Scientists just found a protein that reverses brain aging in mice(sciencedaily.com)
sciencedaily.com
Scientists just found a protein that reverses brain aging in mice
https://www.sciencedaily.com/releases/2025/08/250820000808.htm
75 comments
I wanted the 20s understanding of this. The article says too much FTL1 may decay cognitive ability, so I asked Gemini about the link between that and blood sugar.
High blood sugar increases the amount of iron your body stores, and FTL1 is a mechanism used to store iron in your body. Thus, a contributor to cognitive decline might be a protein that your body makes too much of when your blood sugar is high.
High blood sugar increases the amount of iron your body stores, and FTL1 is a mechanism used to store iron in your body. Thus, a contributor to cognitive decline might be a protein that your body makes too much of when your blood sugar is high.
Clearly we're on the way to a la carte immortality.
This feels like a headline that arrives in my parents' spam folder every two weeks or so for the past two decades.
I feel you. The fact that it cleared Nature’s editorial bar suggests it’s more than a marginal observation. At minimum, the work would have needed rigorous experimental controls, reproducibility across multiple assays, and clear mechanistic insight. “Notability” is high, but skepticism is warranted given the mouse result.
> The fact that it cleared Nature’s editorial bar
This was published in Nature Aging, not Nature. Nature (the company) has 100+ journals, I dont think any of them are as selective as Nature (the journal). That doesn't make this a bad article or a poorly reviewed one, but I wouldnt equate it with an article published in Nature.
This was published in Nature Aging, not Nature. Nature (the company) has 100+ journals, I dont think any of them are as selective as Nature (the journal). That doesn't make this a bad article or a poorly reviewed one, but I wouldnt equate it with an article published in Nature.
It’s almost like they are cashing in on their good name…
Spam folder?
I feel like I see some strongly-worded headline about anti-aging of some sort here every two weeks.
I feel like I see some strongly-worded headline about anti-aging of some sort here every two weeks.
Sorry, this isn’t actually a public forum, we’re all just chatting in your parents spam folder.
Plausible. I once found a group of people who'd somehow infested a VBulletin forum's plugin, that had (for some reason?) its own built in chat system.
Imagine opening up your floorboards, and there's a bunch of rats underneath, chatting about baseball.
Imagine opening up your floorboards, and there's a bunch of rats underneath, chatting about baseball.
Most if them don't age well...
Serious question: With all the advancements in mice medicine, are we theoretically able to create immortal mice?
The robust mouse rejuvenation study is ongoing. Basically they took a lot of mice and threw the kitchen sink of promising age reversing therapies at them: https://www.levf.org/projects/robust-mouse-rejuvenation-stud...
Just off the top of my head, I think the longest they ever got a mouse to live in a study was the C-60 study where they wanted to test whether it was toxic and the mouse lived almost twice their normal lifespan. This paper has been cited over 300 times, so it's not like people haven't taken notice of it. There are a few supplement companies selling c-60 olive oil too:
https://www.sciencedirect.com/science/article/abs/pii/S01429... "Here we show that oral administration of C60 dissolved in olive oil (0.8 mg/ml) at reiterated doses (1.7 mg/kg of body weight) to rats not only does not entail chronic toxicity but it almost doubles their lifespan"
Just off the top of my head, I think the longest they ever got a mouse to live in a study was the C-60 study where they wanted to test whether it was toxic and the mouse lived almost twice their normal lifespan. This paper has been cited over 300 times, so it's not like people haven't taken notice of it. There are a few supplement companies selling c-60 olive oil too:
https://www.sciencedirect.com/science/article/abs/pii/S01429... "Here we show that oral administration of C60 dissolved in olive oil (0.8 mg/ml) at reiterated doses (1.7 mg/kg of body weight) to rats not only does not entail chronic toxicity but it almost doubles their lifespan"
Bearing in mind that the C60 study (from 2012) has never been succesfully replicated since, despite multiple attempts.
Did we manage to accidentally make something live twice as long and then abandon efforts to replicate the results?
Or were there other problems in the data?
No. Originally we sketched out 9 hallmarks of aging, and it has since increased to twelve. We don’t have a full picture of immortality yet, let alone conquering it.
Even if we can't do it biologically i wonder how much we could extend it with artificial organs?
Most deaths seem to be cardiovascular, heart disease, stroke, then followed by cancer.
Most deaths seem to be cardiovascular, heart disease, stroke, then followed by cancer.
Given that you die, when one vital organ dies it will eventaully hapen in this way or another. I read somwhere and that stuck in my brain, that maxmimal logevity for humans is estimated to be approximetly 125 years.
