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Undoing Aging 2019

conference berlin

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#1 caliban

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Posted 28 March 2019 - 07:59 AM




LongeCity Members who are also there in person: please say hi! 


Those elsewhere: feel free to post questions about the talks or to the speakers, I can try to get you some answers. 




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#2 caliban

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Posted 28 March 2019 - 06:40 PM

Day 1: 


Opening: The organisers connected the conference to the legacy of the prior SENS conferences in Cambridge. 

With 500 attendees, this one is the largest so far. 

Barzilai, the opening keynote speaker, explained that the TAME trial was delayed because an NIA reviewer did not support the study. With alternative funding the trial "should start this year" 


Session 1:

Reason introduced his new venture. After all the year in relative seclusion it is wonderful to see him step onto a stage    :happy: 


Moskaleve & Parkhitko both sought to make the case that fruitflies are still useful in intervention-focused geroscience.

Breitenbach-Koller derived insights from protein sythesis in yeast that she hopes to adopt for customised protein synthesis. I missed any achievements since the initial paper in 2013. She mentioned having formed a company which I also can't find straight away. . 


Session 2: Cells in circulation 

Pawelec gave a nice overview of basic aspects of immune aging (watch the video if one goes online), but no new data (although he mentioned that age seems to have no effect on monocytic myeloid-derived suppressor cells=    


Nikolich-Zugich. stressed the importance of "lypmh node fibrosis" in impairing thymus function and regeneration.He has results in primates and humans supporting that. I'm sure Reason listened carefully.    


Lambracht-Washington presented data on immunotherapy vs. Alzheimer's. She acknowledged that all such trials focusing on amyloid have failed but argued that using a DNA AB42 was different. It does affect AD- like pathology in mice, rabbits and monkeys but it seems very early days. If they get an NIA grant this year, they will try to get a GMP vaccine and more preclinical data and aim for a 16 patient trial in year 2.    


Session 3:  Extracellular molecules 

McClure: Argued for the superiority of their biomimic 'peptoids' over peptides and presented plans to use them as an antimicrobic in the ear. More ambitiously, he argued that some types of dementia are infection-related and hopes to use their technology in this context - but presented only flimsy in-house evidence.   

Mata: presented some nifty tools for bio-engineering enamel, with much greater ambitions, but rather failed to demonstrate relevance to the the conference topic      



The day concluded with a debate between Vadim Gladyshev and Aubrey de Grey on "is comprehensive damage repair feasible?" A strange topic as the main interest of most attendees would seem to be "can damage repair be good enough to retard aging significantly?" On this both speakers seemed to agree. But it was nice to hear Aubrey list his current "reasons for optimism" amongst which he listed the unexpected "penunmbra" and "knock-on" effects of interventions that are already working. Unfortunately, the same goes for the "penumbra" of  frailty that comes with the factors that have not yet been 'fixed'  



Great to reconnect with longecity members, and community luminaries, as well as encountering new scientific and policy perspectives. What is always neat with these conferences is the eclectic crowd. Scientists and clinicians mingle with managers, advocates, investors, journalists and other well informed 'lay' stakeholders.  Hoping to gather plenty of feedback for our current planning exercise.     


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#3 Mind

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Posted 29 March 2019 - 08:45 PM

Thanks for the summaries Caliban. Much appreciated.

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#4 Avatar of Horus

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Posted 29 March 2019 - 11:32 PM

Thanks for the summaries Caliban. Much appreciated.

Yes, thanx for the coverage.

#5 caliban

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Posted 29 March 2019 - 11:43 PM

Day 2 


Didier and Jose talked about political activism. I saw it more as a rallying cry.  


Session 4: Cell Therapy


Palla from the Blau lab showed that a PGE2 analog increases muscle function, mass and muscle stem cell numbers in mice – I’m unsure about translatability to humans.


Cai recapped his nature paper on the hypothalamus-stem cell reactions (through exosomal microRNAs). In Q&A he speculated that hypothalamic inflammation was also a factor in aging humans.   


West showed some micro RNA factors in addition to his 'usual' Age-X set 



​Session 5: Counteracting DNA instability


Shay argued that the shortest not the average telomere length was the most indicative measure: “high performing” centenarians have fewer critically short telomeres (decreased NLRP3 expression, higher BAX protein)


Ligner: looked at proteins that contribute to telomere protection. He also speculates that oxidative damage to telomeres may explain the lack of telomere regeneration even in the presence of telomerase.


Gudkov: I really enjoyed this talk. I was not familiar with his work and he managed to connect it in meaningful ways. One line of argument was that aging is driven by genomic instability thrug retrvral junctures (RTL1, LINE1) and that blocking the retrobiome” (with anti-HIV drugs) might be geroprotective. Plus he has inventive projects.  


Session 6: Short talks from submitted abstracts


Foks: Talked about FOXO4, reduced T Cell proliferation, increased Tregs 


Ives: Shift biosciences have a compound that ‘rejuvenates’ mitochondria. Its very early days. Treated mice ‘looked younger’ and had lowered blood glucose    


Toren: examined the genome of grey whales and attributes their longevity to better resilience against cancer and stress


Grońska-Pęski: Presented an idea of transdifferentiating transplanted microglia into neurons in mice. (echos of an old LongeCity project). 


Varvanets:  ApoA-1 Milano is a mutation in among residents of a small village in Northern Italy who don't get plaques. This effort aims at sharing this benefit with a gene therapy. 


Mitteldorf: presented thoughts on data sharing on self experimentation. Hoping to bring him in to collaborate with LongecIty. 


​Session 7/8: Senolysis 


Campisi: reminded us that  (1) suppressing SASP is not easy.  (2) SASP is dynamic and heterogenous  (3) senolytics don’t increase maximum lifespan (4) 


Bulavin: Showed that continuous P16 cell removal had very bad effects in mice, especially in the liver. 



Personally I got more out of Day 2 scientifically compared to yesterday. Not as much socialising as I missed the evening mingle. 

Tomorrow: Last chance for longecity readers to plant questions.  

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