Lifeboat Foundation: Safeguarding Humanity
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Category: biotech/medical – Page 9

The common cold sore virus, which is often caught in childhood, usually stays in the body for life—quietly dormant in the nerves. Now and then, things like stress, illness or injury can trigger it, bringing on a cold sore in some people. But this same virus—called herpes simplex virus type 1—may also play an important role in something far more serious: Alzheimer’s disease.

Over 30 years ago, my colleagues and I made a surprising discovery. We found that this cold sore virus can be present in the brains of older people. It was the first clear sign that a virus could be quietly living in the brain, which was long thought to be completely germ-free—protected by the so-called “blood-brain barrier.”

Then we discovered something even more striking. People who have a certain version of a gene (called APOE-e4) that increases their risk of Alzheimer’s, and who have been infected with this virus, have a risk that is many times greater.

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Organoids, miniaturized, stem cell-derived versions of human organs, are revolutionizing biomedical research by offering human-specific models for disease study and drug testing. While they have limitations, organoids increasingly challenge the dominance of animal models in preclinical science.

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A new gene therapy reversed heart failure in pigs by repairing heart function through cBIN1, showing major promise for future treatment.

A new gene therapy has been shown to reverse the effects of heart failure and restore heart function in a large animal model. The treatment increases the heart’s ability to pump blood and significantly improves survival rates. A paper describing the results calls it “an unprecedented recovery of cardiac function.”

Heart failure is currently irreversible. Without a heart transplant, most treatments aim only to reduce the heart’s workload and slow the progression of the disease. If this gene therapy produces similar outcomes in future clinical trials, it could offer a way to repair the hearts of one in four people expected to develop heart failure during their lifetime.

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A new study led by a pair of researchers at the University of Massachusetts Amherst turns long-held conventional wisdom about a certain type of polymer on its head, greatly expanding understanding of how some of biochemistry’s fundamental forces work. The study, released recently in Nature Communications, opens the door for new biomedical research running the gamut from analyzing and identifying proteins and carbohydrates to drug delivery.

The work involves a kind of polymer made up of neutral polyzwitterions. Because they have a neutral electrical charge, polyzwitterions are not expected to respond to an electric field. However, the team found not only that certain neutral polyzwitterions behave as if they were charged, but also that the electric field surrounding polyzwitterions, once thought to be uniform, varies in strength.

“My interest is in the proteins and , which are the building blocks for protein, inside our body’s cells,” says Yeseul Lee, lead author and graduate student in polymer science and engineering at UMass Amherst.

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The number of people suffering from osteoarthritis is expected to top 1 billion by 2050. The biggest risk factor for the prevalent, often painful, chronic joint disease is aging. And like aging, there is currently no way to stop it.

A discovery by scientists at Henry Ford Health + Michigan State University Health Sciences could pave the way for new breakthroughs in detecting and treating the disease. Their findings were recently published in Nature Communications.

“Our hope is that this discovery will one day allow doctors to catch the disease earlier and intervene before significant joint damage occurs,” said Shabana Amanda Ali, Ph.D., a Henry Ford Health assistant scientist and senior author of the paper. “Osteoarthritis is so complex and so heterogeneous that even with decades of research there hasn’t been a single therapeutic.”

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Thyroid eye disease (TED; also known as Graves’ orbitopathy), causes swollen extraocular muscles and orbital fat. Mechanistically, TED involves lid retraction, oedema and redness of the eyelids and conjunctiva, proptosis, diplopia, and optic neuropathy. Investigation of TED involves assessment of disease activity (inflammation) and disease severity. TED is predominantly mild in 77% of cases, moderate-to-severe in 22%, and rarely sight-threatening in 1% of patients. While most patients with TED have Graves’ hyperthyroidism, up to 5% are euthyroid or even hypothyroid.

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Our eyes could potentially be coaxed into a special repair mode above and beyond our natural self-healing abilities, according to a new study, thanks to the delivery of antibodies that trigger nerve cell regeneration in the retina.

The South Korean research team says the treatment offers hope for restoring lost vision that otherwise can’t be brought back. For now though, it’s only been tested in mice.

Here’s how it works: a compound antibody drug is used to block the prospero homeobox protein 1 (Prox1). This protein isn’t inherently bad, playing an important role in cell regulation, but it appears to stop retinal nerves from regenerating.

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Nicotinamide adenine dinucleotide (NAD) is a ubiquitous electron carrier essential for energy metabolism and post-translational modification of numerous regulatory proteins. Dysregulations of NAD metabolism are widely regarded as detrimental to health, with NAD depletion commonly implicated in aging. However, the extent to which cellular NAD concentration can decline without adverse consequences remains unclear. To investigate this, we generated a mouse model in which nicotinamide phosphoribosyltransferase (NAMPT)-mediated NAD+ biosynthesis was disrupted in adult skeletal muscle. The intervention resulted in an 85% reduction in muscle NAD+ abundance while maintaining tissue integrity and functionality, as demonstrated by preserved muscle morphology, contractility, and exercise tolerance. This absence of functional impairments was further supported by intact mitochondrial respiratory capacity and unaltered muscle transcriptomic and proteomic profiles. Furthermore, lifelong NAD depletion did not accelerate muscle aging or impair whole-body metabolism. Collectively, these findings suggest that NAD depletion does not contribute to age-related decline in skeletal muscle function.

#Aging #Longevity aging and longevity.

NAD depletion in skeletal muscle does not impair tissue integrity and function or accelerate aging, as shown in a mouse model with an 85% decrease in muscle NAD+ levels. Muscle structure, metabolism, and mitochondrial function remain unaffected, suggesting that NAD depletion does not drive age-related muscle decline.

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