Comment

Comment by Dr. Krishna Kumari Challa 1 hour ago

CRISPR gene-editing therapy safely and continuously lowers cholesterol and triglycerides, first-in-human trial shows

A first-in-human clinical trial has shown that a one-time infusion of a gene-editing therapy using CRISPR-Cas9 was effective and safe in reducing LDL ("bad") cholesterol and triglycerides in people with medication-resistant lipid disorders through one year of follow-up across all doses.
In a 15-participant phase I trial, one-time CRISPR-Cas9 therapy targeting hepatic ANGPTL3 lowered LDL cholesterol by 52.5% and triglycerides by 47.8% at 12 months at the highest dose. No treatment-related serious adverse events occurred during one-year follow-up; longer-term safety monitoring is planned.

Luke J. Laffin et al, Durability of CRISPR-Cas9 Gene Editing Targeting ANGPTL3 with CTX310, New England Journal of Medicine (2026). DOI: 10.1056/nejmc2609825

Comment by Dr. Krishna Kumari Challa 1 hour ago

Aging blocks the retina's ability to regrow lost neurons, a first-of-its-kind study finds
Aging markedly reduces transcription factor–driven glial-to-neuron reprogramming in the retina. Reduced cellular plasticity and age-associated inflammation, potentially worsened by barrier dysfunction, contribute to this limitation. Anti-inflammatory steroids partially restored regeneration in aged tissue.

Jugasmita Deka et al, Aging limits neuronal regeneration from glia in the mouse retina, Proceedings of the National Academy of Sciences (2026). DOI: 10.1073/pnas.2612369123

Comment by Dr. Krishna Kumari Challa 1 hour ago

The results of the team's analyses suggest that interconnected neural circuits in the mouse cortex play a key role in regulating the dimensionality of neural activity. In other words, these local circuits help control how many different patterns of activity a group of neurons can exhibit at a given time.

The researchers also found that the dimensionality of cortical activity was not fixed. Over time, they observed shifts between states that involved different numbers of distinct activity patterns.

David Dahmen et al, Strong and localized recurrence controls the dimensionality of neural activity across brain areas, Nature Neuroscience (2026). DOI: 10.1038/s41593-026-02395-w.

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part 2

Comment by Dr. Krishna Kumari Challa 1 hour ago

Local neural wiring may set the brain's range of activity patterns

The human brain contains billions of neurons, specialized nerve cells that receive, transmit and process information through electrical and chemical signals. Human thoughts, sensory perceptions and behaviors are known to emerge not from the activity of individual neurons but from collective patterns of activity distributed across different neuron populations.

One way to characterize the collective activity of neurons is to measure its dimensionality, or, in other words, the number of independent activity patterns (i.e., degrees of freedom) exhibited by a specific neuronal population. High-dimensional activity can encompass various distinct activity patterns, while low-dimensional activity is restricted to a smaller range of possible patterns.

A new study  published in Nature Neuroscience, suggest that the collective activity of cortical networks is strongly influenced by the structure of neural circuits. As a result, local neural wiring could shape the breadth of activity states available to the brain.

The brain contains an astronomical number of neurons, but it is their collective activity that underlies brain function. The number of degrees of freedom that this activity explores (its dimensionality) is therefore a fundamental signature of neural dynamics. However, it is not known what controls dimensionality in the biological brain.

Researchers analyzed neural activity recordings collected in the mouse visual cortex using Neuropixels. These are tiny probes that can be used to monitor the electrical  activity of hundreds of neurons at once.

"Through analysis of high-density Neuropixels recordings, here, we argue that areas across the mouse cortex predominantly operate in a sensitive regime that gives recurrent synaptic networks a strong role in regulating dimensionality," the authors wrote. "This control is expressed across time, as cortical activity transitions among states with different dimensionalities. Moreover, this control is mediated through highly tractable features of synaptic networks (network motifs)."

The researchers tried to determine how many independent activity patterns were required to describe the collective activity of neurons in the mouse visual cortex. They also tracked this dimensionality over time to shed light on whether cortical activity remained in a single state or shifted between states with different dimensionalities.

The researchers also analyzed a dataset that contained physiological measurements of synaptic connections among more than 32,000 pairs of neurons in mouse and human cortical tissue. This allowed them to investigate whether network motifs predicted to affect dimensionality were prevalent in both species.

"Analyzing a massive synaptic physiology dataset, we find that motifs impacting dimensionality are prevalent in both mouse and human brains," the authors wrote. "Thus, local circuitry scales up systematically to help control the degrees of freedom that brain networks may explore and exploit."

Part 1

Comment by Dr. Krishna Kumari Challa 3 hours ago

Could damaged sperm be causing miscarriages?

