Lifeboat Foundation

Acciaroli vila italiana, onde um em cada 10 pessoas vivem além de 100 anos.

Depois de passar seis meses na área, pesquisadores da Universidade de Sapineza de Roma e da Escola de Medicina Sandiego encontraram que os idosos da região têm invulgarmente boa circulação sanguínea para a sua idade.

A equipe de pesquisa analisou amostras de sangue de mais de 80 residentes, e descobriu extraordinariamente baixos níveis de adrenomedullin, um hormônio que alarga os vasos sanguíneos.

Continue reading “Scientists ‘find key to longevity’ in Italian village where one in 10 people live beyond 100 years” »

Ray Kurzweil is a futurist, a director of engineering at Google and a co-founder of the Singularity University think tank at NASA Ames Research Center in Mountain View. He is a nonfiction author and creator of several inventions.

Kurzweil met with the Silicon Valley Business Journal to discuss how technology’s exponential progress is rapidly reshaping our future through seismic shifts in information technology and computing power, energy, nanotechnology, robotics, health and longevity.

Biohacking, nootropics, and the notion of optimizing one’s human performance are on a rapid rise. Nootrobox founders Geoffrey Woo and Michael Brandt are some of the foremost thinkers in this space, and they are here to have intellectual conversations that will make you THINK.

Episode 9 features Aubrey de Grey, the Chief Scientist Officer of the SENS Research Foundation. In this episode, Geoff, Michael, and Aubrey discuss the nuances of aging and health and their differing opinions and tactics of how to fully optimize these notions.

Continue reading “THINKING Podcast” »

No shock to me.

Diamandis claimed that we are gearing towards a future possible of “interface mind-machine, where in human brain’s consciousness could be uploaded to computer and then transferred to a new body—probably a cultured in the lab. He estimates that it will just take 20–30 years to be realized.

The reality of extended life longevity to almost immortality is actually not too hard to believe these days. After all science and technology never failed to amuse us to make the once impossible possible.

Continue reading “We Might Be Getting Closer To ‘Immortality’ Through Medical Nanotechnology” »

The SENS Research Foundation has finally published this anticipated and important paper on mitochondrial gene transfer which has ramifications for mitochondrial diseases and more importantly one of the processes of aging. It is great to see that finally after a decade of criticism Aubrey de Grey has proven his approach is viable.

We explore the possibility of re-engineering mitochondrial genes and expressing them from the nucleus as an approach to rescue defects arising from mitochondrial DNA mutations. We have used a patient cybrid cell line with a single point mutation in the overlap region of the ATP8 and ATP6 genes of the human mitochondrial genome. These cells are null for the ATP8 protein, have significantly lowered ATP6 protein levels and no Complex V function. Nuclear expression of only the ATP8 gene with the ATP5G1 mitochondrial targeting sequence appended restored viability on Krebs cycle substrates and ATP synthesis capabilities but, failed to restore ATP hydrolysis and was insensitive to various inhibitors of oxidative phosphorylation. Co-expressing both ATP8 and ATP6 genes under similar conditions resulted in stable protein expression leading to successful integration into Complex V of the oxidative phosphorylation machinery. Tests for ATP hydrolysis / synthesis, oxygen consumption, glycolytic metabolism and viability all indicate a significant functional rescue of the mutant phenotype (including re-assembly of Complex V) following stable co-expression of ATP8 and ATP6. Thus, we report the stable allotopic expression, import and function of two mitochondria encoded genes, ATP8 and ATP6, resulting in simultaneous rescue of the loss of both mitochondrial proteins.

For cancer research, meanwhile, the situation is more akin to an economic revolution, or disruptive advance in technology. Because all cancers must lengthen their telomeres, and because telomere lengthening is governed by a small number of processes, there is the opportunity to change the focus of cancer research from an endless procession of expensive new therapies, each targeting a tiny number of the hundreds of subtypes of cancer, to one single therapy that can effectively suppress all cancers.

