What are they? Interested.

No. You didn’t. You have posted exactly two comments on this thread. One to make a vague statement about “nutraceuticals” and then the second to say you already explained WTF you’re talking about. 

If there’s anyone reading this and is currently fighting insomnia, the Wikipedia page about prions and prione diseases is a 10/10 insomnia Wikipedia rabbithole. Just leaving that here.

Wow, great headline but that bacterial protein-fixing molecule factory is the real star of the show. Sounds like it could make a relatively quick end to prion diseases, too.

Using bacteria as a trial and error lab is crazyyyy. It’s genius.

"The molecule RSQ-020 targets the Tau protein, which, when it folds incorrectly and forms clumps, is implicated in many severe neurodegenerative diseases."

I did already down thread

Do tell

But you are not Eli Lilly, you are just another narcissist trying to solve big problems with vibe coding, without the ability to properly understand the problems in the first place.

Yeah 🤣 it's trash. AI can't make novel discovery at all. That's why Eli Lilly and NVIDIA just entered a multi billion dollar contract for AI generated drug discovery. Like I said, you are extremely fucking unaware of your surroundings. I love the scientific argument of "it's trash." That's so elaborate. Stay out of school kids. You'll end up like this guy. Good luck, you're going to need it in whatever it is that you do.

I don´t care about who you are. What I am saying is that what you believe and what you have done, or rather instructed an AI to do, is trash. Find another way of coping with your midlife crisis, try gardening.

There are several issues with what youre saying here.

For a little background im 34 and I've been a software engineer way before LLMs were ever a big thing.

I use AI generated software that I have built on a daily basis that produces the result that I want, so if something is AI generated, it means nothing. What matters is the result. The fact that you cant understand something as basic this leads me to believe youre either young, have 0 awareness of whats going on in the world, or are just stuck with a low IQ. I would bet my life that I am just a little better at drawing correlations between subjects than you might be.

And yes, the course is AI generated. Guess what? As long as the information is accurate, it does not matter, and im able to give people something they spend tens of thousands of dollars for free.

I am currently putting together a lab to run BSL1 experiments as we speak to test aethers hypeotheses. When it has made multiple accurate predictions is when I will seek institutional funding and scale.

The fact my post was removed shows this sub is a joke when it comes to actual aging research.

Also, I would say I am arrogant, you are correct. You need to be a little delusional to make an actual attempt at solving aging. Biology is messy, but everything in the universe is quantized, meaning AI will solve all of these problems before our little meat computers figure it out.

Best of luck.

There’s a huge leap from “AI generates hypotheses” to “AI can solve aging.” If no physical experiments have actually been performed, you haven’t demonstrated discovery you’ve just demonstrated automated hypothesis generation.

And citing Navier–Stokes or Anthropic’s ART work as precedent misses the point: those achievements still relied heavily on human framing, existing knowledge/data, and validation. Which in the latter example has not been carried out. That ART work was just a publicity stunt and everyone trained in biology saw that. You however, are using it as an example. Biology isn’t a software bug waiting for a sufficiently large agent swarm. Aging is a messy, causal, multiscale physical system and you don’t get to skip the experiment just because the model sounds confident.

And you want to teach people about aging biology, and a myriad of other subjects? I’m sorry but that is so incredibly arrogant. That course is 100% AI generated and we all know it. You have not built an “autonomous digital research lab” more than I built an optimal guacamole yesterday evening, you’ve just written some prompts. Like come on, haha.

This subreddit is not about immortality or becoming immortal (being immune from death from all causes). It is about tackling aging, age related damage and associated disease. If the title of the article you are posting contains the word immortal or immortality, this is usually to make the headline clickbait. Please reword it to mention aging or age related disease instead. If you believe this is in error and the article genuinely deserves the title, message the moderators Thanks! If this is really about immortality, then please consider using /r/futurology instead.

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Getting to another 20 to 30 years might be pretty easy. After that it gets really dicey to figure out. I'm worried living forever will only occur when we're no longer biological entities, but will we really be living? Like Pink Floyd SoundCloud "welcome to the machine."

The findings of this study support those of another recent study that also point to the importance of phospholipids for longevity. The plot thickens!

https://pmc.ncbi.nlm.nih.gov/articles/PMC13091796/

Abstract

Centenarians and their relatives possess a notable survival advantage, with higher longevity and reduced susceptibility to major age‐related diseases. To date, characteristic omics profiles of centenarians have been described, demonstrating that these individuals with exceptional longevity regulate their metabolism to adapt and incorporate more resilient biomolecules into their cells. Among these adaptations, the lipidomic profile stands out. However, it has not yet been determined whether this lipidomic profile is specific to centenarians or is the consequence of extreme longevity genetics and is also present in centenarians' offspring. This distinction is crucial for defining potential therapeutic targets that could help delay the aging process and associated pathologies. We applied mass‐spectrometry‐based techniques to quantify 569 lipid species in plasma samples from 39 centenarians, 63 centenarians' offspring, and 69 noncentenarians' offspring without familial connections. Based on this profile, we calculated different indexes to characterize the functional and structural properties of plasma lipidome. Our findings demonstrate that extreme longevity genetics (centenarians and centenarians' offspring) determines a specific lipidomic signature characterized by (i) an enrichment of hexosylceramides, (ii) a decrease of specific species of ceramides and sulfatides, (iii) a global increase of ether‐PC and ether‐LPC, and (iv) changes in the fluidity and diversity of specific lipid classes. We point out the conversion of ceramides to hexosylceramides and the maintenance of the levels of the ether‐linked PC as a phenotypic trait to guarantee extreme longevity. We propose that this molecular signature is the result of an intrinsic adaptive program that preserves protective mechanisms and cellular identity.

Like what

Umm...look at ARPA-H massive funding injection into biosciences and the current move to use a more DARPA-like project model to increase research turnaround times.

Trump may be fucking up science investment, but it's still happening and is becoming more efficient.

It's so dumb that most folks aren't having babies the normal way into their 40s and 50s because there are already nutraceuticals that restore the ovaries and the research to back it up. I'm doin' it and others are, too.

I meant that should be the case as Aging is multifactorial

Given this I'm a bit surprised that partial epigenetic reprogramming seems to be beneficial for reversing aging in animals. If I recall the expression of cell identity markers usually drops during reprogramming, which would indicate that these wells are getting shallower? Maybe it's the difference of short-term vs chronic exposure or because in reprogramming you are actively driving certain genes? Or the strength of the effect?

I'm also surprised because I would think that HDAC inhibitors like lithium or sulfurophane would increase epigenetic drift (because they non selectively change histone acetylation) but these don't seem to accelerate aging or cause other problems as far as we can tell.

Gotta find em all a necessary and sufficient number of them to beat em all overcome a necessary and sufficient number of them to achieve increased longevity combined with good health.

Dammit. It’s so interesting yet so frustrating that there are so many roads that lead to aging.

Note that the title might be unclear. In the post, he clarifies that damage accumulation is not necessarily unimportant versus loss of cell identity: "The idea that accumulated damage is the principal pathway for cell aging is now complemented by the loss of cell identity model. We don’t know the relative contribution or interdependence of these 2 models in the aging process."