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Comment by Dr. Krishna Kumari Challa on September 4, 2025 at 12:02pm

Pancreatic insulin disruption triggers bipolar disorder-like behaviors in mice, study shows

Bipolar disorder is a psychiatric disorder characterized by alternating episodes of depression (i.e., low mood and a loss of interest in everyday activities) and mania (i.e., a state in which arousal and energy levels are abnormally high). On average, an estimated 1–2% of people worldwide are diagnosed with bipolar disorder at some point during their lives.

Bipolar disorder can be highly debilitating, particularly if left untreated. Understanding the neural and physiological processes that contribute to its emergence could thus be very valuable, as it could inform the development of new prevention and treatment strategies.

In addition to experiencing periodic changes in mood, individuals diagnosed with this disorder often exhibit some metabolic symptoms, including changes in their blood sugar levels. While some previous studies reported an association between blood sugar control mechanisms and bipolar disorder, the biological link between the two has not yet been uncovered.

Researchers recently carried out a study aimed at further exploring the link between insulin secretion and bipolar disorder-like behaviors, particularly focusing on the expression of the gene RORβ. 

Their findings, published in Nature Neuroscience, show that an overexpression of this gene in a subtype of pancreatic cells disrupts the release of insulin, which in turn prompts a feedback loop with a region of the brain known as the hippocampus, producing alternative depression-like and mania-like behaviors in mice.

The results in mice point to a pancreas–hippocampus feedback mechanism by which metabolic and circadian factors cooperate to generate behavioral fluctuations, and which may play a role in bipolar disorder, wrote the authors.

Yao-Nan Liu et al, A pancreas–hippocampus feedback mechanism regulates circadian changes in depression-related behaviors, Nature Neuroscience (2025). DOI: 10.1038/s41593-025-02040-y.

Comment by Dr. Krishna Kumari Challa on September 4, 2025 at 11:57am

SeeMe detects hidden signs of consciousness in brain injury patients

SeeMe, a computer vision tool tested by Stony Brook University researchers, was able to detect low-amplitude, voluntary facial movements in comatose acute brain injury patients days before clinicians could identify overt responses.

There are ways to detect covert consciousness with EEG and fMRI, though these are not always available. Many acute brain injury patients appear unresponsive in early care, with signs that are so small, or so infrequent, that they are simply missed.

In the study, "Computer vision detects covert voluntary facial movements in unresponsive brain injury patients," published in Communications Medicine, investigators designed SeeMe to quantify tiny facial movements in response to auditory commands with the objective of identifying early, stimulus-evoked behavior.

A single-center prospective cohort included 37 comatose acute brain injury patients and 16 healthy volunteers, aged 18–85, enrolled at Stony Brook University Hospital. Patients had initial Glasgow Coma Scale scores ≤8 and no prior neurologically debilitating diagnoses.

SeeMe tagged facial pores at ~0.2 mm resolution and tracked movement vectors while subjects heard three commands: open your eyes, stick out your tongue, and show me a smile.

Results indicate earlier and broader detection with SeeMe. Eye-opening was detected on average 9.1 (± 5.5) days after injury by SeeMe versus 13.2 (± 11.4) days by clinical examination, yielding a 4.1-day lead.

SeeMe identified eye-opening in 30 of 36 patients (85.7%) compared with 25 of 36 (71.4%) by clinical exam. Among patients without an endotracheal tube obscuring the mouth, SeeMe detected mouth movements in 16 of 17 (94.1%).

In seven patients with analyzable mouth videos and clinical command following, SeeMe identified reproducible mouth responses 8.3 days earlier on average. Amplitude and frequency of SeeMe-positive responses correlated with discharge outcomes on the Glasgow Outcome Scale-Extended, with significant Kruskal-Wallis results for both features.

A deep neural network classifier trained on SeeMe-positive trials identified command specificity with 81% accuracy for eye-opening and an overall accuracy of 65%. Additional observations were lower, with 37% for tongue movement and 47% for smile, indicating a strong specificity for eyes.

Authors conclude that acute brain injury patients can exhibit low-amplitude, stimulus-evoked facial movements before overt signs appear at bedside, suggesting that many covertly conscious patients may have motor behavior currently undetected by clinicians.

Earlier detection could inform family discussions, guide rehabilitation timing, and serve as a quantitative signal for future monitoring or interface-based communication strategies, while complementing standard examinations.

Xi Cheng et al, Computer vision detects covert voluntary facial movements in unresponsive brain injury patients, Communications Medicine (2025). DOI: 10.1038/s43856-025-01042-y

Comment by Dr. Krishna Kumari Challa on September 4, 2025 at 11:44am

Some sugar substitutes linked to faster cognitive decline

Some sugar substitutes may come with unexpected consequences for long-term brain health, according to a study published in Neurology. The study examined seven low- and no-calorie sweeteners and found that people who consumed the highest amounts experienced faster declines in thinking and memory skills compared to those who consumed the lowest amounts.

