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Reporting on the Second Interventions in Aging Conference


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#1 reason

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Posted 02 May 2017 - 12:55 PM


This report captures the state of the research community in a nutshell: progress in the sense that ever more scientists are willing to make the treatment of aging the explicit goal of their research, but, unfortunately, there is still a long way to go in improving the nature of that research. It is still near entirely made up of projects that cannot possibly produce a robust and large impact on human life span. The only course of action likely to extend life by decades in the near future is implementation of the SENS vision for rejuvenation therapies - to repair the molecular damage that causes aging. Everything else on the table is some form of tinkering with the operation of metabolism in order to slightly slow down the accumulation of that damage, such as via capturing some of the calorie restriction response or boosting autophagy. In any machinery, repair is a vastly better strategy for improving function and extending working life span, and our biology is no exception.

In March 2017, the Second Interventions in Aging Conference was held in Cancun, Mexico. The meeting, similar to the earlier event in 2015, was focused on interventional strategies. One notable difference was that this year's meeting was much more directed toward potential interventions to target human aging. The field has been very successful over the last decade in identifying interventions that extend lifespan and healthspan in animal models such as yeast, flies, worms, mice and, to some extent, primates. However, the primary goal is to employ knowledge from basic aging research to develop novel medical strategies aimed at extending human healthspan. Aging is the biggest risk factor for a wide range of chronic diseases that, to date, medical strategies have treated as separate entities, and as they arise. Yet, aging is driven by a limited number of coordinated pathways that can be modulated, and evidence suggests that interventions delaying aging will protect against multiple age-related diseases simultaneously. Discoveries in basic aging research thus point towards a broad-spectrum, preventative, medical strategy for aging-related disease.

There were seven research topics each addressed thematically at the meeting. All were chosen because they embody different strategies to target human aging. Each session combined talks from Platform speakers with those chosen from submitted abstracts. The first and largest theme was targeted toward Organismal Aging, or understanding the intrinsic pathways that govern aging of the entire organism. The interesting aspect of these presentations is that they address strategies to modify aging that touch back to research from the early days of aging research while simultaneously pointing to novel strategies for future interventions: new mechanisms linking growth hormone signaling to aging; using mammalian models to re-evaluate the role of reactive oxygen species; new evidence for links between progeria and normal aging, interpreting these strategies in the context of possible interventions that may affect both normal and "premature" aging; linking NFκB signaling to sarcopenia, a major driver of frailty in aging; mechanisms linking calorie restriction to lifespan extension in primates; strategies to examine the impact of aging pathways in elderly human populations.

The second theme was focused on using Stem Cells to target aging, with exciting presentations on aging of epithelial stem cells in flies and mice, on links between metabolism, autophagy and aging in the hematopoietic system, and on how adult stem cells self-organize into functional configurations. The third theme, addressing Cellular Mechanisms of Longevity Assurance, focused on pathways suspected to modulate aging, including autophagy, mitochondrial function and aging with emphasis on the role of small mitochondrial peptides, and the hypoxia pathway. Theme 4 centered on Epigenetics, which is not only becoming a target for intervention in aging, but is rapidly becoming a leading candidate for providing biomarkers of biological age: mechanisms leading to transgenerational inheritance of epigenetic marks that impact lifespan; links between the epigenome and activation of somatic retrotransposons, and how this activation may drive senescence and aging; further promoting the epigenetic clock as a marker of accelerated and delayed aging.

Theme 5 was designed to take a Systems Aging viewpoint. Such a holistic understanding of the aging process is in a sense the ultimate goal of the research. Is it possible to understand such a complex process as aging not just one gene and pathway at a time but in totality? The final theme centered on Signaling and Metabolism, hitting the major metabolic pathways that are linked to aging and that can be targeted with interventional strategies. These include the mTOR pathway and rapalogs; dietary restriction and links through mTOR to regulation of mRNA splicing; NAD metabolism and sirtuins; mitochondrial roles in regulating aging and metabolism.

Link: http://dx.doi.org/10...32/aging.101221


View the full article at FightAging

#2 alc

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Posted 02 May 2017 - 06:49 PM

... as usual this limited-understanding guy/girl from fightaging blob ... (as what he/she writes cannot be called a "blog") ...

