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Comment by Dr. Krishna Kumari Challa on October 25, 2025 at 10:07am

Furthermore, while AsEVs from control astrocyte cultures tend to favor an anti-inflammatory profile of the GALT (i.e., increased Treg/Th17 ratio), AsEVs derived from corticosterone-treated astrocytes have an opposite action. Similarly, in vitro experiments with disaggregated mesenteric lymph nodes reveal the immunomodulatory functions of AsEVs from corticosterone-treated astrocytes."

The results of this recent study uncover a new brain-to-gut communication pathway mediated by AsEVs via which stress could worsen the symptoms of IBDs.

Liliana Yantén-Fuentes et al, A novel brain-to-gut communication pathway mediated by astrocyte-derived small extracellular vesicles modulates stress-induced intestinal inflammation, Molecular Psychiatry (2025). DOI: 10.1038/s41380-025-03289-2.

Part 2

Comment by Dr. Krishna Kumari Challa on October 25, 2025 at 10:07am

Astrocyte-derived vesicles could link stress to intestinal inflammation

Inflammatory bowel diseases (IBDs), such as Crohn's disease and ulcerative colitis, are chronic and autoimmune conditions characterized by the inflammation of the intestinal tract. This inflammation can cause nausea or vomiting, diarrhea, abdominal pain and cramping, fatigue, fever, and various other debilitating symptoms.

While the underpinnings of IBDs have been widely investigated, the factors that can contribute to its emergence have not yet been clearly elucidated. Past findings suggest that the symptoms of these diseases are often exacerbated by psychological and emotional stress.

Researchers recently carried out a study aimed at shedding new light on the neurobiological mechanisms via which stress could worsen IBDs. Their findings, published in Molecular Psychiatry, hint at the existence of a brain-to-gut communication pathway that is mediated by small communication vehicles known as small extracellular vesicles (sEVs), which are released by astrocytes.

The researchers now hypothesize that psychological stress regulates intestinal inflammation through the release of small extracellular vesicles derived from astrocytes (AsEVs).

The researchers carried out various experiments involving rats, aimed at understanding how stress affected immune responses in their gut. Their study specifically focused on the role of astrocytes, star-shaped glial cells that help to maintain a balanced and healthy environment in the brain, and of small EVs released by these cells.

They  marked astrocytes with a special "tag" protein, using a technique known as in-utero electroporation. This technique allowed them to monitor where signals originating from these cells traveled within the rats' body.

"In-utero electroporation performed to selectively express an AsEV-associated membrane recombinant protein in rat forebrain astrocytes reveals that this protein is transferred to the gut-associated lymphoid tissue (GALT)," wrote the authors.

Similarly, AsEVs isolated from primary astrocyte cell cultures that were stimulated with vehicle or corticosterone (to emulate a stress condition) trafficked to the GALT. Interestingly, the membrane gut homing receptor CCR9 is present on AsEVs and mediates their association with the CCR9-endogenous ligand CCL25."

Interestingly, the researchers discovered that signals originating from astrocytes traveled to immune tissues in the rats' gut. Subsequently, they grew astrocytes in their lab and increased the levels of corticosterone within them. This is a hormone that is naturally released in the animals' body when they are stressed.

The team then injected vesicles released by these cells, as well as vesicles released by "non-stressed" astrocytes into rats and observed their gut responses. They found that vesicles derived from "stressed" astrocytes led to greater gut inflammation, while those released by 'non-stressed' astrocytes helped to calm the gut's immune system.

At the histological level, inflammatory parameters (such as lymph vessel diameter or cell number in them), induced by a stress protocol based on movement restriction, increased by treatment with AsEVs from corticosterone-treated astrocytes.

Part 1

Comment by Dr. Krishna Kumari Challa on October 24, 2025 at 2:35pm

'Forever Chemicals' in Mothers' Blood Linked to Brain Changes in Their Kids

'Forever chemicals' already have a shocking reputation, and now new research has linked these substances – named for the way they stick around in the environment for so long – to brain changes in children born to mothers exposed to common PFAS (per- and polyfluoroalkyl substances).
To reach that conclusion, researchers looked at 51 mother-and-child pairs, measuring PFAS levels in the mother's blood during pregnancy, and then running brain scans on the kids once they reached 5 years old.
These records meant the research team was able to compare different types of PFAS against changes in brain structure and connections between brain regions. Several distinct patterns were revealed, enough to suggest (but not prove) a strong influence.
They were able to measure seven different PFAS in this study, and found that individual compounds had specific associations with offspring brain structure.
In some cases two different PFAS had opposite relationships with the same brain region
For example, perfluorononanoic acid (PFNA) and perfluorooctanoic acid (PFOA) were linked to changes in the corpus callosum, the tract of white matter that connects the brain's left and right hemispheres.
Substantial changes connected to PFAS levels were also detected in the hypothalamus, a part of the brain that controls many of the body's core functions, and in the volume and surface area of posterior grey matter in the occipital lobe, the brain's visual processing centre.
The researchers also found certain types of PFAS more likely to influence brain structure and brain connectivity than others, based on their chemical composition. It's not immediately evident what these changes might mean – but the changes are there.

