Lifeboat Foundation

“Science hasn’t yet found a way to make complex animals like dogs live forever, so the next best thing we can do is find a way to maintain health for as long as possible during the aging process,” said Church.

And the goal was for this to hit a market and use the income to pay for human trials lasting 10 years.

Combination gene therapy developed at Wyss Institute and Harvard Medical School treats four age-related conditions.

Continue reading “Rejuvenate Bio launches to help dogs live longer, healthier lives” »

Ira Pastor, ideaXme exponential health ambassador, interviews Ms. Laura Trejo, General Manager of Los Angeles’s Department Of Aging.

Ira Pastor Comments:

Continue reading “Los Angeles: Healthy Aging” »

In this post, you’ll find why I think SENS Research Foundation (SRF) is great to finance from an EA perspective along with the interview questions I want to ask its Chief Science Officer, Aubrey de Grey. You are welcome to contribute with your own questions in the comments or through a private message. Here is a brief summary of each section:

Introduction: Aging research looks extremely good as a cause-area from an EA perspective. Under a total utilitarian view, it is probably second or third after existential risk mitigation. There are many reasons why it makes sense to donate to many EA cause-areas, such as to reduce risk, if there are particularly effective specific interventions, or if some cause-areas are already well funded.

SRF’s approach to aging research: SRF selects its research following the SENS general strategy, which divides aging into seven categories of damage, each having a corresponding line of research. This categorization is very similar to the one described in the landmark paper The Hallmarks of Aging. This sort of damage repair approach seems more effective and tractable than current geriatrics and biogerontology that are aimed at slowing down aging, as it enables LEV and many more QALYs. It makes rejuvenation possible instead of just slowing down aging as a best-case scenario, and it doesn’t require an in-depth knowledge of our metabolism, which is extremely complicated and full of unknown-unknowns.

The De Grey searching for researchers with work involving longevity… r.p.berry & AEWR.

Thank you for your interest in submitting a proposal for grant funding to SENS Research Foundation (SRF). Primarily, we fund projects by identifying research priorities through our Chief Science Officer’s (CSO) team and then either approaching parties with relevant expertise directly, or if appropriate generating requests for proposals (RFPs).

We do, however, also accept letters of intent for new grant proposals from interested parties for projects that fall specifically within our research mission. All such letters should clearly delineate the specific SENS target to which the proposal relates, and how the proposal would further progress toward developing therapies that remove, repair, replace, or render harmless that target.

All research projects are selected and periodically reviewed by our Research Development Committee (RDC), and its decisions are ratified by our Board of Directors. The RDC convenes twice yearly, at the end of the first and third calendar quarters.

Christian Schafmeister, Ph.D., Professor at Temple University in Philadelphia says: “We are developing “therapeutic catalysts” — small, robust, non-immunogentic catalysts that will permeate the tight spaces within tissues and fix things. Our specific targets include reversing the unwanted cross-links that develop in the extracellular matrix with aging.”

Enzymes, while possessing exquisite substrate-specificity, are limited by their molecular size in their ability to gain access to their substrate when it is embedded within dense material. We have always known that this may be a problem for our approach to restoring the elasticity of aged tissues. Christian’s fascinating work offers the potential to solve this issue with molecules that have the same catalytic function as enzymes but are much smaller and can therefore reach these embedded substrates.

Had a very frank discussion with Greg Mustreader about transhumanism, learned helplessness of society in the face of aging and death, insufficient sense of urgency among researchers of aging, epigenetic rejuvenation, cryonics, and so on. No filter! 😁.

My blog on Medium: https://medium.com/@mustreader

Continue reading “Yuri Deigin on epigenetic rejuvenation, longevity research and transhumanists in politics” »

Turquoise killifish is able to suspend its development for longer than its average lifespan.

Researchers have discovered that the powerhouses of our cells, the mitochondria, also play a role in triggering cells to enter senescence, a dormant state in which cells cease to divide and begin to shut down, ready to die.

Mitochondria trigger cytoplasmic chromatin and inflammation

The new study shows that the mitochondria in each cell communicate with its nucleus, causing it to shut down and enter a senescent state [1]. Dr. Peter Adams, one of the study’s researchers, has spent over a decade investigating how chromatin clusters, a mixture of DNA and proteins typically encountered in the cell nucleus, actually leak out of the nucleus and into the cytoplasm in senescent cells. This leaking then triggers a cascade of inflammatory signals, which are linked to the onset of various age-related diseases.

King’s College in London, UK has been awarded a grant to investigate the role of senescent cells, which accumulate as we age, in the context of the heart and how using a therapy to remove them influences its ability to recover from injury.

What are senescent cells?

As you age, increasing numbers of your cells enter into a state known as senescence. Senescent cells do not divide or support the tissues of which they are part; instead, they emit a range of potentially harmful chemical signals that encourage nearby healthy cells to enter the same senescent state. Their presence causes many problems: they reduce tissue repair, increase chronic inflammation, and can even eventually raise the risk of cancer and other age-related diseases.