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Comment by Dr. Krishna Kumari Challa on April 30, 2024 at 10:50am

Research shows 'profound' link between dietary choices and brain health

A recent study published in Nature Mental Health shows that a healthy, balanced diet is linked to superior brain health, cognitive function and mental well-being. The study, involving researchers at the University of Warwick, sheds light on how our food preferences not only influence physical health but also significantly impact brain health.

The dietary choices of a large sample of 181,990 participants from the UK Biobank were analyzed against and a range of physical evaluations, including cognitive function, blood metabolic biomarkers, brain imaging, and genetics—unveiling new insights into the relationship between nutrition and overall well-being.

The food preferences of each participant were collected via an online questionnaire, which the team categorized into 10 groups (such as alcohol, fruits and meats). A type of AI called machine learning helped the researchers analyze the large dataset.

A balanced diet was associated with better mental health, superior cognitive functions and even higher amounts of gray matter in the brain—linked to intelligence—compared with those with a less varied diet.

The study also highlighted the need for gradual dietary modifications, particularly for individuals accustomed to highly palatable but nutritionally deficient foods. By slowly reducing sugar and fat intake over time, individuals may find themselves naturally gravitating towards healthier food choices.

Genetic factors may also contribute to the association between diet and brain health, the scientists think, showing how a combination of genetic predispositions and lifestyle choices shape well-being.

 Ruohan Zhang et al, Associations of dietary patterns with brain health from behavioral, neuroimaging, biochemical and genetic analyses, Nature Mental Health (2024). DOI: 10.1038/s44220-024-00226-0

Comment by Dr. Krishna Kumari Challa on April 30, 2024 at 10:32am

Study suggests that stevia is the most brain-compatible sugar substitute

Given the known risks of consuming high amounts of sugar, today many people are looking for alternative sweeteners that produce a similar taste without prompting significant weight gain and causing other health issues. While research suggests that the brain can tell the difference between different sweet substances, the neural processes underlying this ability to tell sweeteners apart remain poorly understood.

Researchers recently carried out a study aimed at better understanding what happens in the brain of mice when they are fed different types of sweeteners. Their findings, published in Neuroscience Research, suggest that the response of neurons to sucrose and stevia is similar, suggesting that stevia could be an equally pleasant but healthier sugar substitute.

Stevia is a sweet sugar substitute that is about 50 to 300 times sweeter than sugar. It is extracted from the leaves of Stevia rebaudiana, a plant native to areas of Paraguay and Brazil in the southern Amazon rainforest.The active compounds in stevia are steviol glycosides (mainly stevioside and rebaudioside). Stevia is heat-stable, pH-stable, and not fermentable. Humans cannot metabolize the glycosides in stevia, and therefore it has zero calories. Its taste has a slower onset and longer duration than that of sugar, and at high concentrations some of its extracts may have an aftertaste described as licorice-like or bitter. Stevia is used in sugar- and calorie-reduced food and beverage products as an alternative for variants with sugar.

Interestingly, the team's recordings revealed that compared to other sugar substitutes considered as part of this study, stevia induced activity in the PVT that more closely resembled that elicited by sugar intake. This suggests that stevia is the most "brain compatible" among most widely used sugar alternatives, most closely mirroring the perceived taste of sugar.

Shaolei Jiang et al, Neuronal activity in the anterior paraventricular nucleus of thalamus positively correlated with sweetener consumption in mice, Neuroscience Research (2024). DOI: 10.1016/j.neures.2024.02.002

Comment by Dr. Krishna Kumari Challa on April 29, 2024 at 11:20am

The harm artificial sweeteners can cause

Artificial sweeteners are chemical compounds are up to 600 times sweeter than sugar with very few (if any) calories, and are cheap and easy for manufacturers to use.

