Lifeboat Foundation: Safeguarding Humanity
Toggle light / dark theme

Blog

Category: life extension

Holocene skeletal samples challenge link between sedentary lifestyles and age-related bone weakening

Research led by Vladimír Sládek sheds new light on how bones age, questioning long-standing assumptions that sedentary lifestyles are the primary cause of weakening bone strength in modern humans.

The study analyzed 1,881 adult humeri, femora, and tibiae from European Holocene populations to examine how and structure change with age. Surprisingly, researchers found that patterns of diaphyseal (shaft) aging were consistent across both Early and Late Holocene adults—despite significant differences in physical activity levels between the two groups. The research is published in the journal Science Advances.

“Our findings suggest that lifestyle differences may not fully explain age-related declines in bone strength,” said Dr. Sládek. “Instead, the biology of bone growth and aging itself plays a critical role.”

A cGAS-mediated mechanism in naked mole-rats potentiates DNA repair and delays aging

Efficient DNA repair might make possible the longevity of naked mole-rats. However, whether they have distinctive mechanisms to optimize functions of DNA repair suppressors is unclear. We find that naked mole-rat cyclic guanosine monophosphate–adenosine monophosphate synthase (cGAS) lacks the suppressive function of human or mouse homologs in homologous recombination repair through the alteration of four amino acids during evolution. The changes enable cGAS to retain chromatin longer upon DNA damage by weakening TRIM41-mediated ubiquitination and interaction with the segregase P97. Prolonged chromatin binding of cGAS enhanced the interaction between repair factors FANCI and RAD50 to facilitate RAD50 recruitment to damage sites, thereby potentiating homologous recombination repair.

Age-Defying Health Benefits: New Research Unravels Secrets of the “Longevity” Gene

Deleting the S6K1 protein in mice reduces inflammation and extends lifespan by suppressing inflammatory proteins, highlighting a new mechanism in aging and potential treatments for age-related diseases. S6K1 is a protein that plays a role in regulating aging and age-related diseases. Inhibiting t

Mitochondrial building block balance linked to age-related inflammation

Research led by the Max Planck Institute for Biology of Aging in Cologne reports that misincorporation of ribonucleotides into mitochondrial DNA (mtDNA) initiates an inflammatory cascade.

Mitochondria support cell survival through metabolic and signaling roles. Conversely, their disruption has been associated with inflammation, and disease.

Innate immune activation through the cGAS-STING-TBK1 pathway can move a cell from short-term defense to a chronic state of alarm. cGAS-STING activity is linked to autoimmune and inflammatory diseases and contributes to senescence and aging, intertwining immune signaling with tissue decline.

A New Class of Drug Created That Fights Aging on a Cellular Level

Scientists continue to explore ways we can live longer and ensure those lives are healthier. A new discovery of note in this field comes from experiments in fission yeast (an organism often used for studies of aging).

Researchers from Queen Mary University of London have been testing a new drug called Rapalink-1, building on an existing immunosuppressant called rapamycin that has been shown to extend the life of cells and rodents. In these new tests, Rapalink-1 extended yeast lifespan to a similar degree as rapamycin.

What’s more, molecular analysis revealed that the drug increased the production of enzymes that convert a compound made by gut bacteria, called agmatine, into a variety of other chemicals.

Pan-disease atlas maps molecular fingerprints of health, disease and aging

A new study has mapped the distinct molecular “fingerprints” that 59 diseases leave in an individual’s blood protein, which could enable blood tests to discern troubling signs from those that are more common.

As now published in Science, an international team of researchers mapped how thousands of proteins in human blood shift as a result of aging and serious diseases, such as cancer and cardiovascular and .

The Human Disease Blood Atlas also reveals that each individual’s blood profile has a unique molecular fingerprint, which changes through childhood and stabilizes in adulthood. This provides a baseline for comparison that could one day use to flag early deviations.

Poor sleep may accelerate brain aging

People who sleep poorly are more likely than others to have brains that appear older than they actually are. This is according to a comprehensive brain imaging study from Karolinska Institutet, published in the journal eBioMedicine. The paper is titled “Poor sleep health is associated with older brain age: the role of systemic inflammation.”

Increased inflammation in the body may partly explain the association.

Poor sleep has been linked to dementia, but it is unclear whether unhealthy sleep habits contribute to the development of dementia or whether they are rather early symptoms of the disease.

SHIELD activated: Researchers build defense to protect drones from cyberattacks

Fooled into following a hacker’s rogue commands, a drone is liable to do any number of things. Fly erratically. Speed up. Slow down. Hang suspended in the air. Reverse course. Take a new course. And, most dangerously: Crash.

What the compromised drone cannot do, however, is regain control. Lost to its original assignment—whether it’s delivering a package, inspecting an aging bridge or monitoring the health of crops—the machine is essentially useless.

At FIU, cybersecurity researchers have developed a series of countermeasures to fight back mid-flight against hostile takeovers.

Mitochondria Dump Their Rubbish DNA, And It Could Be Costing Us Our Health

Researchers have discovered a key molecular process that may contribute to chronic inflammation as we age. If this process can be accurately targeted, it could unlock ways to stay healthier in our later years.

The discovery centers on the unique strands of DNA contained within our mitochondria, the power stations of our cells. By banishing their ‘mtDNA’ into the surrounding cytoplasm, mitochondria can cause inflammation. Yet just how or why this happens has never been well understood.

In this study, researchers led by a team from the Max Planck Institute for Biology of Ageing in Germany analyzed tissue samples from humans and test animals, using mice genetically engineered to be models of aging and disease.

/* */