https://www.thelancet.com/journals/lanplh/article/PIIS2542-5196(25)00187-1/fulltext

Comment by Dr. Krishna Kumari Challa on October 24, 2025 at 1:35pm

Pathogen disables plant ‘alarm’ to break in
Phytophthora infestans — a fungus-like mold that causes the devastating disease potato blight — infects plants by disabling their ‘alarm system’. Researchers found that P. infestans secretes enzymes called AA7 oxidases. These enzymes damage the molecules plant cells produce to alert the immune system of an infection, which lets the microbe sneak in without being detected. “It’s like burglars cutting the wires to your home alarm before breaking in,” says biochemist and study co-author Federico Sabbadin. “The microbe has learned the plant’s own language and uses it against it.”

https://www.nature.com/articles/s41467-025-64189-1?utm_source=Live+...

Comment by Dr. Krishna Kumari Challa on October 24, 2025 at 1:32pm

A new human clinical trial has shown that a special procedure to deliver oxygen through the rectum is safe.

The study involved 27 healthy male volunteers in Japan who were tasked with holding between 25 and 1,500 milliliters of perfluorocarbon liquid in their rectum for an hour.

The ‘butt-breathing’ procedure passed its first safety hurdle with flying colors.
Now researchers hope to test what happens when that liquid contains a very high concentration of oxygen.

The hope is that one day, a procedure like this could help people who are struggling to get enough oxygen through their lungs.

Pigs, rodents, turtles, and some fish can breathe through their butts, so why not us?

linkinghub.elsevier.com/retrieve/pii/S2666634025003149

Comment by Dr. Krishna Kumari Challa on October 24, 2025 at 12:21pm

Nighttime light exposure linked to higher heart attack and stroke rates

A new study has found that being exposed to bright light at night can significantly increase the chances of developing serious heart problems, including heart attacks, strokes and heart failure.

Published in JAMA Network Open, the research is the largest study of its kind to explore how personal light exposure affects heart health using data from nearly 89,000 people.

Using wrist-worn sensors, researchers from FHMRI Sleep Health tracked over 13 million hours of light exposure and followed participants for up to 9.5 years.
The study found that people who were exposed to the brightest light at night were much more likely to develop heart problems, with a 56% higher chance of heart failure and 47% more likely to have a heart attack.

These risks remained high even after accounting for other factors like exercise, diet, sleep habits and genetics.

the study highlights a risk factor that many people aren't aware of, but one that's easy to address.

This is the first large-scale study to show that simply being exposed to light at night is a strong and independent risk factor for heart disease.

Disrupting your body's internal circadian clock by repeatedly exposing yourself to bright light at night, when it would typically be dark otherwise, will put you at a higher risk of developing dangerous heart issues, say the researchers.

By using blackout curtains, dimming lights, and avoiding screens before bed, we can help to reduce the health risks associated with light at night.

The study also found that women and younger people were especially vulnerable to the impact of light exposure at night.

Women may be more sensitive to the effects of light disrupting their body clock.

In fact, women exposed to high levels of night light had similar heart failure risks to men, which is unusual because women typically have some natural protection against heart disease.

We need to take our body clocks seriously. Protecting our natural sleep rhythms could be a powerful way to fight heart disease, the researchers conclude.

Light Exposure at Night and Cardiovascular Disease Incidence, JAMA Network Open (2025). DOI: 10.1001/jamanetworkopen.2025.39031

Comment by Dr. Krishna Kumari Challa on October 24, 2025 at 11:56am

A second study, published in the Brain Research Bulletin

focused on IGF2, a growth-factor gene that supports memory formation. As the brain ages, IGF2 activity drops as the gene becomes chemically silenced in the hippocampus.

IGF2 is one of a small number of genes in our DNA that's imprinted, which means it's expressed from only one parental copy. When that single copy starts to shut down with age, you lose its benefit.

The researchers found that this silencing happens through DNA methylation, a natural process in which chemical tags accumulate on the gene and switch it off. Using a precise gene-editing tool, CRISPR-dCas9, they removed those tags and reactivated the gene. The result was better memory in older rats.

Together, the two studies show that memory loss is not caused by a single molecule or pathway and that multiple molecular systems likely contribute to how the brain ages.

