More progress with cancer and using a similar approach to senolytics, no surprise really as cancer and senescent cell share a lot of common ground and approach that work with one may well work with the other if they are aimed at inducing apoptosis.
Apoptosis, or programmed cell death, is a rapid and irreversible process to efficiently eliminate dysfunctional cells. A hallmark of cancer is the ability of malignant cells to evade apoptosis.
Dr Luminita Paraoan, from the University’s Department of Eye and Vision Science in the Institute of Ageing and Chronic Disease, has published new findings in the British Journal of Cancer that identify the requirement of a protein called p63 for the initiation of apoptosis in UM.
Chromosome 3 is one of the 23 pairs of chromosomes in humans. People normally have two copies of each chromosome. One part of chromosome 3 contains the gene for the protein p63. Unfortunately people with aggressive (resistant to apoptosis) UM do not have this part and therefore do not have the p63 protein.
The Goldilocks zone with telomere length is the key.
Ever since researchers connected the shortening of telomeres—the protective structures on the ends of chromosomes—to aging and disease, the race has been on to understand the factors that govern telomere length. Now, scientists at the Salk Institute have found that a balance of elongation and trimming in stem cells results in telomeres that are, as Goldilocks would say, not too short and not too long, but just right.
The finding, which appears in the December 5, 2016, issue of Nature Structural & Molecular Biology, deepens our understanding of stem cell biology and could help advance stem cell-based therapies, especially related to aging and regenerative medicine.
“This work shows that the optimal length for telomeres is a carefully regulated range between two extremes,” says Jan Karlseder, a professor in Salk’s Molecular and Cell Biology Laboratory and senior author of the work. “It was known that very short telomeres cause harm to a cell. But what was totally unexpected was our finding that damage also occurs when telomeres are very long.”
The fourth Lifespan.io campaign and CellAge are using synthetic biology to create an accurate aging biomarker for senescent cells and a new therapy for precision targeting of those problem cells. Senescent cells are one of the processes of aging and this could change the way we age.
Lifespan.io is proud to present our fourth rejuvenation biotechnology project!
As we age our bodies accumulate damage in the form of dysfunctional cells that have entered a state called “senescence”, which secrete toxic signals that can lead to chronic inflammation, higher rates of cancer and additional aging-related conditions.
In Brief
Though aging seems like one of the most natural things, an affair common to all living creatures, the process is actually poorly understood by scientists. A new study detailed in Nature aims to shed light on the phenomenon as a research team led by the Harvard T.H. Chan School of Public Health has uncovered a relationship between lifespan and RNA splicing, a core function of cells that allows a single gene to produce a variety of proteins.
The researchers already knew that mutations in RNA splicing could lead to disease, but they wanted to find out if the act of splicing itself had an impact on the aging process. To find out, they designed experimental setups using the roundworm Caenorhabditis elegans, which show visible signs of aging during their short three-week lifespan.
Infertile women have been offered new hope after scientists found that a common cancer drug triggers the development of new eggs, an outcome which was previously thought to be impossible.
In a discovery hailed as “astonishing”, researchers at the University of Edinburgh proved it is possible to reverse the clock and coax the ovaries back into a pre-pubescent state where they begin to produce new eggs.
Women are born with all their eggs, which is why conceiving becomes harder with age, because the eggs grow old, become damaged and eventually run out entirely.
The full antiaging 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. Fightaging predicts the likely order of arrival of some of these therapies, based on what is presently going on in research, funding, and for-profit development.
1) Clearance of Senescent Cells
Everon Biosciences, Oisin Biotechnologies, SIWA Therapeutics, and UNITY Biotechnology are all forging ahead with various different approaches to the selective destruction of senescent cells. No doubt many groups within established Big Pharma entities are also taking a stab at this, more quietly, and with less press attention. UNITY Biotechnology has raised more than $100 million to date, demonstrating that there is broad enthusiasm for this approach to the treatment of aging and age-related disease.
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The weekend is here so let’s kick it off with a great talk by Dr. Aubrey de Grey at TED in 2014.
Biotechnologist Aubrey de Grey talks about aging as a disease — and how it can be cured.
In the spirit of ideas worth spreading, TEDx is a program of local, self-organized events that bring people together to share a TED-like experience. At a TEDx event, TEDTalks video and live speakers combine to spark deep discussion and connection in a small group. These local, self-organized events are branded TEDx, where x = independently organized TED event. The TED Conference provides general guidance for the TEDx program, but individual TEDx events are self-organized.* (*Subject to certain rules and regulations)
