reasonattlm

22 ms·

91.
by reasonattlm 9y ago
Read their publication list. The SRF collaborates with most of the important research groups in the field: http://www.sens.org/research/publications Also, see their research advisory board, which includes numerous resp
92.
by reasonattlm 9y ago
Aging is the same cell and tissue damage that causes the age-relates diseases you mention. The only difference between aging and disease is how much damage you have, how far the cascade of cause and effect and secondary consequences has pro
93.
by reasonattlm 9y ago
I think it important to note that the SENS research programs are just about 100% funded by philanthropy, with thousands of supporters over the years. This donation is a part of ~$6M from the year end fundraiser: about $500k from a lot of pe
94.
by reasonattlm 9y ago
If you are interested in perusing some of the past decade of science on this topic, some links below. It is about equally devoted to looking at what happens in induced pluripotency versus what happens during embryonic development, induced p
95.
by reasonattlm 9y ago
Only some of the damage repair methods require gene therapy, and in the case of allotopic expression to work around mitochondrial damage that is already demonstrated in human trials by Gensight. You should look over the linked sub-pages her
96.
by reasonattlm 9y ago
There are a wide variety of life courses exhibited in the natural world, when plotting mortality risk over time. The human early start on an exponential increase is just one of them. Flies that reach a mortality risk plateau in late life is
97.
by reasonattlm 9y ago
Senescent cells generate inflammation. So every age-related condition with an inflammatory component - which is most of them - should be improved to some degree by that factor alone when senescent cells are removed, even putting aside other
98.
by reasonattlm 9y ago
I think the problem in the cancer research community is much the same as the one in the aging research community, which is to say pursuing very inefficient strategies. My theory is that the root cause is similar, which is that researchers a
99.
by reasonattlm 9y ago
From other somatic cells, and ultimately from the tissue stem cell population. That population is impacted by aging, as you point out. However, the effects of replacing 1% of tissues over some period of time are going to be negligible in co
100.
by reasonattlm 9y ago
Which is why the SENS portfolio includes a universal cure for cancer. This is not as hard as people have been made to think it is. The present mainstream approach of the past few decades is just not a good one. It is picking strategies that
101.
by reasonattlm 9y ago
They amount to a few percent of tissues in most cases. In mitotic tissues they will be replaced in the same way as any cell is replaced when it dies, by replication. In post-mitotic tissue cell therapy might be needed, but that hasn't
102.
by reasonattlm 9y ago
Senolytics, to clear senescent cells, is a fundamentally different and more theoretically sound approach in comparison to trying to override signaling that is partially downstream of the presence of senescent cells. It also works far more r
103.
by reasonattlm 9y ago
Safe, yes, but I think "promising" is more aimed at the investors than a reflection of reality. Both Alkahest and Ambrosia's results are essentially ambiguous, which reflects the equally ambiguous animal data for plasma trans
104.
by reasonattlm 9y ago
There are a lot of people thinking about beneficial factors in young blood and harmful factors in old blood. Some are looking at period apheresis of blood to remove harmful factors, some are investigating transfusions, some looking at deli
105.
by reasonattlm 9y ago
No-one in the field is particularly impressed with Calico at this point in time. Calico is the second coming of the Ellison Medical Foundation, which is to say they're just analyzing the details of aging and expanding on the NIH budget
106.
by reasonattlm 9y ago
Think about how complex machines fail. Reliability theory is a good tool for this, and has been used to effectively model how aging works, as failure of units in a system of redundant units. https://doi.org/10.1006/jtbi
107.
by reasonattlm 9y ago
And a different, policy-of-medicine-and-rejuvenation interview with de Grey from a politically focused site here: http://merionwest.com/2018/01/08/an-interview-with-anti-agin...
108.
by reasonattlm 9y ago
That would only be the case in the models where senescence is blocked completely. If instead for a short time killing some fraction of all currently existing senescent cells, the effect on cancer risk should be a reduction, due to decreased
109.
by reasonattlm 9y ago
I'll get to publishing a detailed essay on that topic at some point in the near future. The less detailed precursor overview can be found here: https://www.fightaging.org/archives/2017/05/planning-a-singl
110.
by reasonattlm 9y ago
Rejuvenation therapies and treatments that slow the progression of aging won't be tested in humans by waiting to see. They will be tested using quick before/after measures of biomarkers of aging. Those biomarkers are under develop
111.
by reasonattlm 9y ago
Actionable things for humans at the moment appear to look like trying senolytic drug candidates in rational self-experimentation, with before/after tests of metrics linked to tissue stiffness, inflammation, kidney and heart function. C
112.
by reasonattlm 9y ago
The author of this overview, Laura Deming, runs the Longevity Fund, and has a research background in the study of aging. She merits congratulations for being, I think, the first by a few years to put together a longevity-focused fund, now j
113.
by reasonattlm 9y ago
People who think that rejuvenation therapies are only for the rich are not paying attention. Look at first generation senolytic drug candidates that clear ~25% of senescent cells in mice, varying by tissue type. These vary from $100 per dos
114.
by reasonattlm 9y ago
This piece is a great example of entirely the wrong way to think about this issue. The procession of mechanisms is as follows, starting with layer 1: - calcification - cross-linking - vascular smooth muscle dysfunction Which gives you layer
115.
by reasonattlm 9y ago
The biggest thing? Since arguably sometime in the 1930s the technological capacity has existed to store at least the brains of dead individuals at liquid nitrogen temperatures indefinitely, waiting on a future that can restore them. In a di
116.
by reasonattlm 9y ago
It is getting more attention these days, and the older discoveries have had enough following attention to be fairly widely known in the field. It isn't a line of research I've followed specifically, but if you look at PubMed you c
117.
by reasonattlm 9y ago
There is a range of research to suggest that Alzheimer's is a metabolic disorder with high level similarities to type 2 diabetes. You might look up "type 3 diabetes" - which is not an official designation, but sufficiently di
118.
by reasonattlm 9y ago
Paper: https://doi.org/10.1038/nature25158 The research noted here improves the understanding of how inflammation acts to drive the progression of Alzheimer's disease, despite being secondary to the well-known dep
119.
by reasonattlm 9y ago
The research community still lacks a reliable, ready to be productized method of producing vascular networks capable of supporting an organ. However, mass-manufacture of organoids is definitely a thing that can be worked on today. Functiona
120.
by reasonattlm 9y ago
Find research you like, find a syndicate of investors, and do the legwork to bring those two things together. This is going on today in the matter of rejuvenation research - people talking about and funding the early stage startups they lik

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