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Comment by Dr. Krishna Kumari Challa on June 15, 2025 at 9:11am

Analyses drew on 33 years of follow-up from over 12,000 adults across four US communities, with participant age at vascular risk measurement ranging from 45 to 74 years. Dementia incidence was tracked through standardized clinical assessments, proxy interviews, and linked medical records. Analyses were limited to self-identified Black and white participants.

Among participants with vascular risk factors measured at ages 45–54, 21.8% of dementia cases by age 80 were attributable to those risks. This proportion increased to 26.4% when measured at ages 55–64, and to 44.0% at ages 65–74. For dementia occurring after age 80, attributable fractions dropped sharply to between 2% and 8%.

Subgroup analyses revealed higher attributable risk in APOE ε4 noncarriers (up to 61.4% for those aged 65–74), Black participants (up to 52.9%), and females (up to 51.3%). APOE ε4 noncarriers are individuals who lack the gene variant with the strongest known risk factor for Alzheimer's disease. In this lower genetic-risk group, modifiable vascular conditions such as hypertension, diabetes, and smoking accounted for a greater share of dementia risk.

The authors conclude, "Results suggest that maintaining ideal vascular health into late life could substantially reduce dementia risk before age 80 years."

Jason R. Smith et al, Contribution of Modifiable Midlife and Late-Life Vascular Risk Factors to Incident Dementia, JAMA Neurology (2025). DOI: 10.1001/jamaneurol.2025.1495

Roch A. Nianogo et al, Targeting Vascular Risk Factors to Reduce Dementia Risk, JAMA Neurology (2025). DOI: 10.1001/jamaneurol.2025.1493

Part 2

Comment by Dr. Krishna Kumari Challa on June 15, 2025 at 9:08am

Study ties midlife vascular health to later dementia risk

Dementia before age 80 is potentially preventable through early intervention on common vascular risk factors, according to new research. Findings suggest that up to 44% of dementia cases could be attributed to vascular risk factors, specifically hypertension, diabetes, or smoking.

Hypertension, diabetes, and smoking are commonly implicated risk factors, likely acting through arteriosclerotic cerebral small vessel disease (CSVD).

CSVD is a catch-all term for a variety of conditions resulting from damage to small blood vessels in the brain. Narrowing, hardening, or obstruction of small blood vessels in the brain can starve brain cells of oxygen, which can damage nearby brain cells.

Early symptoms are often easily confused with, or overlap with, the normal effects of aging. Mental fog, forgotten names, misplaced objects, can occur naturally throughout a lifetime of remembering things, such that when vascular-related damage reaches the point of a dementia diagnosis, it may appear as a rapid onset, usually presenting later in life.

Attribution is further complicated by the frequent co-occurrence of vascular injury and Alzheimer's pathology, leaving unresolved how much dementia could be prevented by controlling vascular conditions earlier in life.

In the study, "Contribution of Modifiable Midlife and Late-Life Vascular Risk Factors to Incident Dementia," published in JAMA Neurology, researchers designed a prospective cohort analysis to estimate the proportion of dementia attributable to midlife and late-life  vascular risk factors.

Part 1

Comment by Dr. Krishna Kumari Challa on June 14, 2025 at 11:52am

Scientists detect light passing through entire human head, opening new doors for brain imaging

For decades, scientists have used near-infrared light to study the brain in a noninvasive way. This optical technique, known as fNIRS (functional near-infrared spectroscopy), measures how light is absorbed by blood in the brain, to infer activity.

Valued for portability and low cost, fNIRS has a major drawback: it can't see very deep into the brain. Light typically only reaches the outermost layers of the brain, about 4 centimeters deep—enough to study the surface of the brain, but not deeper regions involved in critical functions like memory, emotion, and movement.

This drawback has restricted the ability to study deeper brain regions without expensive and bulky equipment like MRI machines.

Now, researchers  have demonstrated something previously thought impossible: detecting light that has traveled all the way through an adult human head.

Their study, "Photon transport through the entire adult human head," published in Neurophotonics, shows that, with the right setup, it is possible to measure photons that pass from one side of the head to the other, even across its widest point.

To achieve this, the team used powerful lasers and highly sensitive detectors in a carefully controlled experiment. They directed a pulsed laser beam at one side of a volunteer's head and placed a detector on the opposite side. The setup was designed to block out all other light and maximize the chances of catching the few photons that made the full journey through the skull and brain.

The researchers also ran detailed computer simulations to predict how light would move through the complex layers of the head. These simulations matched the experimental results closely, confirming that the detected photons had indeed traveled through the entire head.

Interestingly, the simulations revealed that light tends to follow specific paths, guided by regions of the brain with lower scattering, such as the cerebrospinal fluid.