>> I read somwhere and that stuck in my brain, that maxmimal logevity for humans is estimated to be approximetly 125 years.
Oh, that's just derived from old theology.
Genesis 6:3, 'Then the LORD said, “My Spirit will not contend with humans forever, for they are mortal; their days will be a hundred and twenty years.”'
This kinda got spread throughout the zeitgeist long ago as a "maximal lifespan", but the reality is that only 3 in 10,000 even make it to 100. There's no hard cutoff, but functionally essentially no one gets to 110.
Scientifically, there's no hard reason we couldn't increase our lifespans indefinitely, but we've got a lot of work to do before we'll be able to get a reasonable number of people up to 125.
Oh, that's just derived from old theology.
Genesis 6:3, 'Then the LORD said, “My Spirit will not contend with humans forever, for they are mortal; their days will be a hundred and twenty years.”'
This kinda got spread throughout the zeitgeist long ago as a "maximal lifespan", but the reality is that only 3 in 10,000 even make it to 100. There's no hard cutoff, but functionally essentially no one gets to 110.
Scientifically, there's no hard reason we couldn't increase our lifespans indefinitely, but we've got a lot of work to do before we'll be able to get a reasonable number of people up to 125.
That doesn’t sound like you’re disagreeing with gp.
If we count a permanently inflamed organic blob in roughly the shape of a mouse covered by surgical scars constantly pumped with anti-rejection drugs and hooked up to a blood filter we could probably make the mouse immortal now. It might not enjoy living though.
Funnily enough, chronic inflammation (inflammaging) is also a hallmark of aging.
I mean, that’s a good start honestly. Makes me optimistic about the QoL the mouse might be able to have in 50 years.
Probably quite a bit, but some of the hallmarks (decreased intercellular signaling, reduced ATP activity, decreased macroautophagy) seem so systemic I’m not sure we’re even close.
I think if we were, we would have immortal mice.
Having lived in some of the apartments I've lived in, I'm not sure that we don't.
Are you sure the mice don't change?
One older balding mouse would hold court in the pantry periodically-- he had a little gold ring that he made the other mice kiss before they conferred with him about various happenings around the apartment. I'm pretty sure he was in it for the long haul.
You kill one fucker, twenty show up to its funeral.
That would be very dangerous and possibly the plot of some hard sci-fi thriller. If immortal mice were to somehow escape the lab and breed in the wild we could rapidly end up with massive populations of mice that never die of aging, ultimately collapsing entire ecosystems and food chains, leading to the end of humanity.
1. Of course they should be sterilized.
2. The most common causes of death for wild mice are predation, diseases, and starvation. Theoretically immortal mice have no chance in the real world if not very well-adapted to these conditions.
2. The most common causes of death for wild mice are predation, diseases, and starvation. Theoretically immortal mice have no chance in the real world if not very well-adapted to these conditions.
It’s also not hard to imagine that an immortal organism has higher metabolic needs. Meaning they are more prone to starvation and potentially less fit.
Mice? No, too many predators. Now, crows that would be a different matter. Already seen in the movie "Birds" ;)
It's my understanding that mice don't live long, because slower aging didn't provide a significant evolutionary advantage (lot's of predators, mainly). Instead the rate of reproduction settled at a very high level [1]. So by that logic, engineered, non-aging mice wouldn't have much of an advantage in the wild.
[1] https://biologyinsights.com/the-mice-mating-process-and-thei...
Fascinating, really.
[1] https://biologyinsights.com/the-mice-mating-process-and-thei...
Fascinating, really.
even focusing on age-related death, you assume that such treatment is one-and-done deal instead of continuous pharmaceutical life support
Well there is _Mrs. Frisby and the Rats of N.I.M.H._....
Immortal is not invincible.
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Time for a The Secret of NIMH rewatch.
Summarizes paper "Targeting iron-associated protein Ftl1 in the brain of old mice improves age-related cognitive impairment" [1]
Could lowering FTL1 restore synaptic connectivity and memory in old mice represent a master switch in brain aging, or just one of many parallel mechanisms? If FTL1 is sufficient to induce both structural and functional brain aging in mice, what does that imply about the hierarchy of molecular drivers in neurodegeneration
[1] https://www.nature.com/articles/s43587-025-00940-z
Could lowering FTL1 restore synaptic connectivity and memory in old mice represent a master switch in brain aging, or just one of many parallel mechanisms? If FTL1 is sufficient to induce both structural and functional brain aging in mice, what does that imply about the hierarchy of molecular drivers in neurodegeneration
[1] https://www.nature.com/articles/s43587-025-00940-z
Keywords: In Mice.