Comment by Dr. Krishna Kumari Challa yesterday

Scientists studying cockroach milk and nose-blowing win Ig Nobel prizes for quirky science

Ten research teams were honoured this week at a satirical science awards ceremony that was hosted outside the U.S. for the first time due to travel concerns.
Ig Nobel prizes recognized unconventional work on cockroach milk, nose blowing, kissing evolution, and soil decomposition measured using buried underwear. The ceremony moved to Zurich because of travel and visa concerns, with future events planned across Europe.
Researchers who studied milk from cockroaches and analyzed soil health using underwear received Ig Nobel prizes celebrating unusual and imaginative contributions to science.
Another research team buried 1,000 pairs of underwear in more than 25 countries to study how critters in the soil helped them decompose.

Comment by Dr. Krishna Kumari Challa yesterday

Patients diagnosed with lung cancer found to have more microplastic in their lungs

People with lung cancer are more likely to have microplastics in their lungs and to have larger quantities of microplastics in their lungs, according to research that has been presented at the European Respiratory Society (ERS) Congress in Barcelona, Spain.
Among 100 patients undergoing bronchoscopy, microplastics were detected in 70%, with higher detection frequency and burden in those later diagnosed with lung cancer. Polypropylene and polyethylene predominated. The observational results show an association but cannot determine whether microplastics contribute to cancer or are retained differently by diseased lungs.
Researchers say their study adds to evidence that microplastics are entering our bodies via the air we breathe and suggests that there may be a link between microplastics and lung disease.
Across all samples, the researchers identified a total of 232 microplastic particles. Overall, 70% of patients had detectable microplastics in at least one sample (either the lung wash, tissue or both). When the lung wash and tissue samples from each patient were analyzed together, patients with lung cancer were more likely to have detectable microplastics and had a higher overall microplastic burden than those without cancer.

Patients with lung cancer were also more likely to have detectable microplastics in their lung wash samples (66% versus 46%) and had a higher microplastic burden than patients without lung cancer.

When the researchers compared the lung wash and tissue samples from the same individual, they found that patients with more microplastic in their lung wash tended to have less in the corresponding tissue sample, and vice versa. Because lung wash samples collect particles from the airspaces whereas tissue samples capture particles embedded within the lung itself, this finding suggests that microplastics may not be distributed evenly throughout the lung and that different regions may retain particles differently.

Analysis of the microplastics showed that polypropylene and polyethylene were the most common types of plastic. These are widely used in everyday products such as packaging, textiles, household materials and consumer goods.
This adds to the growing evidence that reducing environmental plastic pollution may have benefits that extend beyond ecosystems and into human health.

‘High respiratory microplastic burden across paired airway and tissue samples in patients with lung cancer’ by Ilias E. Dimeas et al. was presented in session at European Respiratory Society Congress 2026 on Thursday 3rd September.

Comment by Dr. Krishna Kumari Challa yesterday

Cancer cells release antioxidants to prevent immune cells from destroying them

Molecules called reactive oxygen species, which include so-called "free radicals," have long been viewed as damaging by-products of our body's metabolism—a reason antioxidant supplements have been considered a potential way to reduce cancer risk.
Now, scientists have discovered that certain immune cells depend on these molecules to activate and destroy cancer cells and that tumours exploit this dependency by releasing natural antioxidants to shut down the immune attack.
Our immune system keeps us healthy by hunting down and destroying harmful material, including invading bacteria and viruses, as well as cancer cells. It does so by deploying a number of different types of immune cells, including specialized cells known as T cells. These T cells hunt down and destroy tumor cells, but they need small amounts of reactive oxygen species to activate and switch on their killing ability.
Researchers analyzed the fluid surrounding cells within tumours grown in mice and found that cancers chemically 'smother' T cells, stopping their activation and preventing them from destroying cancer cells. Tumours do this by releasing large amounts of a protein that is a natural antioxidant, Peroxiredoxin 1 (PRDX1), which mops up reactive oxygen species and deprives T cells of the activating signals they need to kill cancer cells.

Next, the team used CRISPR gene-editing technology to create mouse cancer cells that could no longer make the antioxidant protein. They found that removing the cancer cells' capacity to produce the antioxidant promoted immune-cell activity and limited tumor growth.

Finally, the team looked for the same mechanism in people. They analyzed published data on the proteins released by human cancer cell lines, examined gene activity across thousands of human tumours, and isolated the fluid surrounding tumours removed from patients. All three approaches pointed the same way: Human cancers also release PRDX1 into their surroundings, where it can strip away the reactive oxygen species that T cells depend on.
Now that the researchers found a new way by which cancers shut down the immune system, we can block this process and make tumours that don't respond to some immunotherapies start responding to treatment. That tells us this is a pathway worth targeting therapeutically, and there are several ways we might be able to achieve this.
The findings also carry broader implications. Several large randomized clinical trials have found that antioxidant supplements fail to reduce cancer risk and, in some cases, worsen outcomes.