This breakthrough suggests that it may be possible to design new optical devices that can reach deeper brain areas than current technologies allow.

While the current method is not yet practical for everyday use—it requires 30 minutes of data collection and worked only on a subject with fair skin and no hair—this extreme case of detecting light diametrically across the head may inspire the community to rethink what is possible for the next generation of fNIRS systems.

With further development, this approach might help bring deep brain imaging into clinics and homes in a more affordable and portable form and better diagnosing platforms. This could eventually lead to better tools for diagnosing and monitoring conditions like strokes, brain injuries, or tumors, especially in settings where access to MRI or CT scans is limited.

Jack Radford et al, Photon transport through the entire adult human head, Neurophotonics (2025). DOI: 10.1117/1.NPh.12.2.025014

Comment by Dr. Krishna Kumari Challa on June 14, 2025 at 10:50am

Some plants make their own pesticide—but at what cost to the atmosphere?

A natural alternative to pesticides may be hiding in a misunderstood plant compound—but it could come at an environmental cost.

For years, scientists knew little about isoprene, a natural chemical produced by plants. New  research 40 years in the making now sheds light on how this natural chemical can repel insects—and how some plants that don't normally make isoprene could activate production in times of stress.

A  research paper in Science Advances uncovers a hormonal response triggered by isoprene that makes insects steer clear of those plants. Insects that munched on isoprene-treated leaves got a stomachache, thanks to indigestible proteins that kick in when the compound is present. Those proteins also stunt the growth of worms that dare to keep eating them.

Another paper, published in the Proceedings of the National Academy of Sciences, reveals that soybeans produce isoprene when their leaves are wounded. This discovery was particularly surprising since researchers previously thought modern crops didn't produce isoprene. This ability could make crops more resilient to heat and pests.

But that benefit could come at a cost. Isoprene is a hydrocarbon that worsens air pollution, especially in areas that already have poor air quality. If more crop plants were engineered to release isoprene, that could further damage Earth's atmosphere. The research also has implications for how soybeans may impact air pollution.

Isoprene is one of the highest emitted hydrocarbons on Earth, second only to methane emissions from human activity. These organic compounds interact with sunlight and nitrogen oxide from coal-burning facilities and vehicle emissions, creating a toxic brew of ozone, aerosols and other harmful byproducts.

Not all plants produce isoprene, however, and the ones that do tend to make more in hot weather. It's mostly found in oak and poplar trees, but unlike similar molecules in pine and eucalyptus trees, isoprene doesn't have a scent.

But as plants make more isoprene, they sacrifice some of their growth potential. When plants make isoprene, they divert carbon away from growth and storage and invest instead in their defense. Some think this is why many plants folded under evolutionary pressure to get rid of the isoprene synthase.

 Abira Sahu et al, Isoprene deters insect herbivory by priming plant hormone responses, Science Advances (2025). DOI: 10.1126/sciadv.adu4637

Mohammad Golam Mostofa et al, Cryptic isoprene emission of soybeans, Proceedings of the National Academy of Sciences (2025). DOI: 10.1073/pnas.2502360122

Comment by Dr. Krishna Kumari Challa on June 13, 2025 at 9:39am

Low sodium in blood triggers anxiety in mice by disrupting their brain chemistry

Hyponatremia, or low blood sodium concentration, is typically viewed as a symptomless condition—until recently. A research team has demonstrated that chronic hyponatremia (CHN) can directly cause anxiety-like behaviors in mice by disrupting key neurotransmitters in the brain.

Their findings, published online in the journal Molecular Neurobiology, reveal that CHN alters monoaminergic signaling in the amygdala, a brain region critical for processing fear and emotion. 

Hyponatremia is usually caused by conditions like liver cirrhosis, heart failure, or syndrome of inappropriate antidiuresis (SIAD). In chronic cases, the brain adapts to the low-sodium environment by adjusting its cellular content through a compensatory mechanism known as volume regulatory decrease (VRD). But this adaptation, while protective, comes at a physiological cost.

This compensation process involves the loss of organic osmolytes and neurotransmitter precursors that help stabilize brain cell volume under low-sodium conditions. Over time, this may lead to disruption in the production, release, or recycling of key mood-regulating chemicals.

The researchers  found that the mice in their experiments exhibited significantly lower serum sodium levels, which were maintained over a prolonged period, consistent with chronic hyponatremia (CHN) and exhibited increased anxiety-like behaviors in both the light/dark transition and open field tests—standard behavioral assays in neuroscience.