The increasing frequency of mouse studies showing reversal of aging symptoms indicates a few things in itself, regardless of whether any single result (like FTL1) holds up in humans:
1. Field Maturation
We’ve moved from “aging is inevitable” → “aging can be slowed” → “specific mechanisms can be reversed in vivo.” That shift means:
- Tools (CRISPR, single-cell omics, proteomics) are now precise enough to pinpoint single culprits.
- Researchers are designing interventions that don’t just extend lifespan, but restore youthful function in cognition, muscle, or immunity.
2. Convergence on a Core Set of Mechanisms
Different labs, different pathways (NAD+, senolytics, plasma dilution, now FTL1), but similar outcomes: old mice regaining youthful traits. This convergence hints aging may not be a diffuse “wear and tear” process, but the result of a relatively small number of upstream regulators.
3. Proof-of-Concept Momentum
Even if each specific intervention fails to translate, the fact that so many are succeeding at all in mice makes it harder to dismiss rejuvenation as fringe. The signal: aging can be manipulated, not just observed.
4. Cultural Shift in Geroscience
Funders, journals, and institutions are increasingly willing to spotlight “reversal” claims, where a decade ago the same results might have been relegated to smaller journals. The fact we’re seeing more of these studies may reflect both real progress and changed editorial appetite.
the trend suggests aging is experimentally tractable and reversible in model organisms. That doesn’t mean translation to humans is imminent, but it reframes aging from “inevitable decline” to “complex but solvable engineering problem.”
1. Field Maturation
We’ve moved from “aging is inevitable” → “aging can be slowed” → “specific mechanisms can be reversed in vivo.” That shift means:
- Tools (CRISPR, single-cell omics, proteomics) are now precise enough to pinpoint single culprits.
- Researchers are designing interventions that don’t just extend lifespan, but restore youthful function in cognition, muscle, or immunity.
2. Convergence on a Core Set of Mechanisms
Different labs, different pathways (NAD+, senolytics, plasma dilution, now FTL1), but similar outcomes: old mice regaining youthful traits. This convergence hints aging may not be a diffuse “wear and tear” process, but the result of a relatively small number of upstream regulators.
3. Proof-of-Concept Momentum
Even if each specific intervention fails to translate, the fact that so many are succeeding at all in mice makes it harder to dismiss rejuvenation as fringe. The signal: aging can be manipulated, not just observed.
4. Cultural Shift in Geroscience
Funders, journals, and institutions are increasingly willing to spotlight “reversal” claims, where a decade ago the same results might have been relegated to smaller journals. The fact we’re seeing more of these studies may reflect both real progress and changed editorial appetite.
the trend suggests aging is experimentally tractable and reversible in model organisms. That doesn’t mean translation to humans is imminent, but it reframes aging from “inevitable decline” to “complex but solvable engineering problem.”
> This convergence hints aging may not be a diffuse “wear and tear” process
About this: it seems to me that the idea itself of "wear and tear" is just silly. It's a metaphor taken from the realm of mechanical objects that have no regeneration abilities. Any living being is continuously repairing localised damages back to a pristine state, while aging is diffuse and organic. This suggests that any "wear and tear" can only be at the cellular level- but still it can't be a biological necessity given the wildly different lifespans of organisms- from a few days to centuries.
About this: it seems to me that the idea itself of "wear and tear" is just silly. It's a metaphor taken from the realm of mechanical objects that have no regeneration abilities. Any living being is continuously repairing localised damages back to a pristine state, while aging is diffuse and organic. This suggests that any "wear and tear" can only be at the cellular level- but still it can't be a biological necessity given the wildly different lifespans of organisms- from a few days to centuries.
It still applies because while organisms all have some form of self-repair ability, most do not have complete self-repair. "Wear and tear" is still possible at the macro level where self-repair is missing or slower than the damage rate -- famously in the articular cartilage, for instance. There's also accumulating damage that does not resemble mechanical wear and tear: toxins, misfolded proteins, DNA damage/mutation, senescent cells, etc.
Biological entities have some regeneration techniques, but that doesn't guarantee a mechanism exists for arbitrary damage to be repaired. For example I can heal a broken bone, but I can't heal a broken tooth.
No but you do grow entire teeth. Some animals regrow entire limbs. Organisms constantly build and rebuild themselves, sometimes (or at some levels) from scratch. Fresh cells can be generated at any time. The capacity to regenerate and repair can be lost but it's not intrinsically absent as the "wear and tear" metaphor suggests.
