Lifeboat Foundation

Werner Syndrome and Hutchinson Gilford Progeria Syndrome are two examples of the rare genetic disorders known as progeroid syndromes that cause signs of premature aging in children and young adults. Patients with progeroid syndromes have pathologies and symptoms that are often linked to aging, including osteoporosis, cataracts, heart disease, and type II diabetes.

This aging is characterized by the gradual loss of nuclear architecture and an underlying tissue-specific genetic program, but the causes are unclear. Scientists have discovered a potential new target for treating these syndromes by preventing nuclear architecture loss.

New imaging of patients with Alzheimer’s demonstrates how a telltale protein spreads throughout the brain based on the phenotype of the disease, i.e., whether the condition is dominated by forgetfulness, or atrophy in a specific brain region. The research offers a host of illuminating clues that ultimately may inform new treatment strategies.

The protein is known as tau and a large multi-disciplinary team of brain researchers at McGill University in Montreal has been able to trace the protein’s patterns in living patients via magnetic resonance imaging (MRI). Alzheimer’s disease is intimately linked to tau, which can form tangles in the brain that irrevocably damage neurons.

The patterns detected by McGill scientists apparently are unique to the phenotype of Alzheimer’s afflicting the patient. This staggering finding opens an intriguing new window into the molecular mechanisms of the disease. And while many features of Alzheimer’s are the same from one patient to the next, phenotypes are a hallmark of the condition. Tracking tau patterns is a specialty of the scientists at McGill, who found that the intrinsic connectivity of the human brain itself provides the scaffolding for the aggregation of tau in distinct variants of the disease.

Viral DNA in human genomes, embedded there from ancient infections, serves as antivirals that protect human cells against certain present-day viruses, according to new research.

The paper, “Evolution and Antiviral Activity of a Human Protein of Retroviral Origin,” published Oct. 28 in Science, provides proof of principle of this effect.

Previous studies have shown that fragments of ancient viral DNA—called endogenous retroviruses —in the genomes of mice, chickens, cats and sheep provide immunity against modern viruses that originate outside the body by blocking them from entering host cells. Though this study was conducted with human cells in culture in the lab, it shows that the antiviral effect of endogenous retroviruses likely also exists for humans.

The finding is a turning point in cancer research.

Two major studies published in Nature.

Continue reading “Major breakthrough in cancer research: Papers reveal ‘dark matter’ that contributes to disease’s growth” »

It’s illegal to use the carcinogenic color additive Red 3 in cosmetics, such as lipsticks or blush, or externally applied drugs. Yet the discredited chemical is lurking in common varieties of candy corn, Nerds, Peeps, Pez, SweeTarts, and hundreds of candies, cakes, and other foods, including dozens of seasonal Halloween items. That’s why the Center for Science in the Public Interest and 23 other organizations and prominent scientists are today urging the Food and Drug Administration to formally remove Red 3 from the list of approved color additives in foods, dietary supplements, and oral medicines.

Since the early 1980s FDA had evidence that Red 3 caused cancer in laboratory animals. The National Toxicology Program considered the evidence “convincing.” As a result, in 1990, the agency eliminated certain “provisionally listed” uses of the chemical—meaning cosmetics and externally applied drugs. In 1990, FDA also said it would “take steps” to ban its use in foods, ingested drugs, and supplements. But those steps were never taken.

“Halloween has never been the healthiest holiday, but few parents would believe that the FDA permits the use of a dye it acknowledges as a carcinogen to be used as a common ingredient in candy,” said CSPI consultant Lisa Y. Lefferts. “Fewer still would believe that the FDA prohibits this carcinogen in makeup but allows it in food.”

A recent study used computational methods to identify novel compounds that activate receptors involved in pain modulation to relieve pain in mouse models without causing sedation. Further research is needed to assess the side effects of these drugs and optimize the compounds for therapeutic use.

In a study using specialized imaging techniques, Johns Hopkins Medicine researchers report distinctive changes in the “white matter” and other brain tissue physiology of those with post-treatment Lyme disease, a condition affecting 10% to 20% of the nearly half a million Americans who contract Lyme disease annually.

The study’s findings, published October 26 in the journal PLOS ONE, substantiate and help validate that memory difficulties and other cognitive difficulties experienced long-term by individuals with post-treatment Lyme disease are linked to functional and structural changes in the brain.

Lyme disease, whose early symptoms may include a characteristic rash, flu-like aches and fever, joint pain, and fatigue, is treated using a rigorous course of antibiotics, which usually clears the illness.

When you cut yourself, a mass migration begins inside your body: Skin cells flood by the thousands toward the site of the wound, where they will soon lay down fresh layers of protective tissue.

In a new study, researchers from the University of Colorado Boulder have taken an important step toward unraveling the drivers behind this collective behavior. The team has developed an equation learning technique that might one day help scientists grasp how the body rebuilds skin, and could potentially inspire new therapies to accelerate wound healing.

“Learning the rules for how individual cells respond to the proximity and relative motion of other cells is critical to understanding why cells migrate into a wound,” said David Bortz, professor of applied mathematics at CU Boulder and senior author of the new study.

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Researchers at the National Institutes of Health have identified a particular protein network that is necessary for cell regeneration to restore hearing in zebrafish. Researchers at the National Human Genome Research Institute (NHGRI) led the research, which may help in the creation of human hearing loss treatments. The findings were recently published in the journal Cell Genomics.

Many animals, like zebrafish, may recover their hearing after injury through the regeneration of hair cells, however, human hair cell loss cannot be restored. The regenerating properties of zebrafish hair cells inspired researchers to use this species to better understand certain fundamental properties of regeneration.