Intramural Research At The SENS Research Foundation

The SENS Research Foundation is a non-profit organization based in Mountain View, California, and its primary functions are scientific research and public relations in rejuvenation. The Methuselah Foundation also performed SENS research before the SRF was founded in 2009. Aubrey de Grey is a founding member for both organizations. The SRF is currently performing its own research in areas such as allotropic expression, the degradation of lysosomal aggregates and the lengthening of telomeres.

Many notable philanthropists have donated to the MF and SRF. The San Francisco Chronicle announced in 2006 that Peter Thiel was pledging $3.5 million to the MF, and entrepreneur Jason Hope pledged $500,000 to the SRF in 2010. Poker player Justin Bonomo pledged five percent of his winnings to the SRF in 2010.

Allotropic Expression

Mutations in mitochondrial DNA may be partially responsible for the aging process. These mutations are caused by exposure to oxygen, which is a highly reactive substance used by mitochondria to generate energy. These mutations continually accumulate because mitochondria are unable to repair themselves efficiently, which is why many mitochondrial genetic disorders such as Parkinson’s disease have symptoms that are similar to those of natural aging.

The SENS Foundation is looking for ways to modify the mitochondrial genome, which could eliminate mitochondrial mutations. A current avenue of research involves creating 13 of the 37 mitochondrial genes that deal with respiratory function. These engineered genes contain a type of protein known as allotropically-expressed proteins. The primary challenge with importing these proteins into mitochondria is that they are repelled by water, although the possibility of an incomplete transfer of proteins is also a danger.

A possible solution to this problem may be to use two processes for translating RNA into protein that will be imported into the mitochondria. Dr. Corral-Debrinski has used this co-translational import technique in previous work with the SENS Research Foundation. This strategy involves tagging the desired RNA sequences in the genes and directing them to the surface of the mitochondria. This method increases the efficiency of the protein importation since the proteins don’t fold as much while they are moving through the mitochondria’s watery environment.

Degradation of Lysosomal Aggregates

Components of the body’s cells also become damaged as a result of undesirable biochemical reactions. The body recycles these materials for future use with a variety of systems such as lysosomes. These cellular bodies contain enzymes that break down most molecules into smaller portions. Molecules that lysosomes are unable to break down are known as lysosomal aggregates, and will accumulate within the lysosome.

Lysosomal aggregates will eventually interfere with the normal functioning of the lysosome, which is especially harmful in cells that can’t be replaced such as those in the brain, heart and retina. This process of impaired tissue function can lead to age-related diseases. For example, macrophages are cells that protect blood vessels from the effects of cholesterol by-products. They consume these toxic materials, which are transported to the macrophage’s lysosomes. This eventually causes the macrophages to become dysfunctional or even rupture, which can lead to arteriosclerosis. Degenerative diseases of the nervous system such as Alzheimer’s and macular degeneration are also caused by lysosomal aggregates, making a solution to this problem especially important in treating age-related diseases.

The most direct solution to the problem of lysosomal aggregates is to locate a source of enzymes that can break down all metabolic wastes. The most likely source of these enzymes is the bacteria that decompose dead bodies, which could result in a treatment known as enzyme replacement therapy. Many disorders such as Gaucher’s disease are caused by lysosomal aggregation, and are already being successfully treated with modified enzymes.

Lengthening Telomeres

A cell’s telomeres normally shorten over time, causing the cell to lose its ability to divide. However, cancer cells are able to preserve their ability to lengthen their telomeres. One line of research into longevity involves looking for ways to impose a replication limit on cancer cells, which would prevent tumors from continuing to grow.

Cells can lengthen their telomeres through two currently known mechanisms. The first mechanism uses the enzyme telomerase and the second mechanism is known as alternative lengthening of telomeres, or ALT. The SRF is currently looking for ways to treat cancer cells with both of these mechanisms, and the most recent SRF project in this area began in 2012. This project’s direct objective is to eliminate ALT, which occurs in about 10 percent of all cancer cells.

ALT is less well studied than the lengthening of telomeres due to telomerase, making the current project of identifying the causes of ALT subject to disruption. The identification and safe disruption of ALT mediators could disable cancers that don’t rely on telomerase for growth. This breakthrough would prevent the cancerous cells from causing many of the problems they currently do.

About Author – April Taylor is a freelance writer. When she is not running around with her kids she is an avid health and medical aficionado.

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