Lifeboat Foundation

Don’t worry you haven’t stumbled onto that strange part of the internet again, but it is true that we never truly did sequence the entire Human genome. For you see what was completed in June 2000 was the so called ‘first draft’, which constituted roughly 92% of genome. The problem with the remaining 8% was that these were genomic ‘dead zones’, made up of vast regions of repeating patterns of nucleotide bases that made studying these regions of the genome effectively impossible with the technology that was available at the time.

However, recent breakthroughs in high throughput nanopore sequencing technology have allowed for these so call dead zones to be sequences. Analysing these zone revealed 80 different genes which had been missed during the initial draft of the Human genome. Admittedly this is not many considering that the other 92% of the genome contain 19889 genes, but it may turn out that these genes hold great significance, as there are still many biological pathways which we do not fully understand. It is likely that many of these genes will soon be linked with what are known as orphan enzymes, which are proteins that are created from an unidentified gene, which is turn opens up the door to studying these enzymes more closely via controlling their expression.

Continue reading “Genes in the Dead Zone” »

Papers referenced in the video:

Sirtuins, Healthspan, and Longevity in Mammals.
https://www.sciencedirect.com/science/article/pii/B9780124115965000034

Continue reading “SIRT6 Positively Affects The Hallmarks Of Aging And Extends Lifespan” »

To keep the longevity train rolling it may not be enough to cure diseases. We may also need to address the underlying condition of aging itself, which is, after all, the primary risk factor for late-life decline.

What happens if we slow down aging?

Enrolling Tens Of Thousands Of Dogs, In 10-Year Study, To Unlock Healthy Aging Secrets — Dr Matt Kaeberlein, Founder / Co-Director, The Dog Aging Project, Professor, University of Washington, joins me on Progress, Potential, And Possibilities Nathan Shock Centers #Rapamycin #Dogs #Aging #Longevity #Healthspan #Geroscience.

#MitochondrialDisease

Continue reading “Dr. Matt Kaeberlein — Founder / Co-Director, Dog Aging Project — Professor, University of Washington” »

The latest from Calico. A bit technical.

Reprogramming of ordinary somatic cells into induced pluripotent stem cells (iPSCs) was initially thought to be a way to obtain all of the patient matched cells needed for tissue engineering or cell therapies. A great deal of work has gone towards realizing that goal over the past fifteen years or so; the research community isn’t there yet, but meaningful progress has taken place. Of late, another line of work has emerged, in that it might be possible to use partial reprogramming as a basis for therapy, delivering reprogramming factors into animals and humans in order to improve tissue function, without turning large numbers of somatic cells into iPSCs and thus risking cancer or loss of tissue structure and function.

Reprogramming triggers some of the same mechanisms of rejuvenation that operate in the developing embryo, removing epigenetic marks characteristic of aged tissues, and restoring youthful mitochondrial function. It cannot do much for forms of damage such as mutations to nuclear DNA or buildup of resilient metabolic waste, but the present feeling is there is nonetheless enough of a potential benefit to make it worth developing this approach to treatments for aging. Some groups have shown that partial reprogramming — via transient expression of reprogramming factors — can reverse functional losses in cells from aged tissues without making those cells lose their differentiated type. But this is a complicated business. Tissues are made up of many cell types, all of which can need subtly different approaches to safe reprogramming.

Today’s open access preprint is illustrative of the amount of work that lies ahead when it comes to the exploration of in vivo reprogramming. Different cell types behave quite differently, will require different recipes and approaches to reprogramming, different times of exposure, and so forth. It makes it very hard to envisage a near term therapy that operates much like present day gene therapies, meaning one vector and one cargo, as most tissues are comprised of many different cell types all mixed in together. On the other hand, the evidence to date, including that in the paper here, suggests that there are ways to create the desired rejuvenation of epigenetic patterns and mitochondrial function without the risk of somatic cells dedifferentiating into stem cells.

Continue reading “A Great Deal of Work Lies Ahead in the Development of In Vivo Reprogramming as a Therapy” »

Ed Whitlock remains at the forefront among older athletes who have led scientists to reassess the possibilities of aging and performance.

Aging is associated with an overall decline in health and increased frailty, and is a major risk factor for multiple chronic diseases. Frailty syndrome, characterized by weakness, fatigue and low physical activity, affects more than 30% of the elderly population. Increasing our understanding of the mechanisms underlying the aging process is a top priority to facilitate the development of interventions that will lead to the preservation of health and improvements on survival and lifespan.

Cumulative evidence suggests that diet and metabolism are key targetable regulators of healthy lifespan. Prof. Haim Cohen, Director of the Sagol Healthy Human Longevity Center at Bar-Ilan University, focuses much of his research on the SIRT6 protein that is involved in regulating many biological processes, such as aging, obesity, and insulin resistance.

In a study just published in the journal Nature Communications, an international team led by Cohen and his Ph.D. student Asael Roichman—together with Prof. Rafael de Cabo, of the National Institute on Aging at the National Institutes of Health, Prof. Manuel Serrani, of the Institute for Research in Biomedicine in Barcelona, and Prof. Eyal Gottlieb from the Technion—report that transgenic mice express high levels of the SIRT6 gene, and show that their life expectancy can be increased by an average of 30% in both males and females. Translated into human terms this means that a 90-year-old could live until nearly 120!

A new discovery could lead to new drugs for faster repairing muscles after injury — or rebuilding muscle mass lost during the normal aging process.

Researchers at the Salk Institute have uncovered a mechanism by which stem cells can help regenerate muscles. The discovery could provide a new drug target for repairing muscles after injury or rebuilding muscle mass lost during the normal aging process.

The breakthrough started with a set of proteins called Yamanaka factors, which have long been studied as a key part of stem cell therapy. These factors are used to convert regular cells – most commonly skin cells – into what are known as induced pluripotent stem cells (iPS), which can then go on to differentiate into a variety of other cell types. That in turn helps regenerate tissue. But exactly how the Yamanaka factors worked their magic remained a mystery.

Continue reading “Scientists discover how stem cells trigger muscle regeneration” »

Hydraulic Instability Decides Who’s to Die and Who’s to Live

In many species including humans, the cells responsible for reproduction, the germ cells, are often highly interconnected and share their cytoplasm. In the hermaphrodite nematode Caenorhabditis elegans, up to 500 germ cells are connected to each other in the gonad, the tissue that produces eggs and sperm. These cells are arranged around a central cytoplasmic “corridor” and exchange cytoplasmic material fostering cell growth, and ultimately produce oocytes ready to be fertilized.

In past studies, researchers have found that C. elegans gonads generate more germ cells than needed and that only half of them grow to become oocytes, while the rest shrinks and die by physiological apoptosis, a programmed cell death that occurs in multicellular organisms. Now, scientists from the Biotechnology Center of the TU Dresden (BIOTEC), the Max Planck Institute of Molecular Cell Biology and Genetics (MPI-CBG), the Cluster of Excellence Physics of Life (PoL) at the TU Dresden, the Max Planck Institute for the Physics of Complex Systems (MPI-PKS), the Flatiron Institute, NY, and the University of California, Berkeley, found evidence to answer the question of what triggers this cell fate decision between life and death in the germline.