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Comment by Dr. Krishna Kumari Challa on August 7, 2025 at 9:39am

Low-oxygen air slows Parkinson's progression and restores movement in mice

Researchers have shown that a low-oxygen environment—similar to the thin air found at Mount Everest base camp—can protect the brain and restore movement in mice with Parkinson's-like disease.

The new research, in Nature Neuroscience, suggests that cellular dysfunction in Parkinson's leads to the accumulation of excess oxygen molecules in the brain, which then fuel neurodegeneration—and that reducing oxygen intake could help prevent or even reverse Parkinson's symptoms.

The fact that researchers actually saw some reversal of neurological damage is really exciting. It tells us that there is a window during which some neurons are dysfunctional but not yet dead—and that we can restore their function if we intervene early enough.

The results raise the possibility of an entirely new paradigm for addressing Parkinson's disease.

Parkinson's disease, which affects more than 10 million people worldwide, causes the progressive loss of neurons in the brain, leading to tremors and slowed movements.

Neurons affected by Parkinson's also gradually accumulate toxic protein clumps called Lewy bodies. Some biochemical evidence has suggested that these clumps interfere with the function of mitochondria—the tiny powerhouses of the cell that Mootha knew were altered in other diseases that could be treated with hypoxia.

Moreover, anecdotally, people with Parkinson's seem to fare better at high altitudes. And long-term smokers—who have elevated levels of carbon monoxide, leading to less oxygen in tissues—also appear to have a lower risk of developing Parkinson's.

Based on this evidence, researchers became very interested in the effect of hypoxia on Parkinson's disease.

The results of their experiments were striking. Three months after receiving α-synuclein protein injections, the mice breathing normal air had high levels of Lewy bodies, dead neurons, and severe movement problems. Mice that had breathed low-oxygen air from the start didn't lose any neurons and showed no signs of movement problems, despite developing abundant Lewy bodies.

The findings show that hypoxia wasn't stopping the formation of Lewy bodies but was protecting neurons from the damaging effects of these protein clumps—potentially suggesting a new mode of treating Parkinson's without targeting α-synuclein or Lewy bodies.

What's more, when hypoxia was introduced six weeks after the injection, when symptoms were already appearing, it still worked. The mice's motor skills rebounded, their anxiety-like behaviors faded, and the loss of neurons in the brain stopped.

However, more work is needed before the findings can be directly used to treat Parkinson's.

 Marutani, E et al. Hypoxia ameliorates neurodegeneration and movement disorder in a mouse model of Parkinson's disease, Nature Neuroscience (2025). DOI: 10.1038/s41593-025-02010-4

Comment by Dr. Krishna Kumari Challa on August 6, 2025 at 3:08pm

Before the first polio vaccine was developed in 1955, the disease—spread mostly from person to person, through contaminated water and via fecal particles—was among the world's most feared, paralyzing hundreds of thousands of children annually. People avoided crowded places during epidemics, and hospital wards filled with children encased in iron lungs after the virus immobilized their breathing muscles.

Polio is mainly spread when people are exposed to water infected with the virus. In countries with poor sanitation, children often become infected when they come into contact with contaminated waste.

WHO says that as long as a single child remains infected, kids everywhere are at risk.
Eradication demands near-perfection—zero polio cases and immunizing more than 95% of children.

But public health leaders and former WHO staffers say campaign efforts are far from perfect, and many question the oral vaccine.
The oral vaccine—proven to be safe and effective—has been given to more than 3 billion children. But there are some extremely rare side effects: Scientists estimate that for every 2.7 million first doses given, one child will be paralyzed by the live polio virus in the vaccine.

In even rarer instances, the live virus can mutate into a form capable of starting new outbreaks among unimmunized people where vaccination rates are low.

Worldwide, several hundred vaccine-derived cases have been reported annually since at least 2021, with at least 98 this year.

Most public health experts agree the oral vaccine should be pulled as soon as possible. But they acknowledge there simply isn't enough injectable vaccine—which uses no live virus and doesn't come with the risks of the oral vaccine—to wipe out polio alone. The injectable vaccine also is more expensive and requires more training to administer.

https://medicalxpress.com/news/2025-08-world-polio-fake-imperfect-v...

