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Hitting the pause button on development in embryos has implications for understanding aging.


UC San Francisco researchers have found a way to pause the development of early mouse embryos for up to a month in the lab, a finding with potential implications for assisted reproduction, regenerative medicine, aging, and even cancer, the authors say.

The new study—published online November 23, 2016 in Nature —involved experiments with pre-implantation mouse embryos, called blastocysts. The researchers found that drugs that inhibit the activity a master regulator of called mTOR can put these early embryos into a stable and reversible state of suspended animation.

“Normally, blastocysts only last a day or two, max, in the lab. But blastocysts treated with mTOR inhibitors could survive up to 4 weeks,” said the study’s lead author, Aydan Bulut-Karslioglu, PhD, a post-doctoral researcher in the lab of senior author Miguel Ramalho-Santos, PhD, who is an associate professor of obstetrics/gynecology and reproductive sciences at UCSF.

Progress towards making a blood scrubber to calibrate the pro aging factors in blood. Irina Conboy has spent the last 20 years working on parabiosis and signalling factors in blood and this is yet another step forward for their research.

Whilst many are seeking the secret sauce in young blood the data suggests it is much more likely the case that old blood contains too many pro-aging factors eg, TGF-beta, TNF-a, IL-6, CD38 etc… The aim is now to filter old blood and calibrate such factors in order to promote a pro-youthful signalling environment. If only this device was small enough to wear or implant.


In what could be a fresh chapter in the never-ending story of the search for eternal youth, scientists are to tinker with people’s blood in the hope of slowing down the ageing process and preventing age-related diseases.

Researchers in California plan to launch a clinical trial of the radical – and highly experimental – approach in the next six months, after a small study in mice found the treatment had promise.

29th November in Berlin there is a meetup for LE enthusiasts.


Announcing our year-end meetup in Berlin.

Join our casual get together of like-minded people. We chat about extending our healthy lifespans and the latest developments in this exciting field.

Again, a lot has happened since our last meetup, great science news and our decision to build a dedicated team for project “Personal Longevity Strategy (see also forever-healthy.org/careers)

This is most likely going to be the last one for this year.

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Destroying and replacing the immune system is one of the approaches to treat the aging process.


Fightaging! provides some commentary about the immune system in relation to aging. Addressing the decline of the immune system is one of the approaches SRF is interested in and is a cornerstone of rejuvenation biotechnology.

“Understanding exactly how aging progressively harms the intricate choreography of the immune response is a massive project, and nowhere near completion. It is possible to judge how far along researchers are in this work by the side effect of the quality of therapies for autoimmune disease, which are malfunctions in immune configuration, and largely incurable at the present time. From a practical point of view, and as mentioned above, the best prospects for effective treatments in the near future involve destroying and recreating the immune system. That works around our comparative ignorance by removing all of the problems that researchers don’t understand in addition to ones that they do.”

#sens #aging

Speculation about what order rejuvenation biotechnologies will arrive.


The first rejuvenation therapies to work well enough to merit the name will be based on the SENS vision: that aging is at root caused by a few classes of accumulated cell and tissue damage, and biotechnologies that either repair that damage or render it irrelevant will as a result produce rejuvenation. Until very recently, no medical technology could achieve this goal, and few research groups were even aiming for that outcome. We are in the midst of a grand transition, however, in which the research and development community is finally turning its attention to the causes of aging, understanding that this is the only way to effectively treat and cure age-related disease. Age-related diseases are age-related precisely because they are caused by the same processes of damage that cause aging: the only distinctions between aging and disease are the names given to various collections of symptoms. All of frailty, disease, weakness, pain, and suffering in aging is the result of accumulated damage at the level of cells and protein machinery inside those cells. Once the medical community becomes firmly set on the goal of repairing that damage, we’ll be well on the way to controlling and managing aging as a chronic condition — preventing it from causing harm to the patient by periodically repairing and removing its causes before they rise to the level of producing symptoms and dysfunction. The therapies of the future will be very different from the therapies of the past.

The full rejuvenation toolkit of the next few decades will consist of a range of different treatments, each targeting a different type of molecular damage in cells and tissues. In this post, I’ll take a look at the likely order of arrival of some of these therapies, based on what is presently going on in research, funding, and for-profit development. This is an update to a similar post written four years ago, now become somewhat dated given recent advances in the field. Circumstances change, and considerable progress has been made in some lines of research and development.

1) Clearance of Senescent Cells

Longevity a challenge or an opportunity?

This autumn, The Economist Events will bring global leaders from business, finance and health care together with policymakers to explore the opportunities of an ageing world.

Together they will discuss how best to adapt financial products and realign business and public policies in ways that will drive economic growth and mitigate problems that ageing societies could otherwise bring.

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New biomarkers for aging is good news for researchers!


“Given the high volume of data being generated in the life sciences, there is a huge need for tools that make sense of that data. As such, this new method will have widespread applications in unraveling the molecular basis of age-related diseases and in revealing biomarkers that can be used in research and in clinical settings. In addition, tools that help reduce the complexity of biology and identify important players in disease processes are vital not only to better understand the underlying mechanisms of age-related disease but also to facilitate a personalized medicine approach. The future of medicine is in targeting diseases in a more specific and personalized fashion to improve clinical outcomes, and tools like iPANDA are essential for this emerging paradigm,” said João Pedro de Magalhães, PhD, a trustee of the Biogerontology Research Foundation.

The algorithm, iPANDA, applies deep learning algorithms to complex gene expression data sets and signal pathway activation data for the purposes of analysis and integration, and their proof of concept article demonstrates that the system is capable of significantly reducing noise and dimensionality of transcriptomic data sets and of identifying patient-specific pathway signatures associated with breast cancer patients that characterize their response to Toxicol-based neoadjuvant therapy.

The system represents a substantially new approach to the analysis of microarray data sets, especially as it pertains to data obtained from multiple sources, and appears to be more scalable and robust than other current approaches to the analysis of transcriptomic, metabolomic and signalomic data obtained from different sources. The system also has applications in rapid biomarker development and drug discovery, discrimination between distinct biological and clinical conditions, and the identification of functional pathways relevant to disease diagnosis and treatment, and ultimately in the development of personalized treatments for age-related diseases.

SENS makes official comment on the excellent news about Mitochondrial repair from UCLA and Caltech.


So the big news is progress has been made on Mitochondrial repair. Our resident expert at the SENS Research Foundation, Dr. Matthew O’Connor of the MitoSENS project had this to say about the exciting news:

“New work from UCLA and Caltech has shown that a genetic pathway can be harnessed to selectively remove mutant mitochondria from the muscles of fruit flies. This work from Kandul et al is exciting because it raises the possibility of someday finding a way to control this genetic pathway in such a way to selectively delete mutant mitochondria. Further they did it in live flies in a tissue (muscle) where we are especially concerned about the impact of mitochondrial DNA mutations. Our ability to selectively control genetic pathways in non-genetically engineered animals (such as humans) is, however, extremely limited so it may be a long time before any clinical benefits can be realized from this research.” — Dr. Matthew O’Connor SRF

#aging #crowdfundthecure