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Comment by Dr. Krishna Kumari Challa on January 22, 2025 at 10:41am

Biotin may shield brain from manganese-induced damage, study finds

While manganese is an essential mineral involved in many bodily functions, both deficiency and excessive exposure can cause health issues. Maintaining a balanced diet typically provides sufficient manganese for most individuals; however, high levels of exposure can be toxic, particularly to the central nervous system.

Chronic manganese exposure may result in a condition known as manganism, characterized by symptoms resembling Parkinson's disease, including tremors, muscle stiffness, and cognitive disturbances.

New research published in Science Signaling employs model systems and human nerve cells to show the mechanisms by which manganese inflicts damage to the central nervous system. The study also suggests that the vitamin biotin may have a protective effect, potentially mitigating manganese-induced damage.

Exposure to neurotoxic metals like manganese has been linked to the development of Parkinsonism. In this study, researchers applied untargeted metabolomics using high-resolution mass spectrometry and advanced cheminformatics computing in a newly developed model of parkinsonism, leading them to the discovery of biotin metabolism as a modifier in manganese-induced neurodegeneration.

Chronic occupational and environmental exposure to manganese, commonly from welding fumes and some sources of rural drinking water, increases the risk of Parkinsonian syndrome, which involves similar but distinct neurological symptoms of Parkinson's disease. Manganese has been previously shown to bind with the protein alpha-synuclein, causing it to misfold and accumulate in the brain.

Using the fruit fly Drosophila, researchers developed a model that mimics occupational manganese exposure in humans and found that manganese induced motor deficits, mitochondrial and lysosomal dysfunction, neuronal loss, and reduced lifespan in flies.

The team validated these findings using human dopaminergic neurons derived from induced pluripotent stem cells (iPSC) and demonstrated that manganese exposure selectively damages these cells. The loss of dopamine-producing cells is a hallmark of Parkinson's disease and Parkinsonian syndrome.

The research indicates that B vitamin biotin, a micronutrient synthesized by gut bacteria, enhances dopamine production in the brain. Biotin supplementation reversed neurotoxicity in flies and iPSC-derived neurons, improving mitochondrial function and reducing cell loss.

This finding aligns with a growing scientific recognition that Parkinson's is a multisystem disorder, with early symptoms often emerging in the gut, and that changes in the gut microbiome may contribute to the disease.

"Biotin supplementation shows potential as a therapeutic strategy to mitigate manganese-induced neurodegeneration, and the safety and tolerability of biotin in humans make it a promising candidate for further exploration," say the researchers.

Biotin-rich prebiotics or biotin-producing probiotics could provide non-pharmacological intervention options.

Biotin rescues manganese-induced Parkinson's disease phenotypes and neurotoxicity, Science Signaling (2025). DOI: 10.1126/scisignal.adn9868

Comment by Dr. Krishna Kumari Challa on January 22, 2025 at 10:19am

Further experiments on mice revealed that shortly after conception, more methyl groups appear on histones near certain genes in uterine fibroblasts. In response, these genes remain inactive, which enables the uterus to support pregnancy.

Over the course of pregnancy, levels of methylation on these histones fade in a slow and steady way, eventually reaching low enough levels that the nearby genes—related to pregnancy events like labor—are activated. This erosion, which does not require KDM6B, functions as a timer.

Essentially, what appears to happen is this timer gets wound up right at the beginning of pregnancy, and then progressively winds down. When histone methylation erodes enough, nearby genes flip on.

When the researchers blocked KDM6B, histones near certain genes accumulated too much methylation early in pregnancy. This increased "setpoint" meant that, despite erosion, these genes were not activated on time, delaying labour.
While the new study did not directly study preterm births, the newly discovered molecular timer could help control pregnancy length in humans.

If the newly studied molecular signals are disrupted in humans, they could be linked to preterm birth risk, his team hypothesizes. For instance, some women could begin pregnancy with lower than usual levels of histone methylation; and this could lead to the erosion of the methylation to turn on labor-related genes too quickly.

 KDM6B-dependent epigenetic programming of uterine fibroblasts in early pregnancy regulates parturition timing in mice, Cell (2025). DOI: 10.1016/j.cell.2024.12.019. www.cell.com/cell/fulltext/S0092-8674(24)01432-6

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Comment by Dr. Krishna Kumari Challa on January 22, 2025 at 10:17am

What's behind preterm birth? Scientists discover a molecular timer

A typical human pregnancy lasts 40 weeks, but most parents know this number is only a rough estimate. Babies are born on a seemingly unpredictable timeline, with a normal pregnancy ranging from 38 to 42 weeks. And 10% of all births are preterm, meaning they occur before 37 weeks of gestation, which puts babies at risk of a host of complications.