Part 2

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Comment by Dr. Krishna Kumari Challa on August 6, 2025 at 3:06pm

The world nearly beat polio. But fake records, an imperfect vaccine and missteps aided its comeback

For the past decade, health care workers have traveled door to door in southeastern Pakistan, pleading with parents to allow children to be vaccinated against polio as part of a global campaign to wipe out the paralytic disease. She hears their demands and fears. Some are practical—families need basics like food and water more than vaccines. Others are simply unfounded—the oral doses are meant to sterilize their kids.

Amid rampant misinformation and immense pressure for the campaign to succeed, some managers have instructed workers to falsely mark children as immunized. And the vaccines, which must be kept cold, aren't always stored correctly.

In many places, their work is not done with honesty. The result: Polio raised its ugly head again.

The World Health Organization and partners embarked on their polio campaign in 1988 with the bold goal of eradication—a feat seen only once for human diseases, with smallpox in 1980. They came close several times, including in 2021, when just five cases of the natural virus were reported in Pakistan and Afghanistan. But since then, cases rebounded, hitting 99 last year, and officials have missed at least six self-imposed eradication deadlines.

Afghanistan and Pakistan remain the only countries where transmission of polio—which is highly infectious, affects mainly children under 5, and can cause irreversible paralysis within hours—has never been interrupted. The worldwide campaign has focused most of its attention and funding there for the past decade.

But in its quest to eliminate the disease, the Global Polio Eradication Initiative has been derailed by mismanagement and what insiders describe as blind allegiance to an outdated strategy and a problematic oral vaccine, according to workers, polio experts and internal materials.

Officials have falsified vaccination records, selected unqualified people to dole out drops, failed to send out teams during mass campaigns, and dismissed concerns about the oral vaccine sparking outbreaks, according to documents shared with some news agencies.

The documents flagged multiple cases of falsified vaccination records, health workers being replaced by untrained relatives and workers improperly administering vaccines.

Part 1

Comment by Dr. Krishna Kumari Challa on August 6, 2025 at 2:59pm

Study finds drinking coffee at night raises impulsivity, especially in females

 A team of  biologists has discovered that nighttime caffeine consumption can increase impulsive behavior, potentially leading to reckless actions.

The study, published in iScience, examined how nighttime caffeine intake affects inhibition and impulsivity in fruit flies.

Drosophila melanogaster, the fruit fly species used in the study, is a powerful model to study complex behaviors due to its genetic and neural parallels with humans. Caffeine is the most widely consumed psychoactive substance in the world.

Interestingly, caffeine consumed by the flies during the daytime did not lead to the same reckless flying, the team said.

The team warns that the findings could have negative implications for shift workers, health care and military personnel who consume coffee at night, particularly females.

Erick Benjamin Saldes et al, Nighttime caffeine intake increases motor impulsivity, iScience (2025). DOI: 10.1016/j.isci.2025.113197

Comment by Dr. Krishna Kumari Challa on August 6, 2025 at 2:54pm

Exposure to nanoplastics could induce spread of Alzheimer's disease from the brain to other organs

A new preclinical study has found exposure to nanoplastics may contribute to the rapid progression of Alzheimer's disease and subsequent spread from the brain to other key organs such as the liver, heart and gut.

The research, "Cerebral to Systemic Representations of Alzheimer's Pathogenesis Stimulated by Polystyrene Nanoplastics," is published in the journal Environment & Health

The study investigated how environmental-level polystyrene nanoplastic exposure influences the progression of Alzheimer's disease from the brain to other parts of the body. Studies in mice revealed that nanoplastic-induced neurological damage is not confined within the brain, but expands systemically through the gut–liver–brain axis.

In mice exposed to polystyrene nanoplastics, Alzheimer's-like symptoms were shown to stimulate 'microglia' immune cell activation in the brain, leading to neuroinflammation and neurodegeneration. This in turn led to peripheral health implications beyond the brain, including fatty liver disease, abnormal build-up of fat and gut microbiota imbalance.

Humans are involuntarily exposed to plastics through inhalation, dermal contact and the consumption of contaminated food and water, and plastic particles have been detected in human lungs, bloodstream and, very recently, in the human brain.

This, however, is the first study to show how rapidly nanoplastics can evolve from the brain to other parts of the body.

