SENS Research Foundation staff spend a fair amount of time analyzing new papers and talking with researchers in the broader community, looking for recent lines of work relevant to rejuvenation biotechnology. There is a lot going on, enough that digesting it would be a full time job: molecular biology is far too large a field for any one group to have a good idea as to what is going on in every last laboratory. Despite the fact that very little of the research community has any great interest in producing ways to treat aging, it is still the case that many scientists are working on technologies that can be adapted or will otherwise contribute to the end goal of repairing the root causes of aging.
Arriving in my in-box today is a new outcome of this ongoing research review, a joint effort between the Methuselah Foundation and SENS Research Foundation to publicize some of the more interesting and relevant research recently uncovered:
As one of The 300, your loyal support of the Methuselah Foundation make up the backbone of our mission. We hope to honor your trust in our shared vision with a curated, quarterly newsletter featuring some of the latest, most exciting developments in reversing or obviating the diseases of aging. We're always on the watch for high-impact efforts that show significant promise for extending healthy human life, and as always, we welcome your input and thoughts. Please let us know if you find this information valuable, readable, and informative. Hope you enjoy!
All the Best,
At SENS Research Foundation, our CSO Team is a full time, internal research team that supports Aubrey de Grey in the work of keeping up-to-date on the most cutting edge science in rejuvenation biotechnology. Michael Rae, Ben Zealley, and Maximus Peto spend many, many hours reviewing the science literature, analyzing new papers, reporting on their findings, and offering suggestions for research priorities for SRF. We are delighted to draw on that work in partnership with Methuselah Foundation, to provide the members of its MF 300 with this newsletter highlighting a handful of the most notable scientific articles and advances, and some of the insights inspired by those advances.
The Methuselah Foundation is thrilled to partner with SENS Research Foundation in order to bring out the most recent advancements in tissue engineering, regeneration, and rejuvenation research for members of The 300. It doesn't take a scientist to understand the vital importance of investing in healthy life extension, so our newsletters will frame these developments as accessibly and approachably as possible. We'll focus on the relevance of three recent studies (within the past 3-6 months) and describe how each one fits into the broader landscape of longevity research.
This first edition of what will hopefully be a regular feature offers commentary on the following papers, and as you can see once you start to delve into the details very little is clear cut. It is rarely easy to see after only a few months whether new and interesting research will turn out to be game-changing, irrelevant, or merely the foundation of an incrementally better treatment that reaches clinical availability five to ten years from now. The forest of science has very thick undergrowth indeed.
You might look back in the Fight Aging! archives to see references to the work on GDF-11 and the C1q paper. I am nowhere near as cautious in my expectations as an actual researcher in the field, and you should bear that in mind: note the differences between my comments and those of the SENS Research Foundation folk.
These results are exciting, but further testing is needed, and there is good reason to be cautious. First, the observation that GDF-11 usually declines with age suggests that the real problem to be addressed is whatever causes its decline in aging. Second, GDF-11 is known to inhibit neurogenesis, and therefore human supplementation with this protein may cause problems. As with any therapeutic, adequate testing will need to be done to ensure safety and efficacy in humans.
A final noteworthy aspect of this study is that GDF-11 was able to reverse cardiac hypertrophy in "wild-type" (non-mutant) mice. A great many studies in aging research use mutant mice to model diseases of aging, and most humans do not have single-gene mutations that cause age-related disease. Thus, research on wild-type mice may more accurately model human diseases associated with advanced age, and lead to more promising therapeutic strategies.
There has been considerable interest in the use of MB as a treatment for human brain diseases in which proteins form toxic aggregates, such as Alzheimer's disease, >Parkinson's Disease, and "tauopathies," wherein mutant forms of the protein Tau aggregate. Aggregation and accumulation of substances in body tissues, particularly the brain, is also a theme in research on aging.
The mechanism of MB's potentially beneficial effects on AD is not known, but it has been speculated to act by assisting the function of mitochondria in the brain. Declining mitochondrial function is another phenomenon which may be associated with diseases of aging, and is an active topic in rejuvenation biotechnology research. It's also important to be aware of the possibility that MB may not represent a cure for AD. It may turn out to be a treatment whose beneficial effects would wear off if it were discontinued, particularly if it functions via mitochondrial antioxidant activity.
We find it important to always be careful when considering whether some scientific observation is a cause or a consequence of aging. The present paper, with its notable 300-fold increase in C1q, can easily tempt one to conclude: "high levels of C1q need to be removed." This may be the case, but not necessarily. Before coming to this kind of conclusion, we strive to ask questions such as: "Is there some aspect of the immune system, related to C1q, which is recruited more highly in aging? If we ameliorate this activation of the immune system, will C1q levels no longer rise so much?"
Finally, the authors noted that while mouse C1q was ~300 fold higher in aging, it was only 8-fold higher in human brains: a noteworthy difference. We hope that further experiments will answer these questions, and others, to inform us about the exact role of C1q in aging dysfunction.