The discovery that T cells depend on reactive oxygen species to fight tumours may help explain why: Antioxidants could inadvertently blunt the immune system's ability to attack cancer.

Tumor-derived antioxidants suppress immunity by depriving T cells of reactive oxygen species, Science (2026). DOI: 10.1126/science.adz8203

Comment by Dr. Krishna Kumari Challa yesterday

Brain scans reveal new link between progesterone and women's mood

The influence of the hormone progesterone on mood is well known. Now, researchers have shown how higher levels of progesterone during the menstrual cycle are linked to less distinct patterns of activity in areas of the brain involved in controlling emotions.
The study, published in Psychological Medicine, explored how natural levels of the ovarian hormones estradiol and progesterone influence parts of the brain involved in emotion control and whether this could help explain differences in mood.

Emotion control is the ability to regulate behaviour in response to emotional information, particularly when automatic emotional responses need to be overridden. For example, if someone needed to ask an unfriendly person for help, their instinct might be to avoid them—emotion control would help overcome that impulse and approach them anyway.
Analysis of MRI scan data from study participants revealed that when progesterone levels were higher, there was a less clear distinction between "easy" and "difficult" emotional situations in the brain scans. This suggests that the brain would be less able to distinguish between different emotional situations in real life.

In contrast, participants whose brain scans had a clearer distinction between "easy" and "difficult" emotional situations tended to report better mood in the preceding week.

This brain mechanism accounted for roughly 7% of the variation in mood scores.
The researchers found that higher progesterone levels were linked to brain activity patterns that made it harder to tell different emotion control situations apart, which also corresponded with lower mood in participants.

This suggests that if the brain can tell different emotional situations apart more clearly, it may be better at regulating emotion in daily life.

Endogenous progesterone blurs frontostriatal representations of emotion control in healthy young women, Psychological Medicine (2026). DOI: 10.1017/S0033291726105315

Comment by Dr. Krishna Kumari Challa yesterday

Healthy aging shaped by more varied biology than previously thought

Molecular changes in aging are far more unique than previously thought, meaning two healthy individuals of identical age can experience significantly different aging journeys.
A new study is the most comprehensive molecular study of aging to date. It demonstrates for the first time that genetic factors and environmental influences continuously interact across a person's lifespan.

The study, published in Science, observed how multiple genetic variants shape how an individual ages.

Notably, researchers found different courses of change among participants with a gene linked to cardiac aging (CXCL9). They also found that levels of the tumour suppressor gene tumour protein p53 (TP53) declined in certain individuals as they grew older, potentially altering their risk of cancer.

Such biological shifts can indicate distinct environmental exposures or reveal an underlying genetic predisposition to disease. Pinpointing individuals at higher risk offers future opportunities for earlier targeted health care interventions.

Importantly, the research also highlights correlations between environmental exposures, such as shifting blood levels of PFAS, commonly referred to as "forever chemicals," and evolving molecular profiles over time. This highlights how public health measures targeting environmental risks can affect the molecular level.

Molecular aging involves the steady accumulation of cellular damage alongside chemical changes in key molecules like DNA, proteins and lipids. Over time, this progression drives a gradual deterioration of tissue function, heightened physical vulnerability and a higher risk of age-related conditions, including cancer as well as cardiometabolic and neurodegenerative disorders.

Understanding how aging happens at the molecular level is vital to preventing or even reversing a range of age-related diseases—as well as increasing longevity.
Rather than there being a single molecular roadmap of aging, this study shows that people follow distinct biological journeys. Two healthy people of the same age can be aging in surprisingly different ways at the molecular level. That raises the possibility of much more personalized approaches to predicting disease risk and maintaining health as we grow older.
Over eight years, the team repeatedly measured blood RNA levels, the activity levels of around 16,000 genes and hundreds of metabolites in the same 335 individuals from TwinsUK during the study, creating one of the most detailed long-term multi-omic studies of healthy aging to date. They found that some study participants had markedly different, and sometimes opposite, molecular changes.

Aging patterns were not uniform across the immune system, which is key to the aging process—molecular changes over time differed between innate and adaptive immune cells. Innate immune cells are the fast, first line of defense you are born with, while adaptive immunity is a slower immune response that builds memory over time.
These findings suggest that human aging at the molecular level is not a uniform process, but one that is dynamic and environment-dependent.

Longitudinal dynamics of gene expression and metabolomics in an ageing population cohort, Science (2026). DOI: 10.1126/science.aed6452

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