Further biochemical analyses revealed that levels of serotonin and dopamine, two key neurotransmitters that regulate mood, were significantly reduced in the amygdala of mice with CHN. These changes were accompanied by a drop in extracellular signal-regulated kinase (ERK) phosphorylation—a molecular signal for emotional regulation.

The data  suggest that CHN disrupts the balance of monoamines in the amygdala, especially serotonin and dopamine, which in turn modulates innate anxiety.

This shows not only that CHN causes anxiety-like symptoms but also that these symptoms can be alleviated with proper correction of sodium imbalance.

While the study focused on mice, the findings could apply to humans. CHN is fairly common among elderly patients and those with chronic illnesses. Identifying and treating its neurological manifestations can improve their quality of life.

Haruki Fujisawa et al, Chronic Hyponatremia Potentiates Innate Anxiety-Like Behaviors Through the Dysfunction of Monoaminergic Neurons in Mice, Molecular Neurobiology (2025). DOI: 10.1007/s12035-025-05024-y

Comment by Dr. Krishna Kumari Challa on June 13, 2025 at 9:24am

Testing their findings across multiple human and mouse cancer cell lines confirmed that cholesterol levels were consistently related to heat resistance. The researchers further validated their discovery in living mice with implanted tumors, using gold nanoparticles and near-infrared light to create localized heating. Tumors treated with both cholesterol depletion and hyperthermia showed dramatic shrinkage, with most tumors completely disappearing—a far superior result compared to heat treatment alone.

This research suggests that measuring cholesterol levels in tumors could help doctors identify which patients are most likely to benefit from hyperthermia treatment. More importantly, the combination of cholesterol-depleting drugs with localized heat therapy could transform hyperthermia from an inconsistent treatment into a powerful weapon against cancer. Since cholesterol depletion primarily triggers necrosis, this approach may also enhance the immune system's ability to recognize and attack the remaining cancer cells.

 Taisei Kanamori et al, Cholesterol depletion suppresses thermal necrosis resistance by alleviating an increase in membrane fluidity, Scientific Reports (2025). DOI: 10.1038/s41598-025-92232-0

Part 2

Comment by Dr. Krishna Kumari Challa on June 13, 2025 at 9:23am

Cancer cells use cholesterol armor to survive heat shock treatment, study discovers

Cancer has been recognized long back as being sensitive to heat. Today, this principle forms the basis of hyperthermia treatment—a promising cancer therapy that uses controlled heat to kill tumor cells while sparing healthy ones.

Unlike chemotherapy or radiation, hyperthermia works by heating cancerous tissue to temperatures around 50°C, causing cancer cell death while simultaneously activating the body's immune system against the tumor. This approach holds particular promise when combined with immunotherapy, as heat-killed cancer cells can trigger a stronger anti-tumor immune response.

Researchers have discovered that some cancer cells—even those from the same organ—react differently to heat shock, with some surprisingly more heat-resistant than others. This resistance involves two distinct cell death types: necrosis, which occurs rapidly through direct physical damage to cell membranes, and apoptosis, a slower, programmed cell death that happens hours later. In particular, how heat-resistant cancer cells regulate necrosis has received little scientific attention, limiting hyperthermia's potential as a standard cancer treatment.

Through a series of experiments in mice and cell cultures, the researchers compared the characteristics and behaviors of heat-sensitive cancer cells with heat-resistant ones. They discovered that cholesterol could act as a protective shield for cancer cells during heat treatment. Heat-resistant cancer cells contained significantly higher levels of cholesterol than heat-sensitive ones. This, in turn, helped maintain the stability of cell membranes when exposed to heat, preventing the rapid membrane breakdown that leads to necrosis.

Notably, when researchers artificially removed cholesterol from cancer cells using a cholesterol-depleting drug, even the most heat-resistant cells became vulnerable to hyperthermia treatment.

Using advanced imaging techniques, the researchers observed that heat treatment causes cell membranes to become more fluid (increased membrane fluidity). In cells with high cholesterol levels, this increase in membrane fluidity was suppressed, thereby protecting the cells from heat damage. However, when cholesterol was removed, membrane fluidity increased, making the cells much more susceptible to heat-induced damage, leading to rapid cell death through necrosis.

Part 1

Comment by Dr. Krishna Kumari Challa on June 13, 2025 at 9:13am

When bacteria get hungry, they kill—and eat—their neighbours!

Scientists have discovered a gruesome microbial survival strategy: when food is scarce, some bacteria kill and consume their neighbours.

The study, published in Science, was conducted by an international team. 

The researchers show that under nutrient-limited conditions, bacteria use a specialized weapon—the Type VI Secretion System (T6SS)—to attack, kill, and slowly absorb nutrients from other bacterial cells.