Traditional artificial sweeteners, such as aspartame, sucralose and acesulfame potassium (acesulfame K) have been found in a wide range of foods and drinks for many years as a way to increase the sweet taste without adding significant calories or costs. However, in the last few years, there has been controversy in the field. Several studies have suggested potential health harms associated with consuming these sweeteners, ranging from gastrointestinal disease to dementia. Although none of these harms have been proved, it has paved the way for new sweeteners to be developed to try to avoid any possible health issues. These next-generation sweeteners are up to 13,000 times sweeter than sugar, have no calories and no aftertaste (a common complaint with traditional sweeteners). An example of this new type of sweetener is neotame. Neotame was developed as an alternative to aspartame with the aim of being a more stable and sweet version of the traditional sweetener. It is very stable at high temperatures, which means it is a good additive to use in baked goods. It is also used in soft drinks and chewing gum.

An artificial sweetener called neotame can cause significant harm to the gut, scientists found.It does this harm in two ways. One, by breaking down the layer of cells that line the intestine. And, two, by causing previously healthy gut bacteria to become diseased, resulting in them invading the gut wall.

The study, published in the journal Frontiers in Nutrition, is the first to show this double-hit negative effect of neotame on the gut, resulting in damage similar to that seen in inflammatory bowel disease and sepsis.

https://www.frontiersin.org/articles/10.3389/fnut.2024.1366409/full

Comment by Dr. Krishna Kumari Challa on April 29, 2024 at 9:42am

In the study, the researchers asked more than 80 people to sit down and grab the handle of a robotic arm, which, in turn, operated the cursor on a computer screen. The subjects reached forward, moving the cursor toward a target. If they succeeded, they received a reward—not a big one, but still enough to make their brains happy.

Sometimes, the targets exploded, and they would get point rewards. It would also make a 'bing bing' sound.

That's when a contrast between the two groups of people began to emerge.

Both the 18 to 35-year-olds and 66 to 87-year-olds arrived at their targets sooner when they knew they would hear that bing bing—roughly 4% to 5% sooner over trials without the reward. But they also achieved that goal in different ways.

The younger adults, by and large, moved their arms faster toward the reward. The older adults, in contrast, mainly improved their reaction times, beginning their reaches about 17 milliseconds sooner on average.

When the team added an 8-pound weight to the robotic arm for the younger subjects, those differences vanished.

The brain seems to be able to detect very small changes in how much energy the body is using and adjusts our movements accordingly. Even when moving with just a few extra pounds, reacting quicker became the energetically cheaper option to get to the reward, so the young adults imitated the older adults and did just that.

The research seems to paint a clear picture. Both the younger and older adults didn't seem to have trouble perceiving rewards, even small ones. But their brains slowed down their movements under tiring circumstances.

The experiment can't completely rule out the brain's reward centers as a culprit behind why we slow down when we age. But if scientists can tease out where and how these changes emerge from the body, they may be able to develop treatments to reduce the toll of aging and disease.

Putting it all together, these results suggest that the effort costs of reaching seem to be determining what's slowing the movement of older adults. 

Erik M. Summerside et al, Slowing of Movements in Healthy Aging as a Rational Economic Response to an Elevated Effort Landscape, The Journal of Neuroscience (2024). DOI: 10.1523/JNEUROSCI.1596-23.2024

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Comment by Dr. Krishna Kumari Challa on April 29, 2024 at 9:38am

Why do we move slower the older we get? New study delivers answers

It's one of the inescapable realities of aging: The older we get, the slower we tend to move.

A new study led by University of Colorado Boulder engineers helps explain why.

The research is one of the first studies to experimentally tease apart the competing reasons why people over age 65 might not be as quick on their feet as they used to be. The group reported that older adults may move slower, at least in part, because it costs them more energy than younger people—perhaps not too shocking for anyone who's woken up tired the morning after an active day.

Why we move the way we do, from eye movements to reaching, walking, and talking, is a window into aging and Parkinson's. Scientists are trying to understand the neural basis of that.

For the study, the group asked subjects aged 18 to 35 and 66 to 87 to complete a deceptively simple task: to reach for a target on a screen, a bit like playing a video game on a Nintendo Wii. By analyzing patterns of these reaches, the researchers discovered that older adults seemed to modify their motions under certain circumstances to conserve their limited supplies of energy.

