Thanks @foresightinst and @allisondman for having me, it was a lot of fun. Thanks to everyone who attended and don't hesitate to contact me if you want to know more or discuss the work!
I agree that aging research is a risky bet. But if we don’t do anything about it then the future - no matter how rich you are - is cancer, cardiovascular disease or dementia.
You might as well take a chance for you and your loved ones will live longer healthier lives.
@LidskyPeter@jpsenescence ... to store less epigenetic information as they have less genome to cover, and this allows them to pay off high fidelity repair with less tradeoff than one might expect.
@LidskyPeter@jpsenescence ... that demands encoding better fidelity.
I would not suggest predation to be the only factor, of course, but bird predation is interesting, as there is an interesting cavet in that bird genomes are much smaller than one might expected. It might be the case they need...
@DrDorotaSK@LidskyPeter@jpsenescence ... each tissue, and so some tissues can 'afford' better fidelity because their storage issues are simpler, their damage is less frequent and the rest of their function is informatically cheap.
@DrDorotaSK@LidskyPeter@jpsenescence That question has quite a complex answer, but in brief, I suggest that the rate of epigenetic damage accrued varies based on tissue and that there is a balance in selection between epigenetic fidelity and other cellular functions that must be found. It'll be different for...
@LidskyPeter@jpsenescence ... the need for high fidelity repair. Furthermore, I speculate that species with high mortality independent of this epigenetic ageing do not 'select' for high fidelity repair. There is no point developing a system to prevent epigenetic damage if you always die to a hawk.
@Halsted_19 @jpsenescence@LivuniILCaMS@InflamAge_UoB@UniofOxford Absolutely, just 'irreversible to evolution in the context of an adult human'. By naked example, 'age' is lost when two cells from old individuals (gametes) combine to form a new, young organism. I think the principles outlined here are a big part of why mammals have kids.
@KarlPfleger@jpsenescence@LivuniILCaMS@InflamAge_UoB@UniofOxford@fedichev 3. I'm not entirely sure what you mean by 'diffs' but the problem with analogies is I like them far too much. Not including them here is a mercy, I assure you. Also, this theory required a very specific description, and I didn't want to muddy the waters.
@KarlPfleger@jpsenescence@LivuniILCaMS@InflamAge_UoB@UniofOxford@fedichev Hi Karl, to respond:
1. I specifically didn't cover this here because we have another paper on the way about this.
2. We actually do make an argument about that, describing how we see these species as requiring fidelity low enough that they lack the typical data storage issue.
Thrilled to finally be able to post our new paper! Honestly a lot went in to getting this one through the door. Still! Excited for feedback!
https://t.co/5XfsnnAo4B
🚨New paper on epigenetic fidelity and ageing
We develop a conceptual model to explain aging based on first principles and conclude that epigenetic aging is inevitable.
Exciting work by @_ThomasDuffield@LivuniILCaMS + @InflamAge_UoB@UniofOxford
1/4
https://t.co/4jcq9rVgRj
It had to happen to me someday.
A reviewer commented that our manuscript “needs to be seen by a native speaker”, and will only comment on the science “once the language issues are fixed” 🙄
#AcademicChatter#AcademicTwitter
https://t.co/QbNjtd9dVP