Now  researchers have discovered a molecular timer in mice that plays a role in controlling when they give birth. Surprisingly, the timer is activated in the very first days of pregnancy and operates within the uterus.

If the same set of molecules is found to be important in human pregnancies, it could lead to new tests to identify women who are at risk of preterm labour, as well as interventions to delay it.

DNA packaging during pregnancy

Throughout pregnancy, the female body undergoes massive biological shifts, with the activity of hundreds of genes going up or down within the uterus.

Researchers were studying a protein called KDM6B which regulates gene activity. They suspected that during pregnancy, KDM6B could help regulate the genes involved in the transition to labor.

KDM6B works by removing methyl chemical groups from histones—structures that help organize and package DNA within cells. In response to KDM6B, DNA becomes more accessible to other factors that regulate gene expression, turning on the activity of nearby genes.

The team noticed that when they blocked KDM6B, pregnancies in the mice became longer, and their babies were born later than usual.

At first, the scientists suspected that, late in pregnancy, KDM6B must be activating genes in the uterus's epithelial cells, which produce hormones known to trigger labor.

But when they carried out detailed analyses on different cell types, they found that KDM6B's effects on pregnancy length were tied to a different cell type called fibroblasts. These structural cells are not typically considered to play a role in the regulation of labor. Moreover, KDM6B regulated these fibroblasts during the first days of pregnancy.

These findings highlight a surprising role for uterine fibroblasts in regulating birth timing.

Part 1

Comment by Dr. Krishna Kumari Challa on January 22, 2025 at 9:55am

To answer this fundamental question, researchers analyzed data from 9,331 patients cataloged in the Cancer Genome Atlas and the Pan-Cancer Analysis of Whole Genomes. By comparing genetic mutations to epigenetic modifications, they found that mutations were predictably correlated with changes in DNA methylation, one type of epigenetic modification.
They found that a single mutation could cause a cascade of epigenetic changes across the genome, not just where the mutation occurred. Using this relationship, the researchers were able to make similar predictions of age using either mutations or epigenetic changes.

Epigenetic clocks have been around for years, but scientists are only now beginning to answer the question of why epigenetic clocks tick in the first place.

This study demonstrates for the first time that epigenetic changes are intricately and predictably tied to random genetic mutations.
The study's authors note that further research is needed to fully understand the relationship between somatic mutations and epigenetic changes in aging. However, the study's findings provide a major breakthrough in our understanding of the aging process and have important implications for the development of new therapies aimed at preventing or reversing aging.
If somatic mutations are the fundamental driver of aging and epigenetic changes simply track this process, it's going to be a lot harder to reverse aging than we previously thought, say the authors of this study.
This shifts our focus from viewing aging as a programmed process to one that's largely influenced by random, cumulative changes over time.

Zane Koch et al, Somatic mutation as an explanation for epigenetic aging, Nature Aging (2025). DOI: 10.1038/s43587-024-00794-x

Part 2

Comment by Dr. Krishna Kumari Challa on January 22, 2025 at 9:51am

Why our biological clock ticks: Research reconciles major theories of aging

Researchers have published results that shed new light on an old question: what causes aging at the molecular level? Their findings, published in Nature Aging, describe a never-before-seen link between the two most accepted explanations: random genetic mutations and predictable epigenetic modifications. The latter, also known as the epigenetic clock theory, has been widely used by scientists as a consistent, quantitative measure of biological aging.

The new research suggests that the process may not be so simple.

Major research institutions and companies are betting on turning back the epigenetic clock as a strategy to reverse the effects of aging, but this new research suggests that this may only be treating a symptom of aging, not the underlying cause.

If mutations are in fact responsible for the observed epigenetic changes, this fact could fundamentally change the way we approach anti-aging efforts in the future.

There are two prevailing theories about the relationship between aging and DNA. The somatic mutation theory suggests that aging is caused by the accumulation of mutations, permanent changes in our DNA sequence that occur randomly. The epigenetic clock theory suggests that aging occurs due to the accumulation of epigenetic modifications, minor changes to the chemical structure of DNA that do not alter the underlying sequence, but instead change which genes are on or off. Unlike mutations, epigenetic modifications can also be reversed in some cases.

Because epigenetic modifications only occur at specific sites on our genome rather than at random locations, they are easier to quantify and have become a go-to way for scientists to determine the "biological age" of cells. However, scientists have long wondered about the source of these epigenetic changes.