All of us, whether young or old, are inherently driven to get the most reward out of our environment while minimizing the amount of effort to do so.

researchers have long known that older adults tend to be slower because their movements are less stable and accurate. But other factors could also play a role in this fundamental part of growing up.

According to one hypothesis, the muscles in older adults may work less efficiently, meaning that they burn more calories while completing the same tasks as younger adults—like running a marathon or getting up to grab a soda from the refrigerator.

Alternatively, aging might also alter the reward circuitry in the human brain. As people age, their bodies produce less dopamine, a brain chemical responsible for giving you a sense of satisfaction after a job well done. If you don't feel that reward as strongly, the thinking goes, you may be less likely to move to get it. People with Parkinson's disease experience an even sharper decline in dopamine production.

Part 1

Comment by Dr. Krishna Kumari Challa on April 27, 2024 at 12:17pm

Given that zoonotic prion disease is absolutely possible, and that transmission to humans has been predicted for some time, the situation, the doctors say, warrants caution and attention.

Although causation remains unproven, this cluster emphasizes the need for further investigation into the potential risks of consuming CWD-infected deer and its implications for public health," they write.

"Clusters of sporadic CJD cases may occur in regions with CWD-confirmed deer populations, hinting at potential cross-species prion transmission. Surveillance and further research are essential to better understand this possible association."

https://www.neurology.org/doi/10.1212/WNL.0000000000204407

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Comment by Dr. Krishna Kumari Challa on April 27, 2024 at 12:16pm

'Zombie Deer' Disease: Zoonotic Transfer Suspected After Two Human Deaths

A medical case report suggests that a deadly prion disease may have made its way from deer into humans.
Two hunters have died after consuming venison from a population of deer known to be infected with chronic wasting disease – an incurable, fatal prion sometimes known as "zombie deer" disease not dissimilar to bovine spongiform encephalopathy, or mad cow disease.
A team of doctors at the University of Texas report a 72-year-old man died after presenting with rapid-onset confusion and aggression.

The man's friend, who was a member of the same hunting lodge, died at a later, unspecified date after presenting with similar symptoms, the doctors note. A post-mortem determined that this second patient had died of Creutzfeldt-Jakob disease, AKA prion disease.

Since prion disease is relatively rare in humans, the two cases could mean that chronic wasting disease – described by the Center for Disease Control as never having been reported in humans – has made the zoonotic leap from animals.
Prion diseases, known as Creutzfeldt-Jakob disease or CJD in humans, are kind of terrifying. Prions are proteins that haven't folded properly, and therefore don't really function the way they should. The problem is that these misfolded proteins teach the proteins around them how to fold badly, too, resulting in a spread of dysfunctional tissue that cannot be halted or cured.
The spread of prions through brain tissue produces symptoms very similar to a kind of fast-tracked dementia, to which the patient eventually succumbs. Since CJD doesn't produce any kind of immune response, it's practically impossible to diagnose in a living patient.

Significant concerns have already been raised about chronic wasting disease. It infects animals such as deer, elk, and moose, and seems to be transmitted fairly easily between them; scientists think it is transmitted via bodily fluids such as blood or saliva, either through direct contact, or contamination in the environment.
It's not known for certain whether the two men described in the case report succumbed to chronic wasting disease, or whether their illness had another source. Prion disease may emerge spontaneously, for example, although that is, as far as we can tell, extremely rare.
The case report also doesn't mention from whence the two men hailed, but the disease can be found across the North American continent in wild populations, including at least 32 states in the US and across Canada. It can also be found among farmed deer.
Part 1

Comment by Dr. Krishna Kumari Challa on April 27, 2024 at 11:10am

With the expansion of machine learning applications in various industries, there's an escalating demand for AI devices that are not only highly computational but also feature low power consumption and miniaturization.

Research has shifted towards physical reservoir computing, leveraging physical phenomena presented by materials and devices for neural information processing. One challenge that remains is the relatively large size of the existing materials and devices.