I fully agree with this GPT copy paste. We rely on these studies for good reason and the "in mice" reflex implies we should disregard important research.
I find them to be an unfortunate mix dismissiveness and principled restraint, that veers to much into the Onions Learned Sage territory.
I find them to be an unfortunate mix dismissiveness and principled restraint, that veers to much into the Onions Learned Sage territory.
It's still something. People are already injecting processed pig brains into their blood stream for many years now: Cerebrolysin
I’m re-reading hitchhikers, this made me chuckle.
Granted with all these science PR posts, what did the paper actually say? And why don't ppl post the actual DOI/paper link? I mean, at least for CS topics people post the arxiv link as a minimum...
The paper was posted as an alternate [1]
[1] https://www.nature.com/articles/s43587-025-00940-z
[1] https://www.nature.com/articles/s43587-025-00940-z
Not an expert, but the amyloid hypothesis for Alzheimers employed the same kind of logic and experiments in mice. For 20 years now every single trial with some intervention targeting the amyloid proteins has failed.
I am by no means an expert on this, but was reading this about the amoloid hypothesis this morning: https://www.astralcodexten.com/p/in-defense-of-the-amyloid-h...
He addresses the specific reasons that the mouse results don't translate, but the interesting part to me is that the scientific community seems to be behind the amyloid hypothesis while the media likes to run with any story that refutes it.
He addresses the specific reasons that the mouse results don't translate, but the interesting part to me is that the scientific community seems to be behind the amyloid hypothesis while the media likes to run with any story that refutes it.
Very interesting post, thanks!
This is interesting. For people with hemochromatosis, I have observed cognitive ability swings as they have their ferritin levels adjusted.
I wonder if they could run tests on regular blood donors as well for those with iron sensitivity and not.
I wonder if they could run tests on regular blood donors as well for those with iron sensitivity and not.
> To investigate the effect of NADH supplementation on cognitive function, young adult mice were administered NADH after viral-mediated neuronal FTL1 overexpression, and hippocampal-dependent memory was assessed by NOR and Y maze (Fig. 4s). Although young mice with increased neuronal FTL1 expression showed no preference for either a novel object or a novel arm, these cognitive deficits were mitigated after NADH supplementation (Fig. 4t,u).
https://www.nature.com/articles/s43587-025-00940-z
https://www.nature.com/articles/s43587-025-00940-z
If epilepsy is essentially “defective” pathways that propagate additional defective pathways I can only assume some “cognitive decline” is actually a protective mechanism
So, how do we differentiate between healthy and unhealthy cognitive decline.
So, how do we differentiate between healthy and unhealthy cognitive decline.
quick reading on that protein suggests to me, a layman, that more aerobic exercise and less red meat should be helping here against such a brain aging. Sounds so familiar.
How is red meat connected to it?
Thank you! I was wondering how this information is useful and applicable to me today.
it gives you something to think about, cognitive exercise has an absoltue possitive effect
also it is known that neural plasticity is just part of how our brains deal with damage of all sorts, so cleaning up "your" act and engaging in
challeging cognitive tasks is almost certainly going to have benificial effects, imediatly
Other studies have suggested that creatine supplementation helps brain function. Red meat is a natural source of creatine.
yes, sure. We'd not be such red meat eaters if it wouldn't be an efficient source of various stuff, at least in some moderate amounts. And our body is like a large enterprise software monolith - you touch something here, and it would reverberate in unexpected ways at some other unexpected places.
The logic i see here is that, having excessive level of iron storage protein, may be it makes sense to cut somewhat back on one of the best sources of hem iron - i.e. red meat.
The logic i see here is that, having excessive level of iron storage protein, may be it makes sense to cut somewhat back on one of the best sources of hem iron - i.e. red meat.
YES, I need this! I think ... I can't remember.
Let's read "Flowers for Algernon" again.
HN needs an automatically generated [in mice] suffix
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Yet another reminder that there has never been a better time to be a lab rat with an awful disease.
Study reveals blood sugar control is a key factor in slowing brain aging 150 points by gnabgib 9 months ago - https://news.ycombinator.com/item?id=42049418
Study Reveals Immune Driver of Brain Aging 232 points by oedmarap on Jan 22, 2021 - https://news.ycombinator.com/item?id=25871347
Brain aging shows nonlinear transitions, suggesting a midlife "critical window" 276 points by derbOac 79 days ago - https://news.ycombinator.com/item?id=44175905