The last few days have arrived for this year’s SENS Research Foundation crowdfunding campaign, focused on important groundwork to establish a universal therapy for all types of cancer. There are still a few thousand dollars left in the matching fund, so donations are still being matched. Cancer is just as much a part of aging that must be ended, brought completely under control, as all of the other line items in the SENS rejuvenation research portfolio, and this year is the first time that the SENS Research Foundation has run a fundraiser for this program.

Hopefully there is no need to remind the audience here that the SENS Research Foundation, and important ally the Methuselah Foundation, have in recent years achieved great progress in the field of rejuvenation research on the basis of our donations and our support. Some of the high points you’ll find mentioned here and there at Fight Aging!: support and ongoing expansion of the mitochondrial repair technologies now under development at Gensight; seed funding Oisin Biotechnologies for senescent cell clearance; unblocking efforts to clear glucosepane cross-links that stiffen tissues; running the lauded Rejuvenation Biotechnology conferences; and many more. If only all charities produced as great an impact with as few resources — and if only we were further along in the bootstrapping of an industry focused on the development of rejuvenation therapies.

Continue reading “Entering the Final Days of the SENS Universal Cancer Treatment Fundraiser” »

Traditional cancer research is well funded but ALT cancers are not. SENS Research is aiming to raise funds to address this vital gap in our scientific knowledge. Most scary thing of all is that some regular cancers that abuse telomerase can switch to this ALT method to keep growing when telomerase blocking therapies are used.

The paper I’ll point out today is a timely one, given that the SENS Research Foundation’s fundraiser for early stage work on a therapy for alternative lengthening of telomeres (ALT) cancers is nearing its close. There are still thousands of dollars left in the matching fund, so give it some thought if you haven’t yet donated. The search for ways to safely sabotage ALT is a useful, important line of research because blocking telomere lengthening is a path to a universal cancer therapy, those research groups presently working on it are all looking to achieve this goal by interfering in the activities of telomerase, cancers can switch from using telomerase to using ALT, and next to no-one is working on ways to suppress ALT mechanisms. It seems fairly clear based on the evidence to date that the universal cancer therapy that lies ahead, built by inhibiting telomere lengthening, must involve a blockade of both telomerase and ALT. The open access paper below reinforces this point, the authors investigating how exactly cancers switch from telomerase to ALT to maintain their dangerous growth.

Cancer research today has a grand strategy problem. There is only so much funding and only so many researchers, but hundreds of subtypes of cancer. Therapies tend to be highly specific to the peculiarities of one type of cancer or a small class of cancers, meaning that great expense and time leads to a treatment that is only applicable for a fraction of cancer patients, all too often a tiny fraction. Further, since tumors evolve at great speed, any one individual patient’s cancer may find its way out from under the hammer by changing its signature and mode of operation. All is not doom and gloom, however. Consider that the research community could build a therapy applicable to all cancers with little to no modification, where the cost of development would be no greater than any one of the highly specific therapies presently in use and under development. That therapy would be, of course, based on the blockade of telomere lengthening.

Continue reading “An Investigation of How Telomerase Cancers can Switch to Become ALT Cancers” »

Calico, a company focused on aging research and therapeutics, today announced that Daphne Koller, Ph.D., is joining the company as Chief Computing Officer. In this newly created position, Dr. Koller will lead the company’s computational biology efforts. She will build a team focused on developing powerful computational and machine learning tools for analyzing biological and medical data sets. She and her team will work closely with the biological scientists at Calico to design experiments and construct data sets that could provide a deeper understanding into the science of longevity and support the development of new interventions to extend healthy lifespan.

Calico will try to use machine learning to understand the complex biological processes involved in aging.

Glad this discovery has been found; however, sad to hear as well. Sharing for my friends involved with anti-aging (Alex) and others work on the cancer cure.

Genetic signature of the brain cancer cell lines used for research is different from the original patient tumor cells.