Part 1

Comment by Dr. Krishna Kumari Challa on January 22, 2025 at 9:15am

Neuronal subtypes study uncovers parallel gut-to-brain pathways that regulate feeding behaviours

The ability to regulate one's own food intake is essential to the survival of both humans and other animals. This innate ability ensures that the body receives the nutrients it needs to perform daily activities, without significantly exceeding calorie intake, which could lead to health problems and metabolic disorders.

Past neuroscience studies suggest that the regulation of food intake is supported by specific regions in the brain, including the hypothalamus and caudal nucleus of the solitary tract (cNTS), which is part of the brainstem. This key region in the brainstem is known to integrate sensory signals originating from the gut and then transform them into adaptive feeding behaviours.

While previous research has highlighted the key role of the cNTS in food intake regulation, the unique contribution of the different neuron subtypes within this brainstem region and the mechanisms by which they regulate feeding remain poorly understood. Better understanding these neuron-specific mechanisms could help to devise more effective therapeutic interventions for obesity and eating disorders.

Researchers recently carried out a study aimed at identifying neuronal subtypes in the mouse cNTS that are involved in how mice control their feeding behaviors. Their findings, published in Nature Neuroscience, show that different types of cNTS neurons process gut-originating signals via distinct sensory pathways, collectively contributing to the regulation of feeding.

The cNTS in the brainstem serves as a hub for integrating interoceptive cues from diverse sensory pathways. Understanding  the mechanisms by which cNTS neurons transform these signals into behaviours is vital too.

So the researchers systematically analyzed the brains and feeding behaviors of mice that were genetically intervened upon to turn "off" and "on" nine types of neurons in the cNTS. The researchers found that two key neuron populations, namely Th⁺ (tyrosine hydroxylase-expressing) and Gcg⁺ (glucagon-like peptide 1-expressing) neurons encoded different aspects of food intake.

Th⁺ cNTS neurons encode esophageal mechanical distension and transient gulp size via vagal afferent inputs, providing quick feedback regulation of ingestion speed.

By contrast, Gcg+ cNTS neurons monitor intestinal nutrients and cumulative ingested calories and have long-term effects on food satiation and preference. These nutritive signals are conveyed through a portal vein–spinal ascending pathway rather than vagal sensory neurons.

New studies could explore the unique contribution of the two broad neuron populations outlined by the researchers (i.e., Th⁺ and Gcg⁺ neurons), as well as their interactions with other brain regions in regulating feeding behaviours.

Hongyun Wang et al, Parallel gut-to-brain pathways orchestrate feeding behaviors, Nature Neuroscience (2024). DOI: 10.1038/s41593-024-01828-8

Comment by Dr. Krishna Kumari Challa on January 21, 2025 at 11:52am

In times of uncertainty, the brain takes the easy route by following the crowd

In uncertain situations where information is lacking, individuals often find themselves imitating the choices of others. 

This behaviour highlights a tendency to conform to others when faced with ambiguity. Computational neuroscience research has shown that the decision to follow others unconditionally serves as an alternative strategy that activates certain brain processes in uncertain environments.

Researchers investigated how the decisions of others influence individual decision-making in uncertain contexts.

Decision-making in social situations typically involves a value judgment process that integrates both personal preferences and the choices of others. This study uncovers the strategies the brain employs when access to individual preferences is compromised.

According to the research findings, now published in PLOS Computational Biology, the brain employs a "heuristic" strategy that reflects social information from the choices of others during decision-making. When value judgments based on individual preferences are not possible, individuals tend to take the shortcut of imitating the decisions made by others.

The research team arrived at these conclusions through experiments conducted on participants with partial damage to the brain's insula or dorsal anterior cingulate cortex (dACC), regions known to play critical roles in processing uncertain information.

The research team noted that the implications of these findings could extend to adolescents, whose individual preferences may be in flux. Both situations of uncertainty and the lack of established personal preferences render value judgments based on individual preferences challenging.

This study sheds light on why individuals with unclear personal preferences may be particularly sensitive to the opinions of those around them. Therefore, the importance of creating a supportive environment and implementing educational approaches to help establish individual preferences as a means of addressing social issues such as addiction.

Mark A. Orloff et al, Social conformity is a heuristic when individual risky decision-making is disrupted, PLOS Computational Biology (2024). DOI: 10.1371/journal.pcbi.1012602

Comment by Dr. Krishna Kumari Challa on January 21, 2025 at 11:40am

Extinction threatens nearly a quarter of all freshwater species

Freshwater ecosystems cover less than 1% of Earth's surface, but are vital for life on this planet. New research reveals that damage to these environments is pushing freshwater animals to the edge of extinction, with 24% of species in danger of being wiped out.

Thousands of fish, crab and dragonfly species could become extinct in the coming decades—and many more could follow.

