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Immortality Without Tumors

face_with_colon_three Year 1998


In ancient Greece, immortality was the province of gods who spun the length of each lifetime. The myth has a kernel of truth, because the ends of chromosomes are protected by specialized stretches of DNA called telomeres. Once these are snipped too much by imperfect copying, a cell goes into senescence and stops dividing. Now two reports show that, with the help of an enzyme called telomerase, human cells can divide forever in the laboratory without turning cancerous. The findings, reported in the January issue of Nature Genetics, could ease the way to new treatments for burn victims, diabetics, and patients with other diseases.

Researchers hoped that adding telomerase would keep cells dividing long enough to replace tissues lost to injury or disease. Normal cells often have proved impractical because they can only divide a limited number of times in culture, and once returned to the body they’re often too old to do much good. The limitation may be that normal cells do not produce active telomerase, which can rebuild the telomeres and keep cells from becoming senescent.

In fact, about a year ago, Jerry Shay and his colleagues at the University of Texas Southwestern Medical Center in Dallas showed that adding the enzyme to normal connective tissue cells called fibroblasts extends their life-span (Science NOW, 13 January 1998). These cells have now lived three times longer than normal in the lab, and they are still going strong. But because cancer cells contain telomerase and also live forever, scientists worried that the newly immortal cells would become malignant when implanted in humans.

CD4 T cells acquire Eomesodermin to modulate cellular senescence and aging

Elyahu and colleagues describe the reciprocal interplay between senescent cells (SCs) and a helper T cell population that accumulates during aging. They show that selective depletion of this T cell population increases SC accumulation, accelerates frailty and limits lifespan in mice.

Men experience more brain atrophy with age despite women’s higher Alzheimer’s risk

Women are far more likely than men to end up with Alzheimer’s disease (AD). This may, at least partially, be due to women’s longer average lifespans, but many scientists think there is probably more to the story. It would be easy to surmise that the increased risk is also related to differences in the way men’s and women’s brains change as they age. However, the research thus far has been unclear, as results across different brain regions and methods have been inconsistent.

Now, a new study, published in Proceedings of the National Academy of Sciences, indicates that it’s men who experience greater decline in more regions of the as they age. Researchers involved in the study analyzed 12,638 brain MRIs from 4,726 cognitively healthy participants (at least two scans per person) from the ages of 17–95 to find how age-related changes occurred and whether they differed between men and women.

The results showed that men experienced declines in cortical thickness and in many regions of the brain and a decline in subcortical structures in older age. Meanwhile, women showed greater decline only in a few regions and more ventricular expansion in older adults. So, while differences in brain aging between the sexes are apparent, the cause of increased AD prevalence in women is still a bit mysterious.

Scientists Extend Lifespan by over 70% in Elderly Male Mice with New Treatment

These findings demonstrate that OT+A5i has a significant ability to extend health span and highlight the sex-specific differences in aging and in responses to longevity treatments. A new study featured in the journal Aging has found that combining oxytocin with an Alk5 inhibitor (OT+A5i) can grea

Longevity gene from supercentenarians offers hope for disease that causes rapid aging in children

A new breakthrough in a rare genetic disease which causes children to age rapidly has been discovered using ‘longevity genes’ found in people who live exceptionally long lives—over 100 years old. The research, by the University of Bristol and IRCCS MultiMedica, found these genes which help keep the heart and blood vessels healthy during aging could reverse the damage caused by this life-limiting disease.

This is the first study, published in Signal Transduction and Targeted Therapy, to show that a gene from long-lived people can slow down heart aging in a model. Also known as Hutchinson-Gilford progeria syndrome (HGPS), progeria is a rare, fatal genetic condition of “rapid-aging” in children.

HGPS is caused by a mutation in the LMNA gene, which leads to the production of a toxic protein called progerin. Most affected individuals die in their teens due to heart problems, although a few, like Sammy Basso, the oldest known person with progeria, have lived longer. Sadly, late last year at the age of 28, Sammy passed away.

Researchers Discover the Cell’s Secret Anti-Aging Mechanism

Activating lysosome biogenesis helps alleviate cellular senescence in progeria. Hutchinson-Gilford progeria syndrome (HGPS) is a rare genetic condition that causes rapid aging and a range of visible and internal symptoms. Individuals with HGPS often experience early skin wrinkling, reduced skin ela

Study Warns of “Ultimate Extinction” as Dolphin Lifespans Plummet

A new study reveals that common dolphins in the North Atlantic are living significantly shorter lives, with female longevity dropping by seven years since 1997. Common dolphins are among the most numerous marine mammals on Earth, yet a new study in Conservation Letters reveals that these animals

Air pollution and Parkinson’s: What a 292,000-person study reveals about hidden risks

Researchers in Northern Ireland examined whether exposure to fine particulate matter (PM2.5) and nitrogen dioxide (NO₂) increases the risk of Parkinson’s disease. While no overall link was found after adjusting for confounders, younger adults under 50 showed a modest association with PM2.5, raising questions about age-related susceptibility and diagnostic misclassification.

Galvanizing blood vessel cells to expand for organ transplantation

Scientists have discovered a method to induce human endothelial cells from a small biopsy sample to multiply in the laboratory, producing more than enough cells to replace damaged blood vessels or nourish organs for transplantation, according to a preclinical study by Weill Cornell Medicine investigators.

Endothelial cells form the inner lining of blood vessels and regulate blood flow, inflammation and healing. Traditional approaches for growing these cells in the lab have yielded only limited numbers before they lose their ability to function. The new method involves treating adult endothelial cells with a small molecule that triggers the hibernating cells to wake up and divide hundreds of times without signs of aging, mutation or loss of function.

The findings, published Oct. 14 in Nature Cardiovascular Research, may provide a reliable way to generate an enormous number of a patient’s own endothelial cells, enabling vascular grafts for , diabetes treatments and and strategies to target abnormal tumor blood vessels.

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