The link was even stronger in people with diabetes. While the study showed a link between the use of some artificial sweeteners and cognitive decline, it did not prove that they were a cause.

The artificial sweeteners examined in the study were aspartame, saccharin, acesulfame-K, erythritol, xylitol, sorbitol and tagatose. These are mainly found in ultra-processed foods like flavored water, soda, energy drinks, yogurt and low-calorie desserts. Some are also used as a standalone sweetener.

Low- and no-calorie sweeteners are often seen as a healthy alternative to sugar, however the new findings suggest certain sweeteners may have negative effects on brain health over time.

The study included 12,772 adults from across Brazil. The average age was 52, and participants were followed for an average of eight years.

After adjusting for factors such as age, sex, high blood pressure and cardiovascular disease, researchers found people who consumed the highest amount of sweeteners showed faster declines in overall thinking and memory skills than those who consumed the lowest amount, with a decline that was 62% faster. This is the equivalent of about 1.6 years of aging. Those in the middle group had a decline that was 35% faster than the lowest group, equivalent to about 1.3 years of aging.

When researchers broke the results down by age, they found that people under the age of 60 who consumed the highest amounts of sweeteners showed faster declines in verbal fluency and overall cognition when compared to those who consumed the lowest amounts. They did not find links in people over 60. They also found that the link to faster cognitive decline was stronger in participants with diabetes than in those without diabetes.

When looking at individual sweeteners, consuming aspartame, saccharin, acesulfame-k, erythritol, sorbitol and xylitol was associated with a faster decline in overall cognition, particularly in memory.

They found no link between the consumption of tagatose and cognitive decline.

https://www.neurology.org/doi/10.1212/WNL.0000000000214023

Comment by Dr. Krishna Kumari Challa on September 4, 2025 at 9:22am

The cephalic furrow is especially interesting because it is a prominent embryonic invagination whose formation is controlled by genes, but that has no obvious function during development. The fold does not give rise to specific structures, and later in development, it simply unfolds, leaving no trace.
With their experiments, the researchers show that the absence of the cephalic furrow leads to an increase in the mechanical instability of embryonic tissues and that the primary sources of mechanical stress are cell divisions and tissue movements typical of gastrulation. They demonstrate that the formation of the cephalic furrow absorbs these compressive stresses. Without a cephalic furrow, these stresses build up, and outward forces caused by cell divisions in the single-layered blastula cause mechanical instability and tissue buckling.

This intriguing physical role gave the researchers the idea that the cephalic furrow may have evolved in response to the mechanical challenges of dipteran gastrulation, with mechanical instability acting as a potential selective pressure.
Flies either feature a cephalic furrow, or if they lack one, display widespread out-of-plane division, meaning the cells divide downward to reduce the surface area. Both mechanisms act as mechanical sinks to prevent tissue collision and distortion.
These findings uncover empirical evidence for how mechanical forces can influence the evolution of innovations in early development. The cephalic furrow may have evolved through genetic changes in response to the mechanical challenges of dipteran gastrulation. They show that mechanical forces are not just important for the development of the embryo but also for the evolution of its development.

Patterned invagination prevents mechanical instability during gastrulation, Nature (2025). DOI: 10.1038/s41586-025-09480-3

Bipasha Dey et al, Divergent evolutionary strategies pre-empt tissue collision in gastrulation. Nature (2025). DOI: 10.1038/s41586-025-09447-4

Part 2

Comment by Dr. Krishna Kumari Challa on September 4, 2025 at 9:18am

Fruit fly research shows that mechanical forces drive evolutionary change

A tissue fold known as the cephalic furrow, an evolutionary novelty that forms between the head and the trunk of fly embryos, plays a mechanical role in stabilizing embryonic tissues during the development of the fruit fly Drosophila melanogaster.

Researchers have integrated computer simulations with their experiments and showed that the timing and position of cephalic furrow formation are crucial for its function, preventing mechanical instabilities in the embryonic tissues.

The work appears in Nature.

The increased mechanical instability caused by embryonic tissue movements may have contributed to the origin and evolution of the cephalic furrow genetic program. This shows that mechanical forces can shape the evolution of new developmental features.

Mechanical forces shape tissues and organs during the development of an embryo through a process called morphogenesis. These forces cause tissues to push and pull on each other, providing essential information to cells and determining the shape of organs. Despite the importance of these forces, their role in the evolution of development is still not well understood.

Animal embryos undergo tissue flows and folding processes, involving mechanical forces, that transform a single-layered blastula (a hollow sphere of cells) into a complex multi-layered structure known as the gastrula. During early gastrulation, some flies of the order Diptera form a tissue fold at the head-trunk boundary called the cephalic furrow. This fold is a specific feature of a subgroup of Diptera and is therefore an evolutionary novelty of flies.