The team's research has pioneered the world's first implementation of physical reservoir computing that operates on the principle of surface-enhanced Raman scattering, harnessing the molecular vibrations of merely a few organic molecules. The information is inputted through ion gating, which modulates the adsorption of hydrogen ions onto organic molecules (p-mercaptobenzoic acid, pMBA) by applying voltage.

The changes in molecular vibrations of the pMBA molecules, which vary with hydrogen ion adsorption, serve the function of memory and nonlinear waveform transformation for calculation.

This process, using a sparse assembly of pMBA molecules, has learned approximately 20 hours of a diabetic patient's blood glucose level changes and managed to predict subsequent fluctuations over the next five minutes with an error reduction of about 50% compared to the highest accuracy achieved by similar devices to date.

This study indicates that a minimal quantity of organic molecules can effectively perform computations comparable to a computer. This technological breakthrough of conducting sophisticated information processing with minimal materials and in tiny spaces presents substantial practical benefits. It paves the way for the creation of low-power AI terminal devices that can be integrated with a variety of sensors, opening avenues for broad industrial use.

Daiki Nishioka et al, Few- and single-molecule reservoir computing experimentally demonstrated with surface-enhanced Raman scattering and ion gating, Science Advances (2024). DOI: 10.1126/sciadv.adk6438

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Comment by Dr. Krishna Kumari Challa on April 27, 2024 at 11:10am

High-precision blood glucose level prediction achieved by few-molecule reservoir computing

A collaborative research team from NIMS and Tokyo University of Science has successfully developed an artificial intelligence (AI) device that executes brain-like information processing through few-molecule reservoir computing. This innovation utilizes the molecular vibrations of a select number of organic molecules.

By applying this device for the blood glucose level prediction in patients with diabetes, it has significantly outperformed existing AI devices in terms of prediction accuracy.

The work is published in the journal Science Advances.

Part 1

Comment by Dr. Krishna Kumari Challa on April 27, 2024 at 9:59am

Study suggests host response needs to be studied along with other bacteriophage research

A team of micro- and immunobiologists  has found evidence suggesting that future research teams planning to use bacteriophages to treat patients with multidrug-resistant bacterial infections need to also consider how cells in the host's body respond to such treatment.

In their paper published in the open-access journal PLOS Biology, the group describes experiments they conducted that involved studying the way epithelial cells in the lungs respond to bacteriophages.

Over the past decade, medical scientists have found that many of the antibiotics used to treat bacterial infections are becoming resistant, making them increasingly useless. Because of this, other scientists have been looking for new ways to treat such infections. One possible approach has involved the use of bacteriophages, which are viruses that parasitize bacteria by infecting and reproducing inside of them, leaving them unable to reproduce.

To date, most of the research involving use of bacteriophages to treat infections has taken place in Eastern Europe, where some are currently undergoing clinical trials. But such trials, the researchers involved in this new study note, do not take into consideration how cells in the body respond to such treatment. Instead, they are focused on determining which phages can be used to fight which types of bacteria, and how well they perform once employed.

The reason so little attention is paid to host cell interaction, they note, is that prior research has shown that phages can only replicate inside of the bacterial cells they invade; thus, there is little opportunity for them to elicit a response in human cells.

In this new study, the research team suggests such thinking is misguided because it fails to take into consideration the immune response in the host. To demonstrate their point, the team conducted a series of experiments involving exposing human epithelial cells from the lungs (which are the ones that become infected as part of lung diseases) to bacteriophages meant to eradicate the bacteria causing an infection.

They found that in many cases, the immune system responded by producing proinflammatory cytokines in the epithelial cells. They noted further that different phages elicited different responses, and there exists the possibility that the unique properties of some phages could be used to improve the results obtained from such therapies. They conclude by suggesting that future bacteriophage research involve inclusion of host cell response.

Paula F. Zamora et al, Lytic bacteriophages induce the secretion of antiviral and proinflammatory cytokines from human respiratory epithelial cells, PLOS Biology (2024). DOI: 10.1371/journal.pbio.3002566

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