It can sometimes be difficult to detect change and progress as it is occurring -- when following and studying a given subject or scientific endeavor, it is not always immediately apparent which data points and events are significant amidst the noise and buzz of journalism, discussion, and argument. But it seems quite certain that things are indeed happening in the realm of longevity science and related research.
For starters, the SENS challenge has been addressed, the MPrize has received generous support this year, and the Longevity Dividend represents, perhaps, one of the first vestiges of mainstream attention to the criticality of addressing the health needs of members of the present and future elderly population (who, of course, have as much a right to stay alive and well anyone else).
I've also linked to several new blogs and information pages that have come into my sphere of awareness over the past few months:
- Ouroboros - Research in the Biology of Aging (lots of good, hard science)
- Partial Immortalization (Biologist, philosopher, and PhD student Attila Csordás reports on longevity research news and interviews various scientists and philosophers on their thoughts and impressions of the current state and projected outcomes of longevity science)
- The Methuselah Foundation Blog (This blog has been reporting on Methuselah Foundation activities since July and gives a nice overview of the kinds of things the Mprize could be applied to.)
- Institute for Ethics and Emerging Technologies (A fascinating source of tech-progressive musings and biotech philosophy. One of my favorite aspects of this group is that there's plenty of heterogeneity of thought, which fits in nicely with my own conviction that since no individual mind can see the overall picture, input from different kinds of minds is necessary when it comes to addressing tough issues.)
However, awareness and support, though indispensible factors, are only part of the equation. Nobody is going to be able to enjoy the benefits of even moderate life extension until the science is there to make it technically feasible. Which is why I am pleased to see the beginnings of actual, laboratory-based investigations.
Lyso-SENS activities have already begin at Arizona State University's Biodesign Institute, heading up an effort to identify enzymes which might help address common "storage diseases" in which accumulated material -- plaques, protein crosslinks, cholesterol, etc., -- contributes to conditions such as Alzheimer's, macular degeneration, diabetes, and cardiovascular illness.
Mito-SENS activities will be conducted at Cambridge University, in an effort to help reduce the effects of mitochondrial DNA vulnerability implicated as a possible contributor to ill health in advanced age -- the goal of the project is to "relocate" the expression of mitochondrial DNA genes to the nucleus, where they will be better protected from the damaging byproducts of cellular metabolism.
The great thing about scientific research (particularly in an era where information and peer-reviewed papers can be transmitted between interested folks on opposite sides of the world in the blink of an eye) is how different studies and even different fields can act in a symbiotic manner -- one person could be working on a particular challenge, and then happen to hear about something his or her colleague is doing that s/he might never have suspected could be relevant.
So, it is quite possible for a person to support, say, SENS research without putting all one's proverbial eggs into one basket; advances anywhere in biotech have the potential to advance SENS science, and vice versa. Speaking of which, I had the fortunate experience recently of being able to assist in proofreading an upcoming book on SENS, intented to bring the ideas of engineered negligible senescence to a wider audience. I am not sure yet when the book is coming out, but I am tremendously excited about it -- even in an unfinished state, what I read was quite fascinating. So, that is definitely something to look out for.
But the question remains -- where do we go from here? Lyso-SENS and Mito-SENS alone are not likely to be "enough", and besides, their efforts are only utilizing a fraction of available biotech-related scientific infrastructure. One thing I would like to see would be more opportunities for regular folks -- people with bachelor's degrees (as opposed to just PhDs and PhD candidates) to contribute more directly to longevity research.
I know from reading various blogs and fora that there is actually a rather impressive "layman's knowledge" base out there -- people who are not necessarily working in university laboratories, but who are reading plenty of peer-reviewed literature and engaging in rigorous self-study on highly technical topics. If all goes well, hopefully these people will be able to find opportunities to contribute productively according to the particular skills and knowledge areas offered by this diverse community.
Tuesday, November 28, 2006
Subscribe to:
Post Comments (Atom)
4 comments:
> advances anywhere in biotech have the potential to advance SENS science
One way to contribute to and learn about biotech research is to participate in distributed computing biotech projects like for instance Rosetta@home (info on Rosetta@home is available in this Betterhumans forum thread).
I'm confused - I know from previous reading that mitochondria are the descendants of once free swimming bacteria that entered into a symbiotic relationship with a different type of bacteria to form our own and all eukaryotic cells. They supply energy to the cell, and will reproduce if more energy is needed - from 70 up to several hundred mitochondria in each cell. Are female ova special places where the degredation of mitochondrial DNA does not happen?
I was also wondering would it be possible to infuse old cells with healthier newer mitochondria, as they are able to reproduce by themselves within the cell, and as far as I know wouldn't be rejected as they are a symbiote. Do you know (I don't) of anyone that has managed to culture mitochondria outside of the interior of a cell? The only site I was able to find was this one, but the fellow tried it in the 1920s:
http://www.dnaftb.org/dnaftb/concept_30/con30bio.html
nerdinium asked:
Are female ova special places where the degradation of mitochondrial DNA does not happen?
Funny you should ask that...I just came across this link, which suggests:
Females live longer than males in many mammalian species, including humans. This natural phenomenon can be explained on the basis of the mitochondrial theory of aging. Mitochondria are a major source of free radicals in cells. Mitochondria from female rats generate half the amount of hydrogen peroxide than those of males and have higher levels of mitochondrial reduced glutathione. The latter is due to females behaving as double transgenic in over-expressing antioxidant enzymes. Estrogens bind to the estrogen receptors and subsequently activate the mitogen activated protein (MAP) kinase and nuclear factor kappa B (NFkappaB) signalling pathways, resulting in an upregulation of antioxidant enzymes. Moreover, the 16S rRNA expression, which decreases significantly with aging, is four times higher in mitochondria from females than in those from males of the same chronological age. On the contrary, the oxidative damage of mitochondrial DNA is fourfold higher in males than in females. Ovariectomy abolishes the gender differences between males and females and estrogen replacement rescues the effect of ovariectomy. The challenge for the future is to find molecules that have the beneficial effects of estradiol, but without its feminizing effects. Phytoestrogens or phytoestrogen-related molecules may be good candidates to meet this challenge.
As for whether it would be possible to infuse old cells with healthier newer mitochondria...I am just talking off the top of my head here, but these newly-infused mitochondria would need to harbor some kind of selective advantage over the nonfunctioning "mutants" that eventually take over the host cell. Part of the problem with the "mutants" is that they can sometimes escape being slated for destruction in the lysosome for longer than would be ideal, because the mutants can still have intact membranes.
Hence, the cell would still be vulnerable to take-over because it could be "tricked" into harboring nonfunctioning mitochondria and allowing these mutants to reproduce and eventually take over, edging out the healthy mitochondria you added. I suppose adding healthy mitochondria periodically might confer some benefit (at least, I can't see why not at the moment) but I am more intrigued by the idea of moving the mtDNA into the nucleus, since evolution has already started that process, and the nucleus is a far "friendlier" environment for such things.
If this were accomplished it wouldn't matter if the local mtDNA mutated, because the proper proteins necessary for mitochondrial functioning would still be produced according to the instructions now contained in the nucleus.
As an aside:
http://www.cnn.com/2006/HEALTH/11/30/hand.transplant.ap/index.html
It's a long way from growing someone a new hand from their own tissue, but we're getting there. :)
Post a Comment