A landmark assessment of the health of nearly 24,000 fresh water species found that just under a quarter are at risk of extinction. Of these, almost 1,000 species are considered Critically Endangered, with 200 having potentially been lost already.

These numbers may only represent the tip of the iceberg, with scientists lacking the information needed to properly understand the extinction risk of thousands of species. The authors of the study, says that urgent action is needed to understand and protect these animals.

"Lack of data on freshwater biodiversity can no longer be used as an excuse for inaction," they say. "Freshwater landscapes are home to 10% of all known species on Earth and key for billions of people's safe drinking water, livelihoods, flood control and climate change mitigation, and must be protected for nature and people alike."

While fresh, clean water is vital for all life on land, freshwater ecosystems are some of the most threatened on Earth. Freshwater environments are being put under pressure as demand for food, water and resources increases.

Wetlands in particular, including bogs, mangroves and saltmarshes, are bearing the brunt of these losses. It's estimated that an area the size of India—a staggering 3.4 million square kilometers—of wetland has been lost since 1700.

The loss of wetlands harms far more than just the animals and plants that live there, as it also limits our ability to fight climate change and stop flooding.

Freshwater sources are also suffering from a cocktail of different challenges. An increase in water abstraction and dams on rivers are reducing the available habitat for wildlife. Some rivers, like the Colorado River, no longer even reach the sea.

The animals that persist in these reduced habitats are then impacted by sewage, industrial and plastic pollution. Yet, despite the rising risk to these species, freshwater environments are significantly understudied compared to the oceans.

While around 10% of all species depend on freshwater, the study was particularly concerned with four groups that are intimately linked to it—the decapods, odonates, mollusks and fishes.

Catherine A. Sayer et al, One-quarter of freshwater fauna threatened with extinction, Nature (2025). DOI: 10.1038/s41586-024-08375-z

Comment by Dr. Krishna Kumari Challa on January 21, 2025 at 11:22am

AI to stop stampedes at world's biggest gathering -Kumbhmela

Science assisting spirituality

Keen to improve India's abysmal crowd management record at large-scale religious events, organizers of the world's largest human gathering are using artificial intelligence to try to prevent stampedes.

Organizers predict up to 400 million pilgrims will visit the Kumbh Mela, a millennia-old sacred show of Hindu piety and ritual bathing that began Monday and runs for six weeks.

Deadly crowd crushes are a notorious feature of Indian religious festivals, and the Kumbh Mela, with its unfathomable throngs of devotees, has a grim track record of stampedes.

More than 400 people died after being trampled or drowned at the Kumbh Mela on a single day of the festival in 1954, one of the largest tolls in a crowd-related disaster globally. Another 36 people were crushed to death in 2013, the last time the festival was staged in the northern city of Prayagraj.

So AI is helping the police avoid reaching that critical mass in sensitive places.

This time, authorities say the technology they have deployed will help them gather accurate estimates of crowd sizes, allowing them to be better prepared for potential trouble. Police say they have installed around 300 cameras at the festival site and on roads leading to the sprawling encampment, mounted on poles and a fleet of overhead drones. Not far from the spiritual center of the festival at the confluence of the Ganges and Yamuna rivers, the network is overseen in a glass-paneled command and control room by a small army of police officers and technicians.

The footage fed into an AI algorithm that gives its handlers an overall estimate of a crowd stretching for miles in every direction, cross-checked against data from railways and bus operators.

They are using AI to track people flow, crowd density at various inlets, adding them up and then interpolating from there. The system sounds the alarm if sections of the crowd get so concentrated that they pose a safety threat.

Organizers say the scale of this year's festival is that of a temporary country -- with numbers expected to total around the combined populations of the United States and Canada.

Organizers have been eager to tout the technological advancements of this year's edition of the Kumbh Mela and their attendant benefits for pilgrims. Even the Pilgrims think  that the fact that there are cameras and drones makes them feel safe!

Yes, science and tech makes people feel safe!

Source: News agencies

Comment by Dr. Krishna Kumari Challa on January 19, 2025 at 12:18pm

Sepsis can be incredibly challenging to treat in such cases. The systems that control blood clotting and bleeding become dangerously unbalanced.

The study, conducted in nonhuman primates, found that when bacteria containing LPS entered the bloodstream, it quickly activated the clotting system. This included coagulating proteins like factor XII, which seems to initiate the clotting process, causing a chain reaction.

Even when we know the bacteria causing the infection, different strains can behave differently. By understanding this,  scientists hope to develop precision therapies.

André L. Lira et al, The physicochemical properties of lipopolysaccharide chemotypes regulate activation of the contact pathway of blood coagulation, Journal of Biological Chemistry (2024). DOI: 10.1016/j.jbc.2024.108110

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