Part1

Comment by Dr. Krishna Kumari Challa on September 4, 2025 at 9:12am

New tool enables rapid, large-scale profiling of disease-linked RNA modifications

Researchers have developed a powerful tool capable of scanning thousands of biological samples to detect transfer ribonucleic acid (tRNA) modifications—tiny chemical changes to RNA molecules that help control how cells grow, adapt to stress and respond to diseases such as cancer and antibiotic‑resistant infections. This tool opens up new possibilities for science, health care and industry—from accelerating disease research and enabling more precise diagnostics, to guiding the development of more effective medical treatments for diseases such as cancer and antibiotic‑resistant infections.

Cancer and infectious diseases are complicated health conditions in which cells are forced to function abnormally by mutations in their genetic material or by instructions from an invading microorganism. The SMART-led research team is among the world's leaders in understanding how the epitranscriptome—the over 170 different chemical modifications of all forms of RNA—controls growth of normal cells and how cells respond to stressful changes in the environment, such as loss of nutrients or exposure to toxic chemicals. The researchers are also studying how this system is corrupted in cancer or exploited by viruses, bacteria and parasites in infectious diseases.
Current molecular methods used to study the expansive epitranscriptome and all of the thousands of different types of modified RNA are often slow, labor‑intensive, costly and involve hazardous chemicals which limit research capacity and speed.

To solve this problem, the SMART team developed a new tool that enables fast, automated profiling of tRNA modifications—molecular changes that regulate how cells survive, adapt to stress and respond to disease. This capability allows scientists to map cell regulatory networks, discover novel enzymes and link molecular patterns to disease mechanisms, paving the way for better drug discovery and development, and more accurate disease diagnostics.

SMART's automated system was specially designed to profile tRNA modifications across thousands of samples rapidly and safely. Unlike traditional methods—which are costly, labor‑intensive and use toxic solvents such as phenol and chloroform—this tool integrates robotics to automate sample preparation and analysis, eliminating the need for hazardous chemical handling and reducing costs. This advancement increases safety, throughput and affordability, enabling routine large‑scale use in research and clinical labs.

Jingjing Sun et al, tRNA modification profiling reveals epitranscriptome regulatory networks in Pseudomonas aeruginosa, Nucleic Acids Research (2025). DOI: 10.1093/nar/gkaf696

Comment by Dr. Krishna Kumari Challa on September 4, 2025 at 8:52am

In the paper, they argue that fusions are a specific example of a more general and extensive internal force that applies across mutation types. Rather than local accidents arising at random locations in the genome disconnected from other genetic information, mutational processes put together multiple meaningful pieces of heritable information in many ways.

Genes that evolved to interact tightly are more likely to be fused; single-letter RNA changes that evolved to occur repeatedly across generations via regulatory phenomena are more likely to be "hardwired" as point mutations into the DNA; genes that evolved to interact in incipient networks, each under its own regulation, are more likely to be invaded by the same transposable element that later becomes a master-switch of the network, streamlining regulation, and so on. Earlier mutations influence the origination of later ones, forming a vast network of influences over evolutionary time.

Previous studies examined mutation rates as averages across genomic positions, masking the probabilities of individual mutations. But these new studies suggest that, at the scale of individual mutations, each mutation has its own probability, and the causes and consequences of mutation are related.
At each generation, mutations arise based on the information that has accumulated in the genome up to that time point, and those that survive become a part of that internal information.
This vast array of interconnected mutational activity gradually hones in over the generations on mutations relevant to the long-term pressures experienced, leading to long-term directed mutational responses to specific environmental pressures, such as the malaria and Trypanosoma–protective HbS and APOL1 mutations.
New genetic information arises in the first place, they argue, as a consequence of the fact that mutations simplify genetic regulation, hardwiring evolved biological interactions into ready-made units in the genome. This internal force of natural simplification, together with the external force of natural selection, act over evolutionary time like combined forces of parsimony and fit, generating co-optable elements that themselves have an inherent tendency to come together into new, emergent interactions.
Co-optable elements are generated by simplification under performance pressure, and then engage in emergent interactions—the source of innovation is at the system level.
Understood in the proper timescale, an individual mutation does not arise at random nor does it invent anything in and of itself.
The potential depth of evolution from this new perspective can be seen by examining other networks. For example, the gene fusion mechanism—where genes repeatedly used together across evolutionary time are more likely to be fused together by mutation—echoes chunking, one of the most basic principles of cognition and learning in the brain, where pieces of information that repeatedly co-occur are eventually chunked into a single unit.

Yet fusions are only one instance of a broader principle: diverse mutational processes respond to accumulated information in the genome, combining it over generations into streamlined instructions. This view recasts mutations not as isolated accidents, but as meaningful events in a larger, long-term process.

