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Category: life extension – Page 6

Muscle in Space Sheds Light on Ageing-Related Muscle Loss

Sarcopenia, which is a progressive and extensive decline in muscle mass and strength, is common with aging and estimated to affect up to 50% of people aged 80 and older. It can lead to disability and injuries from falls and is associated with a lower quality of life and an increased mortality. Apart from lifestyle changes, there is no current clinical treatment for sarcopenia.

Space flight with the associated absence of gravity and limited strain on muscles causes muscle weakness, a prominent feature of sarcopenia, within a short period of time, providing a time lapse view on age-related atrophy-associated changes in the muscle. This relatively short window of time in space provides a microgravity model for muscular aging and opens opportunities for studying sarcopenia, which normally takes decades to develop in patients on earth.

To understand the changes of muscle in microgravity, Siobhan Malany, Maddalena Parafati, and their team from the University of Florida, USA, engineered skeletal muscle microtissues from donor biopsies and launched them to the International Space Station (ISS) aboard SpaceX CRS-25. Their findings were published today in Stem Cell Reports. The microtissues were taken from both young, active donors and from aged, sedentary donors and cultured in an automated mini lab, which besides regular feeding and monitoring of cultures also enabled electrical stimulation to simulate exercise. On earth, the contraction strength of microtissues from young, active individuals was almost twice as much as the strength of tissues from older, sedentary individuals. After only two weeks in space, muscle strength trended to decline in the young tissues and was now more comparable to the strength of old tissues. A similar trend was seen for the muscle protein content, which was higher in young microtissues on earth compared to old microtissues but decreased in microgravity to levels measured in old tissues. Further, space flight changed gene expression, particularly in the younger microtissues and disturbed cellular processes related to normal muscle function. Interestingly, electrical stimulation could mitigate these changes in gene expression to some extent.

A potential replacement for bone marrow sampling: New blood test may detect leukemia risk

What if a blood test could reveal the pace of our aging—and the diseases that may lie ahead? The labs of Profs. Liran Shlush and Amos Tanay at the Weizmann Institute of Science have been conducting in-depth studies into the biology of blood to better understand the aging process and why some people become more susceptible to disease over the years.

Their research teams, made up of physicians, biologists and , have been tracking changes in the , including the emergence of genetic changes in these cells in about one-third of people over the age of 40. These changes not only increase the risk of blood cancers such as leukemia, but have also been linked to heart disease, diabetes and other age-related conditions.

In a new study published today in Nature Medicine, Shlush and Tanay present findings that may lead to an innovative for detecting a person’s risk of developing leukemia. This test may potentially replace the invasive diagnostic procedure of bone marrow sampling.

Restoring youth: Scientists use engineered cells to restore vitality in primates

Researchers from the Chinese Academy of Sciences and Capital Medical University utilized gene editing to create senescence-resistant human mesenchymal progenitor cells (SRCs). In a 44-week trial on aged macaques, biweekly intravenous SRC injections induced no adverse effects and spurred multi-system rejuvenation in 10 major physiological systems and 61 tissue types. Treated macaques displayed enhanced cognitive function and diminished age-related degeneration. The SRCs work by releasing exosomes that curb cellular senescence and inflammation. This study presents the first primate-level proof of cell therapy’s safety and efficacy in reversing aging, presenting a potential multi-system approach for human anti-aging research.

Dissecting the cell cycle regulation, DNA damage sensitivity and lifespan effects of caffeine in fission yeast

Caffeine has long been associated with health benefits, including a reduced risk of age-related diseases. However, the specifics of how caffeine interacts with cellular mechanisms and nutrient and stress-responsive gene networks have remained elusive — until now.

In this pioneering research, published in the journal Microbial Cell, scientists used fission yeast, a single-celled organism with surprising similarities to human cells, to delve deeper into caffeine’s impact.

The researchers discovered that caffeine influences aging by engaging an ancient cellular energy system.

A few years ago, the same team found that caffeine prolongs cell life by acting on a growth regulator known as TOR (Target of Rapamycin). TOR is a molecular switch that regulates cell growth based on available food and energy and has been part of the evolutionary landscape for over 500 million years.

However, their latest study unveiled a surprising new finding: caffeine does not directly act on the TOR switch. Instead, it activates AMPK, a cellular fuel gauge that is conserved through evolution in both yeast and humans.

“When your cells are low on energy, AMPK kicks in to help them cope,” senior author Charalampos (Babis) Rallis, a reader in genetics, genomics and fundamental cell biology at Queen Mary University of London, said in a news release. “And our results show that caffeine helps flip that switch.”

Intriguingly, AMPK is also the target of metformin, a common diabetes medication currently under scrutiny for its potential to extend human lifespan when used alongside rapamycin.

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Diglycerides Are Associated With An Older Biological Age

And an increased all-cause mortality risk…

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Scientists use gene editing to correct harmful mitochondrial mutations in human cells

In a step toward treating mitochondrial diseases, researchers in the Netherlands have successfully edited harmful mutations in mitochondrial DNA using a genetic tool known as a base editor. The results, published in the open-access journal PLOS Biology, offer new hope for people with rare genetic conditions.

Mitochondria have their own small set of DNA. Mutations in this mitochondrial DNA can lead to a wide range of maternally inherited diseases, cancer, and aging-related conditions. While the development of CRISPR technology has given scientists new ways to correct mutations in nuclear DNA, this system cannot effectively cross the mitochondrial membrane and reach mitochondrial DNA.

In the new study, the researchers used a tool called a base editor—specifically, a DdCBE (double-stranded DNA deaminase toxin A-derived cytosine ). This tool allows scientists to change a single letter in the DNA code without cutting it, and it works on mitochondrial DNA.