In 2012, SENS Research Foundation was able to support expenses that were double those from the previous year . This was made possible through not only the continued support of our generous donors, but the first in a series of annual disbursements from the de Grey family trust, which together caused SRF’s income to increase by about $2 million. Our expenses in 2013 should increase by an amount equal to 2012’s increase . Given our secure base of funding sources, we expect to sustain this higher level of operation indefinitely.
So the life extension research funding level looks like it should go to $4 to 5 million per year and will be sustainable at that level.
Some cellular wastes are so chemically snarled that even the lysosome is unable to shred them . With no way to eliminate these compounds, the cellular garbage simply builds up over time, progressively interfering with cell function.
Identifying enzymes in other life forms that can degrade such wastes, and modifying these enzymes so they can be delivered to — and function in — our own lysosomes, would restore cellular function and prevent or reverse these diseases.
In 2013, the team will put a recombinant form of SENS20 to the test, assessing its ability to degrade A2E in vitro and in RPE cells, and verifying that it is not toxic to the cell.
Estimates of the global cost of visual impairment due to age-related macular degeneration is US$343 billion, including US$255 billion in direct health care costs. Estimates of the direct health care costs of visual impairment due to age-related macular degeneration in the US, Canada, and Cuba (WHO subregion AMR-A), collectively, is approximately US$98 billion.
If SENS is able to make a major contribution against a major disease then the funding level should scale into the billions of dollars per year.
Our cells’ energy-producing mitochondria are at constant risk of major mutations in their internal genes, because they are housed close to where the mitochondria produce both cellular energy and the toxic byproducts of its generation . The Research Center’s Mitochondrial Mutations team is working to engineer “backup copies” of vulnerable mitochondrial genes, located in the safer location of the cell’s nucleus . This would let mitochondria keep producing energy normally, even after mitochondrial mutations have occurred.
SRF-RC scientists are now working to master and refine a superior method for accomplishing this goal . Our team has taken four cell lines from patients suffering from severe diseases caused by inherited mitochondrial mutations, and made stable lines that express their improved mitochondrial gene constructs . They have begun collecting data confirming the targeting of gene transcripts and proteins to their mitochondrial locations, and the functional activity of the mitochondrial energy system, in such re-engineered cells.
Cancer is a disease of unlimited cellular division . Healthy cells have a built-in limit on the number of times they can divide: with each division, a stretch of DNA called the telomere progressively shortens, until it becomes so short that it prevents the cell from dividing or kills it outright . To bypass this limit, would-be cancer cells must exploit one of two escape systems . The most common method is to activate the gene for an enzyme called telomerase, which re-lengthens shortened telomeres . The other, less common approach is to activate a poorly-understood system known as alternative lengthening of telomeres (ALT) . The goal of the SRF-RC’s Cancerous Cells project is to identify the mechanisms of the latter, and to use this knowledge to disrupt the system, opening up the power to strongly suppress cancer.
Our researchers have recently developed an innovative version of the standard, radioisotope C-circle assay that instead uses a non-radioactive digoxigenin (DIG)-labeled probe, and are also working to establish new protocols for ALT-associated PML nuclear bodies, another key marker of ALT activity . Establishing these two assays is a critical step towards deciphering the molecular mechanisms behind ALT, developing novel diagnostics, and finding ways to shut ALT cancers down
Enabling Technology: Maximally Modifiable Mouse
If a mouse could be engineered to readily take up significant genetic modification at any point during its life, it would substantially contract the timeline needed to gather critical data regarding the effectiveness of applied interventions.
The Maximally Modifiable Mouse project aims to generate a new line of transgenic mice with the needed site engineered into their genomes . The Bxb1 integrase system could then be used at any time during the mice’s lifespan to insert therapeutic genes of any size into their genomes, with no risk of mutational disruption of their own genes and with rapid testing turnaround times.
Brian Wang is a Futurist Thought Leader and a popular Science blogger with 1 million readers per month. His blog Nextbigfuture.com is ranked #1 Science News Blog. It covers many disruptive technology and trends including Space, Robotics, Artificial Intelligence, Medicine, Anti-aging Biotechnology, and Nanotechnology.
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