Lifeboat Foundation: Safeguarding Humanity
Toggle light / dark theme

Blog

Category: life extension

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.

Smart blood: How AI reads your body’s aging signals

Could a simple blood test reveal how well someone is aging? A team of researchers led by Wolfram Weckwerth from the University of Vienna, Austria, and Nankai University, China, has combined advanced metabolomics with cutting-edge machine learning and a novel network modeling tool to uncover the key molecular processes underlying active aging.

Their study, published in npj Systems Biology and Applications, identifies aspartate as a dominant biomarker of physical fitness and maps the dynamic interactions that support healthier aging.

It has long been known that exercise protects mobility and lowers the risk of chronic disease. Yet the precise molecular processes that translate physical activity into healthier aging remain poorly understood. The researchers set out to answer a simple but powerful question: Can we see the benefits of an active lifestyle in elderly individuals directly in the blood—and pinpoint the molecules that matter most?

How non-neuronal brain cells communicate to coordinate rewiring of the brain

A study by Dorothy P. Schafer, Ph.D., and Travis E. Faust, Ph.D., at UMass Chan Medical School, explains how two different cell types in the brain—astrocytes and microglia—communicate in response to changes in sensory input to remodel synapses, the connections between neurons.

Published in Cell, these findings are in an emerging area of interest for neurobiologists who want to understand how different cells in the brain interact to rewire the brain.

This novel mechanism has the potential to be targeted by translational scientists hoping to one day prevent synaptic damage incurred during neurodegenerative diseases such as Alzheimer’s or ALS as well as age-related cognitive decline. It may also lead to new insights into neurodevelopmental and psychiatric disorders such as autism and schizophrenia, where the brain’s circuit refinement process may have been compromised during development.

Extreme lifespan multiomics

Recent studies suggest that the steady rise in life expectancy observed over the past 200 years has now stagnated. Data indicate that a limit has been reached, and that medical and healthcare advances no longer affect longevity in developed countries as they did in previous decades. Today, ageing itself, rather than disease, is the real frontier of human longevity. But what exactly is ageing? And can it be addressed in the same way as a disease?

A research team has just published the final peer-reviewed data from the study of the longest-lived person ever recorded, who far exceeded 117 years: the Catalan woman Maria Branyas. The analysis, based on samples obtained using minimally invasive techniques, takes a multi-omic approach with genomic, proteomic, epigenomic, metabolomic and microbiomic technologies, and represents the most exhaustive study ever undertaken on a supercentenarian.

In the paper, published in the prestigious journal Cell Reports Medicine, the international and multidisciplinary team explains that individuals who reach supercentenarian age do not do so through a general delay in ageing but, as the author notes, thanks to a “fascinating duality: the simultaneous presence of signals of extreme ageing and of healthy longevity.”

Reprogramming cellular senescence and aging clocks for advanced cancer immunotherapy

Cellular senescence has gradually been recognized as a key process, which not only inhibits the occurrence of early tumors but also promotes advanced malignant progression through secretory and immunomodulatory functions. Initially, cellular senescence manifested as irreversible cell cycle arrest, but now it encompasses a broader phenotype regulated by the p53-p21CIP1 and p16INK4A-Rb pathways. Although secretory phenotypes related to aging can recruit immune effectors to clear new tumor cells, persistent senescent cell populations often trigger chronic inflammation, promoting immune escape and fibrosis. In this review, we first discuss the molecular underpinnings of cellular senescence, highlighting its induction pathways and diverse physiological or pathological roles. We then examine the composition of the tumor microenvironment, where senescent cells accumulate and secrete pro-inflammatory cytokines, reshaping immune surveillance and extracellular matrix architecture. Against this backdrop, we explore how aging clocks refine our understanding of individual susceptibility to malignancy by distinguishing biological from chronological aging. We also present current therapeutic prospects, including senolytic agents targeting senescent stromal cells that promote tumor growth, and the utilization of aging clock metrics to tailor immunotherapies more effectively for older patients. Finally, we consider the major challenges facing clinical translation, from standardizing multi-omics data pipelines to clarifying the ethical implications of measuring biological age. By bridging senescence biology with geroscience and cutting-edge oncology, we posit that aging clocks may catalyze a transformation in cancer care, enabling more personalized, effective, and age-conscious treatment strategies.

/* */