The latest SENS Research Foundation monthly newsletter turned up in my in-box yesterday, along with a reminder that the 2014 Rejuvenation Biotechnology conference will be held on August 21st in Santa Clara, California. This event has a strong focus on creating the stronger ties between academia and industry that will be needed to speed the development of applied longevity science, building the life-extending therapies of tomorrow to help bring aging under medical control. There's still time to register.
Don't miss this landmark event! Here are 4 reasons to attend RB2014:
1) Meet expert researchers from multiple age-related disease areas in a setting designed to enable true cross-functional learning and partnering.
2) Impact the creation of the emerging Rejuvenation Biotechnology industry by sharing your research, regulatory, finance, academic and industry perspective.
3) Participate in meaningful discussion and productive networking opportunities in the heart of Silicon Valley.
4) Engage with industrial and academic leaders like Eli Lilly, California Institute for Regenerative Medicine (CIRM), Harvard University, GE Healthcare Life Sciences, and Wake Forest Institute for Regenerative Medicine.
The speakers list contains the usual impressive line up characteristic of a SENS conference:
Ajay Royan, Mithril Capital
Ajay Royan co-founded Mithril Capital and heads the firm as its managing general partner. At Mithril, he has led investments in innovative companies located both in Silicon Valley and around the world.
Ajay frequently speaks on technology investing at technology and finance conferences as well as public forums, such as Bloomberg, CNBC, the Financial Times, and The Wall Street Journal. He has been a guest lecturer on macro investing at Yale University and has served as a participant in the Hoover Institution's Working Group on Global Markets and as one of the Churchill Club's Tech Trends experts.
Ajay serves as an external adviser to Oak Ridge National Laboratory and the University of Michigan Risk Science Center and also serves on the board of the Thiel Foundation. He was educated at Yale University.
Dr. George Church, Harvard
Dr. George Church is Professor of Genetics at Harvard Medical School and Director of PersonalGenomes.org, in addition to being the author of the book, Regenesis: How Synthetic Biology Will Reinvent Nature and Ourselves. His 1984 Harvard thesis work pioneered the first methods for direct genome sequencing, molecular multiplexing and barcoding, which led to the first commercial genome sequence in 1994.
Dr. Church's innovations in "next generation" genome sequencing and synthesis and cell/tissue engineering resulted in 12 companies spanning fields including medical genomics and synthetic biology as well as new privacy, biosafety and biosecurity policies. He is director of the NIH Center for Excellence in Genomic Science, and his honors include election to NAS (National Academy of Sciences), NAE (National Academy of Engineering) and Franklin Bower Laureate for Achievement in Science.
As always the real gem of these newsletters is the scientific question of the month - which this month is actually a question asked in a comment to a recent post here at Fight Aging! The lesson to take away here is that you should always ask questions when you have them, as the world is flat these days and an expert is often closer than you think.
Question Of The Month #5: Must Mitochondrial Mutation Management Account For Humanin?
Q: SENS Research Foundation is working to develop a system of "backup copies" of the genes in the mitochondria that code for proteins as a way to bypass the harmful effects of mutations in mitochondrial DNA. But in addition to these 13 proteins, researchers have found a peptide called humanin that is produced from mitochondrial DNA and that seems to have some physiological functions. How would moving the mitochondrially-encoded genes to the nucleus potentially impact other, less well known, products of mtDNA such as humanin?
A: Humanin is a recent and still somewhat controversial product of mitochondrial DNA. What to do about it as part of generating "backup copies" of the protein-encoding genes in the mitochondrial genome turns on how things ultimately shake out.
First, it's not yet clear whether humanin really is produced by mitochondria to serve a physiological function, or is just a byproduct left over from the of unusual way that mitochondria process their RNA. True, humanin seems to bind to a variety of receptors and to have various functions in models of stress and disease, which some have taken as evidence of function - but of course, the same thing is true of various drugs, including synthetic peptides, and that doesn't mean that they are somehow physiological substances. Also, many of these disease models are very artificial, and may not reflect the real conditions under which cells must respond to stress, or in which humanin would exert any activity. If humanin is just a byproduct of mitochondrial RNA processing, its loss will be harmless.
Second, if humanin is indeed a genuinely physiologically functional peptide, the sequence encoding it may be much less vulnerable to age-associated mutation than the genes encoding the proteins of the electron transport chain. Its putative encoding sequence is located by the minor arc of the mtDNA loop, which is rarely affected by deletions in aging. If that's so, then most of the cells that suffer major deletions in their mitochondrial DNA with age and have to draw on their engineered "backup copies" would still have their native humanin-encoding sequences on which to draw, with no special work on our part.
Third, even if humanin is physiologic and the sequence that encodes it is sufficiently susceptible to mutations as to be problematic for the cell in which that sequence is mutated, the mutation of this sequence isn't necessarily all that big a deal. Remember, only a very small number of cells accumulate large deletions of mtDNA with age. We worry so much about these mutations not so much because of the harm they cause to the individual cells in which they occur, but because such cells appear to adopt an abnormal metabolic regime to continue producing energy, and this abnormal metabolic state seems likely to spread metabolically harmful effects across the rest of the body in turn. So even if we find that a small number of cells do lose the ability to synthesize humanin with age, and even if those cells in isolation might be harmed by its absence, still the dysfunction or death of so small a number of cells will not cause the dysfunction of an entire tissue (or the body generally) in the way that a rising burden of cells unable to produce energy normally probably does. And any cells hypothetically rendered dead or dysfunctional for lack of humanin could be periodically replaced using cell therapy, which is already an essential component of comprehensive human rejuvenation.
Finally: if there turns out to be some really compelling reason why it's important to prevent cells from losing humanin expression with age, we do have the option of developing nuclear "backup copies" of the humanin sequence that can fill in in case of shutdown of translation by age-related mutations.