Yue Wang et al, Cerebral to Systemic Representations of Alzheimer's Pathogenesis Stimulated by Polystyrene Nanoplastics, Environment & Health (2025). DOI: 10.1021/envhealth.5c00160

Comment by Dr. Krishna Kumari Challa on August 6, 2025 at 2:50pm

Researchers debunk long-standing concern about flu treatment in children

For decades, medical professionals debated whether a common antiviral medication used to treat flu in children caused neuropsychiatric events or if the infection itself was the culprit.

Now researchers at Monroe Carell Jr. Children's Hospital at Vanderbilt have debunked a long-standing theory about oseltamivir, known as Tamiflu.

According to the study, published in JAMA Neurology, oseltamivir treatment during flu episodes was associated with a reduced risk of serious neuropsychiatric events, such as seizures, altered mental status and hallucination.

These findings demonstrated what many pediatricians have long suspected, that the flu, not the flu treatment, is associated with neuropsychiatric events.

"In fact, oseltamivir treatment seems to prevent neuropsychiatric events rather than cause them."

Key points:

• Influenza itself was associated with an increase in neuropsychiatric events compared to children with no influenza, regardless of oseltamivir use.
• Among children with influenza, those treated with oseltamivir had about 50% reduction in neuropsychiatric events.
• Among children without influenza, those who were treated with oseltamivir prophylactically had the same rate of events as the baseline group with no influenza.

Taken together, these three findings do not support the theory that oseltamivir increases the risk of neuropsychiatric events. It's the influenza, conclude the researchers.

James W. Antoon et al, Influenza With and Without Oseltamivir Treatment and Neuropsychiatric Events Among Children and Adolescents, JAMA Neurology (2025). DOI: 10.1001/jamaneurol.2025.1995

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Comment by Dr. Krishna Kumari Challa on August 6, 2025 at 2:34pm

New study shows that E. coli can evolve antibiotic resistance during treatment

Scientists have documented a notable case of antibiotic resistance evolving within a critically ill patient during treatment for an E. coli bloodstream infection, providing genomic evidence of how drug resistance can emerge in real time.

This new study published in the Journal of Medical Microbiology, details the rapid evolution of resistance in an E. coli strain exposed to piperacillin/tazobactam (TZP), a first-line treatment for serious bacterial infections that pairs an antibiotic with a compound that inhibits beta-lactamase enzymes, a widespread antibiotic resistance gene.

While the initial infection appeared treatable, the bacteria quickly developed a mechanism to escape the drug's effects, not by acquiring new resistance genes, but by amplifying one it already carried, overcoming the effects of the resistance inhibitor.

This is a striking example of resistance evolving under antibiotic pressure.

The researchers identified a tenfold increase in copies of a key resistance gene within the bacterial isolate, leading to a 32-fold increase in the level of antibiotic required to kill the bacteria, ultimately causing the treatment to fail, and all within the course of a single patient's illness.

The research team, which included genomic scientists, microbiologists and clinicians used high-resolution whole-genome sequencing to confirm the genetic changes.

The amplified resistance gene in E. coli, named blaTEM-1, produces a beta-lactamase enzyme that breaks down the antibiotic piperacillin. Although the TZP drug combination is meant to inhibit these enzymes, the sheer volume produced following gene duplication overwhelmed its protective effect, allowing the infection to persist. Further lab experiments confirmed that exposure to TZP led E. coli to generate even more copies of the gene.

This form of "within-patient evolution" presents a major diagnostic challenge. Routine resistance tests may underestimate the risk of treatment failure if they don't detect bacteria capable of rapidly increasing enzyme production under antibiotic pressure.

The study also highlights that 40% of new antibiotic candidates in the pipeline are beta-lactamase inhibitor combinations like TZP, raising critical concerns for drug developers and frontline clinicians alike.

This study underscores why relying on static resistance profiles can be misleading.

The findings underscore the need for greater investment in diagnostics and surveillance tools that can detect dynamic, hard-to-spot resistance mechanisms before they undermine treatment.

