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Berkeley researchers find evidence for a "molecular fountain of youth"

Berkeley researchers find evidence for a "molecular fountain of youth" | Longevity science | Scoop.it

 

A group of medical researchers at the University of California at Berkeley has found a protein that is able to rejuvenate aged blood stem cells...

 

The ravages of aging appear to be related to oxidative stress combined with telomere exhaustion, along with many other known and unknown factors. The subject of the new Berkeley study is a class of proteins called sirtuins that are known to play a central role in regulating aging and longevity in many non-human models (such as mice).

 

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Merridee Wouters's curator insight, March 28, 2013 12:03 PM

Relevant pathophysiology

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Sierra Sciences, LLC - Cure Aging or Die Trying

Sierra Sciences, LLC - Cure Aging or Die Trying | Longevity science | Scoop.it

The root cause of aging is very straightforward: we age because our cells age.

In 1961, Leonard Hayflick, a researcher at the Wistar Institute in Philadelphia, discovered that there was a limit to the number of times a human cell could divide.1 After about 70 divisions, a cell derived from embryonic tissue enters a stage where its ability to divide slows and eventually stops. This stage is called cellular senescence. Hayflick also observed that the number of times a cell could divide was governed by the age of the cells: cells from a twenty-year-old could divide more times than cells from a fifty-year-old, which in turn would divide more times than cells from a ninety-year-old.

 

 

Ray and Terry's 's insight:

An interesting discussion on telomerase and aging. We are not yet sure whether attempting to increase telomere length, particularly with current available methods, is the answer to aging. There is some indication that cancer can be triggered by these efforts.

 

The research is promising, but we cannot yet recommend the therapies.

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Telomerase Gene Therapy Extends Mouse Lifespan by 24%

Telomerase Gene Therapy Extends Mouse Lifespan by 24% | Longevity science | Scoop.it
Inducing cells to express telomerase, the enzyme which is supposed to slow down the metabolic clock, has enabled researchers boost the lifespan of mouse by 24% with a single treatment.

 

The gene therapy acts on specific genes and is applied in adult life, not from the embryonic stage. Researchers at the Spanish National Cancer Research Center (CNIO) have demonstrated that the mouse lifespan can be extended by the application of one treatment acting directly on the animal’s genes in adult life. The therapy has been found to be safe and effective in mice.

 

Adult and aged mice were treated with the gene therapy, delivering a rejuvenating effect. On average, the mice lived 24% longer. The older mice lived 13% longer. The therapy produces an appreciable improvement on the animal’s health and delayed the onset of age-related diseases.

 

The genes were treated with a DNA-modified virus. The viral genes were replaced by those of the telomerase enzyme, which plays a key role in aging. Telomerase repairs the extreme ends of chromosomes, and slows the cells and therefore the body’s biological clock.

 

There is a potential to develop a telomerase-based anti-aging gene therapy that won’t increase the risk of cancer. Telomeres are the caps that protect the end of chromosomes, but each time the cell divides, the telomeres get shorter until they lose all functionality. The cell then stops dividing or dies. Telomerase prevents telomeres from shortening or even rebuilding them.

 

In most cells, telomerase is only active before birth. The cells of adult organisms contain no telomerase. There are some exceptions such as adult stem cells and cancer cells, which divide limitlessly and could be immortal.

 

The risk of cancer tumor promotion is a risk that has set back telomerase-based anti-aging therapies. The kind of virus employed to carry the telomerase gene to the cells is very important. The viruses used is in this study have been successfully used in gene therapy treatment of hemophilia and eye disease. They are non-replicating viruses derived from others that are non-pathogenic in humans.


Via Dr. Stefan Gruenwald
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Caloric restriction has a protective effect on chromosomes

Caloric restriction has a protective effect on chromosomes | Longevity science | Scoop.it

According to a study carried out by a team led by María Blasco, the director of the Spanish National Cancer Research Centre (CNIO) and head of the Telomeres and Telomerase Group, a sustained lowering of food intake over time results in an increase of telomere length -- the ends of chromosomes -- in adult mice, which has a protective effect on the DNA and genetic material.

 

 

Ray and Terry's 's insight:

Caloric restriction is step 6 of the Transcend program. Moderate CR (10%) is manageable and easier to sustain over the long term.

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Protecting Cellular Telomeres with Omega Fatty Acids

Protecting Cellular Telomeres with Omega Fatty Acids | Longevity science | Scoop.it
Researchers are working to find ways to strengthen a microscopic cellular defender that has the power to boost cellular health and longevity.
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Telomerase Gene Therapy Extends Lives Of Mice By Up To 24 Percent

Telomerase Gene Therapy Extends Lives Of Mice By Up To 24 Percent | Longevity science | Scoop.it

The latest in the fight against ever dying is a gene therapy that gives mice a healthy dose of telomerase, the enzyme that keeps our chromosomes – and thus our cells and bodies – “young.”

 

The therapy extended the lifespans of mice by 24 percent and, at least so far, the therapy appears to be completely safe...

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