Daniel Melamed et al, De novo rates of a Trypanosoma -resistant mutation in two human populations, Proceedings of the National Academy of Sciences (2025). DOI: 10.1073/pnas.2424538122

Part 3

Comment by Dr. Krishna Kumari Challa on September 4, 2025 at 8:49am

The new findings challenge the notion of random mutation fundamentally.
Historically, there have been two basic theories for how evolution happens— random mutation and natural selection, and Lamarckism—the idea that an individual directly senses its environment and somehow changes its genes to fit it. Lamarckism has been unable to explain evolution in general, so biologists have concluded that mutations must be random.
This new theory moves away from both of these concepts, proposing instead that two inextricable forces underlie evolution. While the well-known external force of natural selection ensures fitness, a previously unrecognized internal force operates inside the organism, putting together genetic information that has accumulated over generations in useful ways.
To illustrate, take fusion mutations, a type of mutation where two previously separate genes fuse to form a new gene. As for all mutations, it has been thought that fusions arise by accident: one day, a gene moves by error to another location and by chance fuses to another gene, once in a great while, leading to a useful adaptation. But researchers have recently shown that genes do not fuse at random.
Instead, genes that have evolved to be used together repeatedly over generations are the ones that are more likely to get fused. Because the genome folds in 3D space, bringing genes that work together to the same place at the same time in the nucleus with their chromatin open, molecular mechanisms fuse these genes rather than others. An interaction involving complex regulatory information that has gradually evolved over generations leads to a mutation that simplifies and "hardwires" it into the genome.
Part 2

Comment by Dr. Krishna Kumari Challa on September 4, 2025 at 8:47am

Mutations driving evolution are informed by the genome, not random, study suggests

A study published in the Proceedings of the National Academy of Sciences by scientists  shows that an evolutionarily significant mutation in the human APOL1 gene arises not randomly but more frequently where it is needed to prevent disease, fundamentally challenging the notion that evolution is driven by random mutations and tying the results to a new theory that, for the first time, offers a new concept for how mutations arise.

Implications for biology, medicine, computer science, and perhaps even our understanding of the origin of life itself, are potentially far reaching.

A random mutation is a genetic change whose chance of arising is unrelated to its usefulness. Only once these supposed accidents arise does natural selection vet them, sorting the beneficial from the harmful. For over a century, scientists have thought that a series of such accidents has built up over time, one by one, to create the diversity and splendor of life around us.

However, it has never been possible to examine directly whether mutations in the DNA originate at random or not. Mutations are rare events relative to the genome's size, and technical limitations have prevented scientists from seeing the genome in enough detail to track individual mutations as they arise naturally.

To overcome this, researchers developed a new ultra-accurate detection method and recently applied it to the famous HbS mutation, which protects from malaria but causes sickle-cell anemia in homozygotes.

Results showed that the HbS mutation did not arise at random, but emerged more frequently exactly in the gene and population where it was needed. Now, they report the same nonrandom pattern in a second mutation of evolutionary significance.

The new study examines the de novo origination of a mutation in the human APOL1 gene that protects against a form of trypanosomiasis, a disease that devastated central Africa in historical times and until recently has caused tens of thousands of deaths there per year, while increasing the risk of chronic kidney disease in people with two copies.

If the APOL1 mutation arises by chance, it should arise at a similar rate in all populations, and only then spread under Trypanosoma pressure. However, if it is generated nonrandomly, it may actually arise more frequently where it is useful.

Results supported the nonrandom pattern: the mutation arose much more frequently in sub-Saharan Africans, who have faced generations of endemic disease, compared to Europeans, who have not, and in the precise genomic location where it confers protection.

Part 1

Comment by Dr. Krishna Kumari Challa on September 3, 2025 at 12:44pm

When the germ-free mice were just a handful of days old, the researchers found fewer neurons in their PVN, even when microbes were introduced after birth. That suggests the changes caused by these microorganisms happen in the uterus during development.

These neural modifications last, too: the researchers also found that the PVN was neuron-light even in adult mice, if they'd been raised to be germ-free. However, the cross-fostering experiment was not continued into adulthood (around eight weeks).

The details of this relationship still need to be worked out and researched in greater detail, but the takeaway is that microbes – specifically the mix of microbes in the mother's gut – can play a notable role in the brain development of their offspring.
Rather than shunning our microbes, we should recognize them as partners in early life development. They're helping build our brains from the very beginning, say the researchers.
While this has only been shown in mouse models so far, there are enough biological similarities between mice and humans that there's a chance we're also shaped by our mother's microbes before we're born.

One of the reasons this matters is because practices like Cesarean sections and the use of antibiotics around birth are known to disrupt certain types of microbe activity – which may in turn be affecting the health of newborns.

https://www.sciencedirect.com/science/article/pii/S0018506X25000686...

Part 2

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