Lifeboat Foundation

Research labs are pursuing technology to “reprogram” aging bodies back to youth.

Recent evidence points out the role of the gut microbiota in the aging process. However, the specific changes and relevant interventions remain unclear. In this study, Senescence Accelerated Mouse-Prone 8 (SAMP8) mice were divided into four groups; young-FMT-group transplanted fecal microbiota from young donors (2–3°months old) and old-FMT-group transplanted from old donors (10–11°months old); additionally, other two groups either adult mice injected with saline solution or untreated mice served as the saline and blank control groups, respectively. All mice were intervened from their 7-months-old until 13-months-old. The open field test at 9 and 11°months of age showed that the mice transplanted with gut microbiota from young donors had significantly better locomotor and exploration ability than those of transplanted with old-donors gut microbiota and those of saline control while was comparable with the blank control. 16S rRNA gene sequencing showed that the gut microbiome of recipient mice of young donors was altered at 11°months of age, whereas the alternation of the gut microbiome of old-donor recipient mice was at 9°months. For comparison, the recipient mice in the blank and saline control groups exhibited changes in the gut microbiome at 10°months of age. The hallmark of aging-related gut microbiome change was an increase in the relative abundance of Akkermansia, which was significantly higher in the recipients transplanted with feces from older donors than younger donors at 9°months of age. This study shows that fecal microbiota transplantation from younger donors can delay aging-related declines in locomotor and exploration ability in mice by changing the gut microbiome.

Aging is inherently accompanied by the decline of physical and mental abilities, including locomotor, cognition, and bodily functions, to subsequently cause frailty syndrome, neurodegenerative diseases, and other age-related diseases, which reduce the quality of life of the aging population (Hou et al., 2019). Aging mechanisms and anti-aging interventions have long been a major focus of biomedical research, which is particularly relevant given the rapidly aging society.

The gut is a major organ for nutrients absorption, metabolism, and immunity, and contains hundreds of millions of microorganisms and their metabolites, which comprise the gut microbiota (Heintz and Mair, 2014) that interacts with host cells and tissues (Huang et al., 2021). Our previous study reported continuous changes in the gut microbiome of centenarians during their transition from a healthy status to death. The most significant changes of gut microbial communities in the period were found to occur at 7°months prior to death, suggesting that this may be a turning point of significant changes in the gut microbiome of centenarians (Luan et al., 2020). Recent studies have revealed an important relationship between the gut microbiome and aging-related diseases such as Alzheimer disease (Ticinesi et al., 2018; Haran and McCormick, 2021), suggesting that the gut microbiome plays an essential role in the aging process.

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We teach the scientific rationality of age reversal, radical life-extension, & we provide fellowship for longevity enthusiasts. Longevity lives here!

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RIYADH, Saudi Arabia—(BUSINESS WIRE)— Hevolution Foundation, a non-profit organization that provides grants and early-stage investments to incentivize research and entrepreneurship in healthspan science, announces a new grants program to encourage research into the aging process in Saudi Arabia, as part of the growing Saudi scientific ecosystem. The program, Hevolution’s Open Call for Grant Applications in Saudi Arabia, will provide funding of up to 500,000 Saudi Riyals for local researchers with an interest in the mechanisms of aging.

“This grants program is the first of many through which we aim to encourage the development of the field of aging research in Saudi Arabia” Tweet this

“Saudi Arabia’s population is relatively young but has high rates of age-related conditions such as heart disease and diabetes,” commented Mehmood Khan, MD, Hevolution Foundation’s Chief Executive Officer. “Our hope is that by tackling the aging process itself, we can alleviate the burden of diseases and conditions of aging for the people of Saudi Arabia and worldwide. With this pilot program and others that we have in the works, we hope to enable Saudi Arabia’s scientific community to be a key player in the global charge to reduce the burden of age-related diseases and conditions that affect most of humanity.”

The Aging and Drug Discovery Conference (ARDD) 2022 is pleased to present David Sinclair from Harvard Medical School, who shares new unpublished results from his lab at Harvard Medical School.