 Yeeun Bae et al, Age-related dysregulation of proteasome-independent K63 polyubiquitination in the hippocampus and amygdala, Neuroscience (2025). DOI: 10.1016/j.neuroscience.2025.06.032

Shannon Kincaid et al, Increased DNA methylation of Igf2 in the male hippocampus regulates age-related deficits in synaptic plasticity and memory, Brain Research Bulletin (2025). DOI: 10.1016/j.brainresbull.2025.111509

Part 2

Comment by Dr. Krishna Kumari Challa on October 24, 2025 at 11:54am

Scientists find ways to boost memory in aging brains

Memory loss may not simply be a symptom of getting older. New research  shows that it's tied to specific molecular changes in the brain and that adjusting those processes can improve memory.

In two complementary studies, researchers used gene-editing tools to target those age-related changes to improve memory performance in older subjects. The work was conducted on rats, a standard model for studying how memory changes with age.

Memory loss affects more than a third of people over 70, and it's a major risk factor for Alzheimer's disease. 

This work shows that memory decline is linked to specific molecular changes that can be targeted and studied. If we can understand what's driving it at the molecular level, we can start to understand what goes wrong in dementia and eventually use that knowledge to guide new approaches to treatment.

In the first study, published in the journal Neuroscience one research team examined a process called K63 polyubiquitination. This process acts as a molecular tagging system that tells proteins inside the brain how to behave. When the system functions normally, it helps brain cells communicate and form memories.

They found that aging disrupts K63 polyubiquitination in two distinct areas of the brain. In the hippocampus, which helps form and retrieve memories, levels of K63 polyubiquitination increase with age. Using the CRISPR-dCas13 RNA editing system to reduce these levels, the researchers were able to improve memory in older rats.

In the amygdala, which is important for emotional memory, the researchers noted that K63 polyubiquitination declines with age. By reducing it even further, they were able to boost memory in older rats.

Together, these findings reveal the important functions of K63 polyubiquitination in the brain's aging process. In both regions, adjusting this one molecular process helped improve memory.

Part 1

Comment by Dr. Krishna Kumari Challa on October 24, 2025 at 11:42am

Not all gas is bad: Hydrogen gas found to play key role in supporting gut health

 Scientists have revealed how hydrogen is made and used in the human gut. Though infamous for making flatulence ignite, hydrogen also has a positive role supporting gut health.

In a study published in Nature Microbiology, researchers  analyzed how microbes control hydrogen levels in the gut.

Hydrogen gas is naturally produced in the gut when bacteria ferment undigested carbohydrates from our diets. Some of this gas is exhaled, much is recycled by other gut bacteria, and the rest exits the body as flatulence.

The results revealed hydrogen had an even bigger role in gut function than previously thought.

Most people release about a liter of gas per day and half of that is hydrogen. But hydrogen is more than just the gas behind flatulence—it's a hidden driver of gut health.

Gas production in the gut is a normal process. Hydrogen is made in large amounts when gut bacteria break down food and is then used by other microbes for energy.

The study shows hydrogen shapes the gut microbiome in surprising and varied ways. It helps some beneficial bacteria thrive in the gut and keeps digestion going.

However, excessive hydrogen production can signal gut problems. Abnormal hydrogen levels are associated with infections, digestive disorders, and even cancer, and are often measured in breath tests to assess gut health.

They also  saw signs that hydrogen production was disrupted in people with gut disorders, but it's unclear if this is a cause or consequence of disease.

The researchers' work was focused on understanding the fundamental role of hydrogen in gut function, rather than improving diagnostics or developing therapies.

The study found that a specific enzyme called Group B [FeFe]-hydrogenase was mainly responsible for making hydrogen in the gut. This enzyme is found in many gut bacteria and is very active.

The researchers studied bacteria from stool samples and gut tissue and found that this enzyme helps bacteria grow and produce hydrogen, especially in the primary health associated groups. They also discovered that this enzyme works by using a specific chemical reaction involving iron and another protein called ferredoxin.

As an example, healthy people have a lot of these enzymes in their gut, but people with Crohn's disease have fewer of them and more of the other types of hydrogen-producing enzymes.

The researchers hope their discovery will highlight the need to expand fundamental knowledge of how our gut works so it can be used to design new treatments for gastrointestinal issues.

 Caitlin Welsh et al, A widespread hydrogenase supports fermentative growth of gut bacteria in healthy people, Nature Microbiology (2025). DOI: 10.1038/s41564-025-02154-w

Comment by Dr. Krishna Kumari Challa on October 24, 2025 at 11:29am

Tigers in trouble as Malaysian big cat numbers dwindle

Malaysia's national animal is in trouble.

Poaching, food loss and diminishing habitat have slashed the population from 3,000 in the 1950s to less than 150 roaming free today, according to official estimates.

The government said last month it was ramping up efforts to combat wildlife crime, introducing AI-enabled camera traps and methods to detect smuggling at airports.

But experts and officials admit that resources fall far short of what is needed to protect the country's famed big cat, listed as critically endangered.

The next 10 years will decide whether we can bring back the roar of the Malayan tiger.

Source: News agencies

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