Lifeboat Foundation

Powered by data produced by its AI-driven discovery platform, clinical-stage biotech BioAge Labs is rapidly developing a pipeline of therapies to extend healthy lifespan by targeting the molecular causes of aging. Having raised more than $120 million in funding, and with multiple clinical trials already under its belt, the company is focused on building a broad pipeline of potential longevity therapies in three main areas: muscle, immune, and brain aging.

Longevity. Technology: There are few companies in the longevity biotech field that appear to be executing on their vision as quickly and consistently as BioAge. When the company wowed the sector with a $90 million funding round in 2020, talk of multiple imminent clinical trials may have sounded optimistic to some, but BioAge has delivered on its promise time and again. Beyond the trials already underway, the company’s much-vaunted AI discovery platform also appears to be churning out the data, this year spawning a new programme exploring the potential of NLRP3 inhibitors in brain aging. To learn more, we caught up with BioAge co-founder and CEO Kristen Fortney.

Looking back at 2022, Fortney says it has been “immensely gratifying” to see so many new companies and investors coming into the longevity field.

In this #webinar, Dr Vincenzo Sorrentino from the Department of Biochemistry and Healthy Longevity Translational Research Programme at the Yong Loo Lin School of Medicine, shared about his research on the relationship between metabolism, nutrition and proteostasis and their impact on health and ageing, and engaged in discussion about the role of mitochondrial proteostasis in ageing and related diseases.

Register for upcoming #HealthyLongevity #webinar sessions at https://nus-sg.zoom.us/webinar/register/7916395807744/WN__sypkX6ZSomc7cGAkK3LbA

Continue reading “Targeting the mitochondria-proteostasis connection in ageing and disease | Dr Vincenzo Sorrentino” »

Aging appears to progress similarly across species, from worms and flies to mice and humans, and involves pathways related to early development. Guest Linda Partridge talks with Gordon while visiting the Buck Institute to discuss the evolutionary trade offs of aging mechanisms, the role of nutrient-sensing pathways, and how we might get the most benefit from preventative interventions in midlife.

Linda Partridge, born in 1950 in Bath, England, studied and graduated in biology at the University of Oxford. After three years of postdoctoral research at the University of York, she was Demonstrator, Lecturer, Reader and finally Professor at the University of Edinburgh. After many years in Scotland, in 1994 she became Professor of Biometry, University College London. She is both a founding director of the new Max Planck Institute for Biology of Ageing in Cologne and Director of the UCL Institute of Healthy Ageing. Linda Partridge’s research is directed to understanding both how the rate of aging evolves in nature and the mechanisms by which healthy lifespan can be extended in laboratory model organisms. Her work has focussed in particular on the role of nutrient-sensing pathways, such as the insulin/insulin-like growth factor signaling pathway, and on dietary restriction.

Interesting interview about the future of Ageing with leading expert with Aubrey De Grey.

This week we interview the phenomenal Aubrey De Grey, the world’s foremost authority on longevity and developing strategies to slow or eliminate aging altogether. The author of The Mitochondrial Free Radical Theory of Aging (1999) and Ending Aging (2007), De Grey is probably best known for the concept of Longevity Escape Velocity, a view that soon medical technology will enable human beings to prevent age-related deterioration, and eventually eliminated aging entirely.

The future of Ageing with Aubrey De Grey.

Billionaires are funding immortality tech. And in theory, such techology would allow those billionaires to compound their wealth and power forever. Gulp.

Our DNA is made up of genes that vary drastically in size. In humans, genes can be as short as a few hundred molecules known as bases or as long as two million bases. These genes carry instructions for constructing proteins and other information crucial to keeping the body running. Now a new study suggests that longer genes become less active than shorter genes as we grow older. And understanding this phenomenon could reveal new ways of countering the aging process.

Luís Amaral, a professor of chemical and biological engineering at Northwestern University, says he and his colleagues did not initially set out to examine gene length. Some of Amaral’s collaborators at Northwestern had been trying to pinpoint alterations in gene expression—the process through which the information in a piece of DNA is used to form a functional product, such as a protein or piece of genetic material called RNA—as mice aged. But they were struggling to identify consistent changes. “It seemed like almost everything was random,” Amaral says.

Then, at the suggestion of Thomas Stoeger, a postdoctoral scholar In Amaral’s lab, the team decided to consider shifts in gene length. Prior studies had hinted that there might be such a large-scale change in gene activity with age—showing, for example, that the amount of RNA declines over time and that disruptions to transcription (the process through which RNA copies, or transcripts, are formed from DNA templates) can have a greater impact on longer genes than shorter ones.

Many neurodegenerative diseases, including Alzheimer’s.

Alzheimer’s disease is a disease that attacks the brain, causing a decline in mental ability that worsens over time. It is the most common form of dementia and accounts for 60 to 80 percent of dementia cases. There is no current cure for Alzheimer’s disease, but there are medications that can help ease the symptoms.

Let me assure you that my intent in this article is not to refute any empirical data or established theories about telomeres. Instead, I will explain why I believe that the historical course of scientific discoveries and an outdated paradigm about the biological cause of aging have led to the use of inaccurate language in describing the roles and functions of telomeres.

Aubrey De Grey discusses the progress and potential of therapies related to his ideas on anti-aging medicine, including the four therapies that will be tested in a mouse rejuvenation trial. He also shares his thoughts on partnering with organizations and individuals in the field, integrating AI into his work, and the importance of structure in maximizing impact. Aubrey de Grey discusses the potential for Yamanaka factors to be used in organ rejuvenation, and the role of transcription factors in creating induced pluripotent stem cells. He also provides advice for those interested in getting involved in the field and shares his views on time management and productivity. Aubrey De Grey discusses the potential for reversing the pathology of aging to address mechanical issues and mentions promising research being conducted by MAIA Biotechnology on cancerous cells that express telomerase. He also expresses his optimism about the possibility of reaching “longevity escape velocity” within the next 15 years.

Youtube:
Aubrey De Grey links.
https://twitter.com/aubreydegrey?ref_src=twsrc%5Egoogle%7Ctw…r%5Eauthor.
https://www.levf.org/
https://www.linkedin.com/in/aubrey-de-grey-24260b/

Continue reading “Aubrey De Grey: longevity escape velocity, longevity, mouse rejuvenation, Altos Labs, Yamanaka factor” »