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The Longevity Medical Research Fund "More Life, More Life Worth Living" |
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BeneficiariesThe following are the beneficiaries of the funds raised by The Longevity Medical Research Fund. In keeping with LMRF's tax-exempt status, all recipients are also 501(c)(3) organizations. LysoSENSLysoSENS is a SENS initiative to tackle atherosclerosis and other diseases caused by the accumulation of normally benign material in the body. Atherosclerosis is their first and most urgent target. Due to its role in stroke and cardiovascular disease, it kills kills more Americans each year than all cancers combined. The first stages of the work are being carried out at Arizona State. The strategy is based on work done by John Archer (Cambridge), Jay Jerome (Vanderbilt), Ana Marie Cuervo (Albert Einstein), Roscoe Brady (NINDS), Perry McCarty (Stanford), Pedro Alvarez (Rice), and Bruce Rittman (Arizona State). Their strategy is to target build-up of usually-benign metabolic by-products that in sufficient quantity become precursors to age-related disease. LysoSENS currently focus on the subset of these molecules that accumulate in lysosomes, the cell's garbage can and degredation site of last resort. Most molecules absorbed by lysosomes are decomposed by powerful enzymes and rereleased. There are macromolecules that our lysosomes can't degrade. Lysosomes does us a favor of just containing such molecules, instead of rereleasing them. In certain cases this eventually backfires, the lysosomes bloating enough to create a cascade of cellular malfunction and damage to surrounding tissue. The solution is similar to that currently used for people born without the normal range of lysosomal enzymes: periodic enzyme injections. The twist for LysoSENS is to develop enzymes that don't normally occur in humans. For more on their work, check out the following links. How you can contribute more directly to this effort More on how you can contribute directly to this effort MitoSENSMitoSENS is a SENS initiative to test medical interventions based on the mitochondrial free radical theory of aging. Mitrochondria used to be bacteria, before plants and animals split off from each other over a billion years ago. They gave an evolutionary advantage to the single-celled organisms they infected by giving the host cell an additional source of energy. Over time, most of their thousand genes have migrated into the nucleus, where far more DNA repair mechanisms are available and the genes are safe from the damaging free radicals naturally produced inside mitochondria. In mammals, 13 genes haven't made the jump. Given aging mitochondria's complicity in the negative effects of aging, MitoSENS is working on gene therapy to place engineered versions of these 13 genes into the safer environment of the cell nucleus. The trick is to design genes with the same function, but whose proteins can make the full journey into mitochondria, just like a thousand other proteins the mitochondrion needs to function. For more on their work, check out the following links. Experimental support for the mitochondrial free radical theory of aging Why damage to mitochondrial DNA matters, and an alternate approach to its reduction Detailed explication of the chain of events from mitochondrial DNA damage to disease How you can contribute more directly to this effort The MprizeThe Mprize is a competition, actually two competitions, to foster practical research in countering the negative effects of aging. The award goes to competitors who break the world record for longest-living Mus musculus, or lab mouse (normal lifespan: 3 years). The rejuvenation prize concerns mice who begin rejuvenation therapy at age 2. The longevity prize concerns mice that begin treatment from birth. The award amount is a proportion of the total cash pot, reflective of the proportion by which the new world record holder beats the prior record. Since healthy lifespan is the aim, the rejuvenation prize is the main focus, since it betters tests the ability of a therapy to reverse the negative effects of aging, as opposed to forestalling them. The longevity prize, however, is easier for the media to explain to the general public. Therefore, the main point of this competition is extended longevity as a result of improved quality of health, not extending longevity for its own sake. The prize was first formulated by entrepreneur David Goebel, who was inspired by a prize that Napoleon offered to improve battlefield food preservation beyond mere smoking and salting. Before the prize, people died regularly from famine as a result of poor food preservation, because insufficient numbers had tried to solve the problem. Ultimately, a French chef invented canning and claimed the prize of 12,000 francs. A small investment led to an enormous stride forward. This model of small prizes designed to mobilize many resources has been used to great effect much more recently as well, from the Orteig Prize and the first non-stop trans-Atlantic flight to the $10M Ansari X Prize that led to commercial space flight. Currently, another $10M X Prize is being offered to whoever accurately sequences 100 human genomes in 10 days for less than $10,000 per genome. The Mprize is not currently a beneficiary of LMRF. We emphasize LysoSENS and MitoSENS for now, to first put the tools for winning such a competition more within competitors' reach. For more on the Mprize, check out the following links. How you can contribute directly to the Mprize pot How to make a recurring pledge, more directly to the Mprize, for the price of a cup of coffee a day |