 20 volunteers registered a whopping 226 percent increase in cognitive capacity as measured by a word list test commonly used to evaluate memory.
The exact protocol is as follows: Participants provided an odorant diffuser made by Diffuser World
Provided seven essential oils: rose, orange, eucalyptus, lemon, peppermint, rosemary, lavender
Participants were asked to turn on the diffuser before bedtime—producing scent for two hours
Rotate through different scents each night
Continue nightly for six months
While this study was conducted in older adults aged 60-85, with no cognitive issues at all, there is some chance this may help younger groups as well. At a minimum, the side effects, or risks of sleeping with scented aromas, are quite minimal.
The finding supports past studies, including a 2021 report in the journal Geriatric Nursing indicating olfactory stimulation could prove a “simple and convenient new intervention for alleviating, maintaining [and managing] cognitive function and [behavior and psychological symptoms] in older adults with dementia .”
So, why is the sense of smell so critical to cognition, emotion , and general neural function? Smell Directly Linked to Memory
Unlike the other senses, such as eyesight and hearing, the olfactory nerves are linked directly to a white matter pathway in the brain—the uncinate fasciculus—which plays a significant role in learning and memory encoding. It is part of the brain’s limbic system, which governs emotions and behavior.
It is this pathway that deteriorates due to aging and the development of neurodegenerative disorders like Alzheimer’s and Parkinson’s disease, authors of the July 2023 journal article state. In fact, the sense of smell is much like the canary in the cave, where the bird’s sensitivity to adverse conditions and resulting death, is a warning to miners to get out quickly. Loss of smell can prove a warning of the onset of some 70 different neurological disorders or neural infections. Traumatic brain injuries can also modify or interfere with olfactory discrimination .
The researchers were quick to point out that olfactory stimulation does not directly affect areas of the brain responsible for controlling sleep. However, they say the use of natural fragrances can deepen slow-wave sleep. Slow-wave sleep is considered “the most restful portion of the sleep cycles,” study authors write. “Odorants enhance normal sleep, and…also improve abnormal sleep at a magnitude similar to that of sleep medications.”
Meanwhile, the National Sleep Foundation says that smell can affect “how long it takes to fall asleep, [as well as] overall sleep quality and quantity. Distinct scents may promote better sleep, help people wake up in the morning, or even [potentially] influence dreams and memory formation during sleep.”
Key components of what is defined as “quality sleep” include duration, continuity (number of times one awakens during the night), and amount of beneficial slow wave (deep) sleep, which is important in enhancing memory, strengthening the immune system, repairing bone and tissue, and regenerating cells. Lavender Most Studied, But Other Oils Also Beneficial
The most studied fragrance for improving sleep has been lavender, but past reports also cite the appealing effects of natural oils like jasmine, rose, and Roman chamomile, which reportedly is effective in easing anxiety and depression , and even cedarwood. All of these are extracts derived from plants.
In a 2021 article published in Complementary Therapies in Medicine , authors review 30 aromatherapy studies and conclude the use of fragrant oils has a “statistically significant” effect on improving sleep quality and reducing “ stress , pain, anxiety, depression, and fatigue.” Indeed, aromatherapy also appears effective for controlling cases of acute insomnia , they state. And now, of course, the latest study indicates the smell of these oils can make the user smarter in terms of cognition, recall, and judgment.
The therapeutic effects of natural fragrances are not a new concept. Pedanius Discorides, a Greek physician considered the father of pharmacognosy, discussed the medicinal properties of natural plant oils in his book De Materia Medica , written in the first century. Later, in the 12th century, Saint Hildegard, a German Benedictine abbess, composer, philosopher, and medical writer, used distilled lavender for healing purposes. Finding the Best Way to Use Fragrances
Having a scientifically approved approach to enhancing sleep quality, while building cognition and memory, through the use of natural fragrances could benefit tens of thousands of Americans. Impaired sleep is reaching epidemic proportions in the United States. The National Sleep Foundation estimates more than a third of adults fail to sleep the required number of hours. The Centers for Disease Control and Prevention says the number is closer to 35 percent.
Chronic insomnia and other forms of sleep deprivation are linked to a variety of physical, mental, and psychological symptoms. These include mood shifts and increased irritability, concentration and attention problems, failures in judgment and executive decision-making , physiological changes, such as impairments in brain function and hormone production, reduced immunity protection from disease, overstimulated appetite and weight gain, higher risk for diabetes and various dementias, an overactive nervous system , chronic fatigue—even earlier death. This list includes a range of psychiatric disorders, including elevated anxiety, depression, and obsessive compulsiveness.
As the […]