The T6SS is like a microscopic harpoon gun. A bacterium fires a needle-like weapon into nearby cells, injecting toxins that fatally rupture them.

Historically, scientists thought this system was mainly for competition, clearing out rivals to make space, but the multi-institutional research team discovered that bacteria aren't just killing for territory, they're strategically killing for dinner, and to help themselves grow.

Using time-lapse imaging, genetic tools, and chemical labeling, the scientists watched in slow-motion the microscopic assassins at work.

In both ocean bacteria and human gut microbes, bacteria equipped with T6SS attacked neighbors when starved of nutrients, and then grew by feeding off the deceased's leaking remains.

To prove this wasn't just coincidence, the researchers then genetically "turned off" the T6SS in some strains. When these genetically edited bacteria were placed in a nutrient-poor environment with potential prey, they couldn't grow. But the unedited bacteria, the ones still able to kill, thrived.

Their survival depended on murder.

The team also analyzed bacterial genomes across marine environments and found that these killing systems are widespread.

This isn't just happening in the lab. It's present in many different environments and it's operational and happening in nature from the oceans to the human gut.

This insight has wide-ranging implications.

If scientists can better understand how and why these bacterial weapons work, they can begin to design smarter probiotics, ones that don't just coexist in your gut, but actively protect it by taking out harmful microbes.

It could also lead to new antibiotics, at a time when drug resistance is on the rise. The same harpoon that bacteria use to extract nutrients from competitors could be harnessed to deliver drugs directly into problem pathogens—offering a new frontier in targeted, resistance-proof therapies.

And beyond our bodies, in the ocean, bacteria help regulate the planet's carbon cycle. When killer bacteria take out the ones breaking down algae and recycling carbon, it can shift how we understand how much carbon stays in the ocean or gets released back into the atmosphere.

By decoding how microscopic bacteria kill and consume each other, the research could reshape how we think about ecosystems—from the human gut to the vast oceans that regulate Earth's climate.

Astrid K. M. Stubbusch, Antagonism as a foraging strategy in microbial communities, Science (2025). DOI: 10.1126/science.adr8286. www.science.org/doi/10.1126/science.adr8286

Comment by Dr. Krishna Kumari Challa on June 13, 2025 at 8:56am

Humans have unique breathing 'fingerprints' that may signal health status

A study published in Current Biology demonstrates that scientists can identify individuals based solely on their breathing patterns with 96.8% accuracy. These nasal respiratory "fingerprints" also offer insights into physical and mental health.

The study found that the respiratory fingerprints correlated with a person's body mass index,sleep-wake cycle, levels of depression and anxiety, and even behavioral traits. For example, participants who scored relatively higher on anxiety questionnaires had shorter inhales and more variability in the pauses between breaths during sleep.

 The results suggest that long-term nasal airflow monitoring may serve as a window into physical and emotional well-being.

Humans Have Nasal Respiratory Fingerprints, Current Biology (2025). DOI: 10.1016/j.cub.2025.05.008. www.cell.com/current-biology/f … 0960-9822(25)00583-4

Comment by Dr. Krishna Kumari Challa on June 13, 2025 at 8:49am

Cellular assays measured oxidative stress, antioxidant protein expression, nitric oxide bioavailability, endothelin production, and fibrinolytic capacity. Capillary electrophoresis immunoassay and ELISA were used to quantify expression of superoxide dismutase-1 (SOD-1), catalase, endothelial nitric oxide synthase (eNOS), phosphorylated eNOS, endothelin-1 (ET-1), and tissue-type plasminogen activator (t-PA).

Cells exposed to erythritol exhibited a substantial increase in oxidative stress. Reactive oxygen species levels rose by approximately 75% relative to untreated controls. Antioxidant defense markers were also elevated, with SOD-1 expression increasing by approximately 45% and catalase by approximately 25%.

Nitric oxide production declined by nearly 20% in response to erythritol. Although total eNOS expression remained unchanged, phosphorylation at the Ser1177 site, which is associated with enzymatic activation, fell by approximately 33%. In contrast, phosphorylation at the inhibitory Thr495 site increased by approximately 39%.

In another test, t-PA release in response to thrombin stimulation was blunted in erythritol-treated cells, indicating reduced fibrinolytic responsiveness.

The researchers conclude that erythritol exposure disrupts multiple mechanisms vital to maintaining cerebral endothelial health. Although results are limited to acute in vitro conditions, the findings align with prior epidemiological associations between erythritol and elevated stroke risk.

Auburn R. Berry et al, The Non-Nutritive Sweetner Erythritol Adversely Affects Brain Microvascular Endothelial Cell Function, Journal of Applied Physiology (2025). DOI: 10.1152/japplphysiol.00276.2025

Part 2

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