Held in Copenhagen at the glorious Ceremonial Hall, this meeting gathers the most prominent figures of the aging and longevity research field, from scientists to clinicians, investors, developers, and everything in between. The fast growth of the conference is evidence of its great quality. In 2022 we had around 400 people on-site, and many others joined through the web.

Continue reading “David Sinclair at ARDD2022: Great release of unpublished data from David Sinclair’s Lab” »

The Inaugural Rejuvenation Startup Summit 2022, brought to you by the Forever Healthy Foundation, took place with over 400 participants from over 30 countries in October. It is a vibrant networking event that aims to accelerate the development of the rejuvenation biotech industry. The Summit brings together startups, members of the longevity venture capital / investor ecosystem, and researchers interested in founding or joining a startup – all aiming to create therapies to vastly extend the healthy human lifespan. We started to publish videos with a first set of selected speakers on the 2022 summit:

Foresight Biotech & Health Extension Meeting sponsored by 100 Plus Capital.
Program & apply to join: https://foresight.org/biotech-health-extension-program/

This video was recorded at the Foresight Longevity Workshop.

Continue reading “Reason | An 80/20 Gene Therapy that Just Works — Challenge” »

ROS are short lived molecular species containing an unpaired electron which makes them highly reactive as they search for another electron to pair with, and in the process can damage biomolecules such as DNA, proteins and lipids⁵⁴. ROS induced oxidative stress is known to have multiple deleterious effects on host cells⁵⁵. However, we have reported that, paradoxically, when ROS is artificially generated outside the cell in the extracellular spaces of the body, they can have wide ranging therapeutic effects^{18,19,20,26,27}. Admixing R with Cu leads to generation of oxygen radicals by virtue of the ability of R to reduce Cu (II) to Cu (I)^23,25. Oxygen radicals that are generated in the stomach upon oral administration of R–Cu are apparently absorbed to have systemic effects in the form of deactivation/eradication of extracellular cfChPs. We have shown that cfChPs have wide-ranging damaging effects on host cells. For example, cfChPs can readily enter into the healthy cells to damage their DNA, activate inflammatory cytokines and promote apoptosis via the mitochondrial pathway^13,14. Given that 1 × 10⁹–1 × 10¹² cells die in the body every day^56,57, we have hypothesised that repeated and lifelong assault on healthy cells by cfChPs derived from the dying cells may be the underlying cause of ageing^15,16. In support of this hypothesis we show in this article that prolonged oral administration of R–Cu to ageing mice down-regulated multiple biological hallmarks of ageing and neurodegeneration by virtue of its ability to deactivate cfChPs. Our results suggest that R–Cu may qualify as an ideal anti-ageing agent since it has the potential to simultaneously retard or delay the many conditions that are associated with ageing². To be globally applicable, an ideal anti-ageing agent should also be inexpensive and non-toxic—the two criteria that are also met by R–Cu. The latter can be easily administered orally, and both R and Cu are already approved for human use. An illustrated summary of the study design and the mechanisms by which R–Cu generated oxygen radicals eradicate cfChPs from brain micro-environment leading to down-regulation of ageing hallmarks is provided in Fig. 10.

The mechanism(s) by which R–Cu down-regulates the multiple biological hallmarks of ageing and neurodegeneration needs elaboration. Reversal of telomere shortening by R–Cu may suggest that telomere shortening could be a consequence of DNA damage inflicted by cfChPs which shear off telomere ends causing them to shorten. We observed differential effects between female and male mice with respect to telomere abnormalities. R–Cu effects in preventing telomere abnormalities in female mice were statistically significant for all parameters tested, while this was not the case in male mice. The biological explanation for this discrepant finding remains to be determined. Breakage of telomere ends may also help to explain our detection of persistent γ-H2AX signals in telomere regions of brain cells (DNA-SCARS)—an established signature of senescence⁴³. The bare chromosomal ends can fuse with each other to lead to chromosomal instability and aneuploidy⁴⁸, as was detected in our study.