Alice J. Fraser et al, A high-resolution genomic and phenotypic analysis of resistance evolution of an Escherichia coli strain from a critically unwell patient treated with piperacillin/tazobactam, Journal of Medical Microbiology (2025). DOI: 10.1099/jmm.0.002018

Comment by Dr. Krishna Kumari Challa on August 6, 2025 at 2:19pm

In this study, AUN exhibits transcendent antitumor effects through uniquely orchestrated bacterial mechanisms, including:

Selective destruction of tumor vasculature and cancer cells
Structural transformation of A-gyo (filamentation) triggered by tumor metabolites, enhancing its antitumor potency
Functional optimization via intratumoral population shift—although the initial bacterial mixture is A-gyo : UN-gyo ≈ 3:97, it dramatically shifts to 99:1 within the tumor microenvironment
Suppression of pathogenicity and minimization of side effects, including the avoidance of CRS
Notably, UN-gyo functions as a regulatory partner only when coexisting with A-gyo, helping to suppress the pathogenicity of both strains while simultaneously enhancing their tumor-specific cytotoxicity. This "cooperation of labor" mirrors the Japanese philosophical concept of AUN—perfect harmony between opposites. It is this delicate and dynamic interplay between the two bacterial species that unlocks the remarkable antitumor efficacy—a feat previously unattainable through conventional therapies.

Tumour-resident oncolytic bacteria trigger potent anticancer effects through selective intratumoural thrombosis and necrosis, Nature Biomedical Engineering (2025). DOI: 10.1038/s41551-025-01459-9

Part 2

Comment by Dr. Krishna Kumari Challa on August 6, 2025 at 2:18pm

Bacterial duo eliminates tumors without immune system help in new cancer therapy

A  research team has developed an immune-independent bacterial cancer therapy using a novel microbial consortium called AUN.

Cancer immunotherapy originated in 1868 when the German physician Busch reported a case of a cancer patient who was intentionally infected with bacteria and subsequently cured. In 1893, Dr. William Coley proposed the use of bacteria for cancer treatment, and immunotherapies have been evolving into modern treatments such as checkpoint inhibitors and CAR-T cells for over 150 years. While powerful, these approaches fundamentally depend on immune cells—making them ineffective for many cancer patients with compromised immune systems due to chemotherapy or radiotherapy.

The newly developed AUN therapy overturns this long-standing limitation. The research is published in Nature Biomedical Engineering.

AUN is composed of two naturally occurring bacteria:

• Proteus mirabilis (A-gyo), a tumor-resident microbe
• Rhodopseudomonas palustris (UN-gyo), a photosynthetic bacterium

Working in perfect synergy, these AUN bacteria produce exceptional tumor eradication in both murine and human cancer models, even in immunocompromised environments—all without the help of immune cells. The therapy exhibits high biocompatibility and minimal side effects, including suppression of cytokine release syndrome (CRS).

Part 1

Comment by Dr. Krishna Kumari Challa on August 6, 2025 at 2:14pm

Study finds Ozempic may weaken muscles even as muscle size remains stable

As use of the popular anti-diabetic and weight-loss drug Ozempic skyrockets, so have concerns about the medication's side effects. One such side effect is loss of "lean mass"—body weight that isn't fat—raising concerns that Ozempic could be reducing muscle mass and strength.

New research in mice suggests that muscle mass changes less than expected, but muscles may still get weaker, pointing out an urgent need for clinical studies to pin down the full effects of the popular medications.

Researchers found that Ozempic-induced weight loss did decrease lean mass by about 10%. Most of this lost weight wasn't from skeletal muscles but instead from other tissues like the liver, which shrank by nearly half. The researchers emphasize that more research is needed to determine whether similar changes to organ size occur in humans—and whether those changes come with any risks.

Interestingly, when the researchers tested the amount of force the mice's muscles could exert, they found that, for some muscles, strength decreased as the mice lost weight, even when the size of the muscle stayed roughly the same. For other muscles, strength was unchanged. It's unknown how weight loss drugs affect this balance in people, the researchers say.

A potential loss of strength when taking Ozempic may be of particular concern for adults over the age of 60, who are at higher baseline risk for muscle loss and reduced mobility. "The loss of physical function is a strong predictor of not just quality of life but longevity," they add.

However,  mice and humans gain and lose weight in different ways and unless tested in humans, we can't apply the same results to human beings. 

Unexpected effects of semaglutide on skeletal muscle mass and force-generating capacity in mice, Cell Metabolism (2025). DOI: 10.1016/j.cmet.2025.07.004. www.cell.com/cell-metabolism/f … 1550-4131(25)00331-6

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