In a new study published in Aging Cell [1], researchers report that transient activation of the Yamanaka factor Oct4 allowed partial reprogramming of cells, which led to rejuvenation in these cells and in a mouse model of premature aging.
For the first time, researchers have shown that reduced oxygen intake, or “oxygen restriction,” is associated with longer lifespan in lab mice, highlighting its anti-aging potential. Robert Rogers of Massachusetts General Hospital in Boston, US, and colleagues present these findings in a study published May 23rd in the open access journal PLOS Biology.
Research efforts to extend healthy lifespan have identified a number of chemical compounds and other interventions that show promising effects in mammalian lab animals— for instance, the drug metformin or dietary restriction. Oxygen restriction has also been linked to longer lifespan in yeast, nematodes, and fruit flies. However, its effects in mammals have been unknown.
To explore the anti-aging potential of oxygen restriction in mammals, Rogers and colleagues conducted lab experiments with mice bred to age more quickly than other mice while showing classic signs of mammalian aging throughout their bodies. The researchers compared the lifespans of mice living at normal atmospheric oxygen levels (about 21%) to the lifespans of mice that, at 4 weeks of age, had been moved to a living environment with a lower proportion of oxygen (11%—similar to that experienced at an altitude of 5,000 meters).
It sucks that the primary reason this has not gone forward is because it is off patent.
This video is reproduced from a presentation I gave to the Euro-Geroscience Task Force “Challenges in Developing Geroscience Drug Trials” held March 23, 2022 in Toulouse, France. It gives an introduction to the state of research on rapamycin as a potential longevity and healthspan drug and some of the challenges and opportunities for clinical development.
The 2023 edition of the exclusive Longevity Investors Conference is fast approaching, bringing together investors, companies and researchers in Gstaad, Switzerland in September. One of the speakers at this year’s conference is scientist, writer and presenter Dr Andrew Steele, the author of the best-selling book Ageless: The new science of getting older without getting old. When it comes to his views on longevity, Steele sits firmly in the camp that aging, like cancer, is something that humanity should be focused on curing.
Longevity. Technology: Last year, Steele told us he was “absolutely convinced” curing aging is possible, but that significant questions remain around how quickly we can get there. As he prepares to speak to more than 100 investors at LIC, we caught up with Steele to see how his views on longevity have evolved, and what he would say to those considering investing in the field.
First and foremost, Steele, who recently published a new, free chapter of Ageless on the moral, ethical and social consequences of treating aging, believes that longevity represents a huge “human opportunity” for investors.
The winners of the Non-Profit Organisation Awards 2023 by Acquisition International have just been announced and The Millennium Project has been awarded for Excellence in Innovation – USA!
The Non-Profit Organisation Awards aim to reward Non-profit organizations that globaly that play a monumental role in solving some of our biggest global challenges. The awards reward commitment, innovation, and determination of the best NPOs from across the world by selecting the most innovative, creative and compassionate NPOs, and provide a platform for NPOs to demonstrate that they are a true leader within the non-profit sphere.
The approach for nominations includes gathering and evaluating the nominees, research and judging on various criteria, including client dedication, innovation, business growth, longevity, online reputation, client feedback and business performance, and announcement of the winners.
The ancient, 18-foot-long crocodile — the world’s largest living in captivity — is healthy but occasionally displays signs of trauma from his troubled youth in the wild.
Busso also said we don’t yet know the long-term effects of these treatments on normal cells or what the long-term impact of killing zombie cells might be. Additionally, because zombie cells play an important role in wound healing, “We don’t want to remove all of them,” he said. “We don’t know the ideal regimen, daily versus weekly versus monthly.”
Hopefully, we won’t have to wait long for answers about the best way to get rid of zombie cells on the skin. “Major breakthroughs and contributions to delaying of the aging process are expected in the near future,” Busso said.
Although it’s still unclear whether zombie cells can be safely and effectively cleared from the skin, it is possible to prevent some zombie cells from forming in the first place. Collins explained that zombie cells are formed as the result of both biological and environmental factors. “The internal factors, like aging or genetic disease, are not so much within our control,” but the external factors can be controlled, she said.
The African turquoise killifish is an emerging vertebrate model organism with great potential for aging research due to its naturally short lifespan. Thus far, turquoise killifish aging omic studies using RNA-seq have examined a single organ, single sex and/or evaluated samples from non-reference strains. Here, we describe a resource dataset of ribosomal RNA depleted RNA-seq libraries generated from the brain, heart, muscle, and spleen from both sexes, as well as young and old animals, in the reference GRZ turquoise killifish strain. We provide basic quality control steps and demonstrate the utility of our dataset by performing differential gene expression and gene ontology analyses by age and sex. Importantly, we show that age has a greater impact than sex on transcriptional landscapes across probed tissues. Finally, we confirm transcription of transposable elements (TEs), which are highly abundant and increase in expression with age in brain tissue. This dataset will be a useful resource for exploring gene and TE expression as a function of both age and sex in a powerful naturally short-lived vertebrate model.
The authors have declared no competing interest.
Research from the Babraham Institute has developed a method to ‘time jump’ human skin cells by 30 years, turning back the ageing clock for cells without losing their specialised function. Work by researchers in the Institute’s Epigenetics research programme has been able to partly restore the function of older cells, as well as rejuvenating the molecular measures of biological age. The research is published today in the journal eLife and whilst at an early stage of exploration, it could revolutionise regenerative medicine.
What is regenerative medicine?
As we age, our cells’ ability to function declines and the genome accumulates marks of ageing. Regenerative biology aims to repair or replace cells including old ones. One of the most important tools in regenerative biology is our ability to create ‘induced’ stem cells. The process is a result of several steps, each erasing some of the marks that make cells specialised. In theory, these stem cells have the potential to become any cell type, but scientists aren’t yet able to reliably recreate the conditions to re-differentiate stem cells into all cell types.
Immunotherapy is a fast-growing field designed to stimulate the immune system and target different diseases, including cancer. Some immunotherapies include immune cell activation therapies such as checkpoint inhibitors that block the interaction of cell markers which in turn allows the cell to kill the bound tumor cell. One example of a checkpoint inhibitor is anti-programmed cell death-1 (Anti-PD-1). Programmed cell death-1 (PD-1) is expressed on immune cells, specifically T cells. On responsibility of T cells include killing infected cells, such as cancer. The PD-1 marker is bound to PD-L1 on the infected cell and blocks the T cell’s ability to kill the tumor. Checkpoint inhibitors are effective in some subsets of cancer patients, but in more aggressive cancers such as liver cancer, immunotherapy is limited. Interestingly, a recent study in Nature Medicine by Dr. Miriam Merad and colleagues from the Ichan School of Medicine at Mount Sinai recently reported a new strategy to improve immunotherapy in liver cancer.
Merad and colleagues have uncovered a “trio of immune cells” within the tumor that helps improve immunotherapy. Researchers discovered this cohort of cells specifically in hepatocellular carcinoma (HCC), an aggressive and deadly liver cancer. It was demonstrated that specific populations in the tumor would be needed to activate T cells with immunotherapy, specifically anti-PD-1. Increased activation of T cells in HCC is critical because it demonstrates that an aggressive tumor has become sensitized to the immune system.
Researchers studied this phenomenon in patients to determine why some immune cells present in the tumor allow improved immunotherapy response, while others do not. The research team analyzed patient samples before and after checkpoint inhibitor treatment. Analysis was performed through computational methods, which allowed Merad and others to determine the immune cells necessary that help patients improve with immunotherapy. Through this computational cell analysis researchers are able to improve patient outcomes by determining if the “trio of cells” is present in the tumor.