 

"

 

The only course of action likely to extend life by decades in the near future is implementation of
the sens vision for rejuvenation therapies - to repair the molecular damage that causes aging.
Everything else on the table is some form of tinkering with the operation of metabolism in
order to slightly slow down the accumulation of that damage, such as via capturing some of
the calorie restriction response or boosting autophagy.

 

"

 

blah, blah, blah ... same bs every day ...

 

so here are couple of the serious teams working on rejuvenation technologies, that are just "tinkering" with metabolism ...

 

1. Izpisua Belmonte Lab:

 

http://belmonte.salk.edu/

 

cellular reprogramming is NOT "tinkering" with metabolism, as this limited guy/girl is keep repeating.

 

this is a clear example, that he simply do not understand what is going on in the real world.

 

http://belmonte.salk.edu/inthenews.php

 

 

2. George Church Lab:

 

http://arep.med.harvard.edu/gmc/

 

http://arep.med.harv...u/gmc/news.html

 

http://www.lifeexten...-School/Page-01

 

CRISPR gene editing is NOT (though will result in) "tinkering" with metabolism ... so yeah, this guy/girl is keep typing same non-sens all over the places ...

 

As a matter of fact degrey was very reluctant that CRISPR can lead to reverse aging (yup, sour grapes) ... but that is usual when people do not understand the technology, as it is the same with Calico: they keep attacking Calico without understanding what AI will lead to in the reverse aging field ...

 



#3 to age or not to age

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Posted 03 May 2017 - 08:04 PM

alc - I am with you on your criticism and I responded on the fight aging blog to to that effect.

Irina Conboy told me on camera that blocking one or two aging damage factors in the blood

seems to make stem cells begin to act young. She and Michael Conboy's point is that in this case

the body does the heavy lifting; i.e. if you set the stage the body will make the myriad choices

modern science cannot do. This meme that tinkering with the rate of aging via altering this or that pathway

just helps on the edges of health span is shortsighted in my view. And, the salk paper and crispr technology are other clear

examples that the body knows what to do.  Further, in terms of low hanging fruit, it is possible that intermittent down regulation of the mtor 1 gene

(via rapalogues)  may actually reverse aging elements of the immune system. I know and like Aubrey but I don't  believe this is an either or situation.  


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#4 alc

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Posted 03 May 2017 - 08:39 PM

@ to age or not to age  -

sens are good at being "crusaders" for rejuvenation, but they have lots of issues with their theories (just see the mitochondria work, or their "understanding" of telomere/telomerase, etc.).

 

one majer issue is that their "solution" is very alembicated and require a lot of "and", "and", "and", etc.

 

they do not take it well whenever a study shows the ability of the body to "reset" itself to a younger state.

and that is because all those studies will make obsolete their approach.

 

anytime a study like this appear, you will see the duo fightaging guy/girl + michael rae writing bunch of explanations and casting doubts

about that research paper.

 

what bothers me most is that this guy/girl cast doubts on anybody else (except sens), without having any/much proof that something from sens works.

now, there is the recent senscent cells story ... but, sens and others piggybacked on others work.

my closed family is in medical field, and I recall back in 90s when they were discussing about senescent cells and their role in aging.

but at that time there was not much research done.

 

anyway, casting doubts on everybody's work, and claiming that everybody else except sens is "tinkering" with metabolism, this is something

really, really stupid and ought to STOP.  

 

this is not political election, this is pure science that we need to conquer in order to reverse aging.

 

... btw here is another researcher I forgot to put on that list, researcher that is "tinkering" with metabolism: Michael West.

 

now you tell me how in the world "Induced Tissue Regeneration" is "tinkering" with metabolism???

 

when you compare what Michael West, Izpisua Belmonte or George Church have published on this field with the theories of sens guys, there is a difference from sky to earth ... so let's just call this guy/girl out to stop this non-sens(e)

 

here is Michael West group (let's not forget that Michael West is the one who put intelligence in Geron):

 

http://michaelwest.org/

 

http://michaelwest.org/subsidiary.htm

 

 

 

"BioTime Forms New Subsidiary AgeX Therapeutics, Inc. to Develop its Programs Focused on Human Aging"

 

http://investor.biot...icle&ID=2260328

 

(would be nice if you can interview Michael West about his upcoming research on ITR to reverse aging in organs).

 

thanks for your comments.






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