With yearly budget of several million dollars, the SENS Research Foundation has grown a long way beyond the founding group of a few advocates and researchers. Life scientists in laboratories around the world, including the Foundation's research center in California, presently work on the foundations of human rejuvenation detailed in the Strategies for Engineered Negligible Senescence (SENS). There are forms of cellular and intracellular damage that harm us and cause degenerative aging, and in every case researchers can clearly describe what needs to be accomplished in order to repair that damage. The only obstacles to rapid progress towards the medical control of aging are (a) funding and (b) obtaining the widespread public support and understanding needed to generate that funding.
Aging is the greatest form of harm to humanity that presently exists: it causes more death and suffering than all forms of disease, violence, and accident combined. The golden future of medicine involves finding ways to reduce the cost of aging, and preferably eliminate it altogether through periodic repair procedures. Curing degenerative aging will save more lives than any other human endeavor to date, and more lives than any other endeavor can possibly save. Research into human rejuvenation is the most important activity presently taking place in the world today by any rational measure.
(And yet it is also probably the least funded in comparison to its importance. Little medical research is well funded of course, in comparison to the benefits it can produce, but that is the way of the world. We spend billions on circuses and war, billions more on trying to cope with the consequences of sickness and aging, but next to nothing on ways to dramatically improve the human condition by eliminating that sickness and aging. Given how small a sliver of economic activity is devoted to improving medicine, it's amazing that progress is as fast as it is).
The SENS Research Foundation is presently running a series of profiles of the researchers and interns who are helping to push forward the boundaries of the possible in medical science. Few people are doing work that is more important than that funded by the Foundation:
Before I joined SRF, I started out as a curious and active member of the Do-It-Yourself (DIY) bio community. As a young teen, I got involved with BioCurious in its earliest days to help build the BioCurious lab. I also participated in other organizations like the Health Extension Salon and Thiel Fellowship Under20 Summits before applying for a 20Under20 Fellowship this past year.
Currently I volunteer at SRF four days a week. I spend my time conducting research to understand a poorly understood pathway that plays a key role in cancer cell immortality called alternative lengthening of telomeres, or ALT. I keep current with new developments in my field by reading scientific papers at the cutting edge of ALT work, and I am currently in charge of studying POT1, a protein that could negatively affect ALT activity. I am also performing experiments on cancer cells to test for ALT activity.
When I'm not at SRF, I've designed my own home schooling curriculum, where I get to choose which subjects I want to study. I take local college classes that I feel will assist me in my research goals, like chemistry and public speaking. I love telling people about the latest discoveries in science, and have spoken at The University of California, Santa Cruz (UCSC) about genetic modification.
After moving to the Bay Area I was looking for mitochondria research labs that would fit my experience and expertise where I could further my career. I came across the MitoSENS project at SRF's Research Center and was very excited. It seemed like 'the' perfect place, almost like an extension of what I was doing in my postdoc lab. So I sent my CV, cold, to the info address listed, and Daniel forwarded my CV to Oki [Matthew O'Connor, SRF's Principal Investigator]. We had a good talk about the project and I volunteered for a short bit before coming on full-time this year.
We all know that mitochondria are the cell's "powerhouse" for energy. One interesting fact about these organelles is that they have their own DNA in addition to the nuclear DNA that we are all aware of. However, the mitochondrial DNA is prone to mutations due to constant exposure from ROS (reactive oxygen species) generated through the OX-PHOS system. This is because the mitochondrial DNA is not encased in a nuclear envelope nor does it have efficient repair mechanisms to correct mutations as they occur. To mitigate this weakness, our goal here at SRF is to move the mitochondrial genes to the nucleus, where it's safer to express them for function. This would let mitochondria keep producing energy normally, even after mitochondrial mutations have occurred.
Here at SRF, we're working to engineer expressions of "backup" copies of vulnerable mitochondrial genes, located in the safer location of the cell's nucleus. To explore and refine methods to safely accomplish this, we've taken four cell lines from patients suffering from inherited mitochondrial mutations, and made stable lines that express their improved mitochondrial gene constructs. We've begun collecting data which confirms the targeting of gene transcripts and proteins, as well as the functional activity of the mitochondrial energy system.
Our two primary goals this year are to definitively confirm the localization of allotopically-expressed proteins at the inner membrane of mitochondria, and to demonstrate that our allotropic expression systems can functionally rescue cells with each of several missing or severely mutated mitochondrial genes. I spend most of my time engineering different targeting tags on the various proteins we are trying to target to the mitochondrial OxPhos system and testing the engineered genes in the cell lines.
Aging is a sad thing, and it's important to me to contribute to research that helps understand and alleviate suffering. Mitochondrial abnormalities contribute to general problems of aging most people traditionally think of as inevitable, but also affect acute diseases such as diabetes, Parkinson's and Alzheimer's. Our mission is a noble one.
Mission isn't everything, though; you have to like the people your work with, too. I really like that everyone here is not only abstractly passionate about SRF's mission, but also truly committed to uncovering the real scientific truths in what they want to accomplish. Some more traditional workplaces have such a product or hierarchically-oriented management focus that it's hard to get real research done; here, if I have a question or a research problem, it's really natural to just go talk to someone about it honestly face-to-face.