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.
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.
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.
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"
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.
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.
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 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.
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
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.”
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...
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.
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.
Readit News
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
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.
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.
I feel like I see some strongly-worded headline about anti-aging of some sort here every two weeks.
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"
Most deaths seem to be cardiovascular, heart disease, stroke, then followed by cancer.
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.
[1] https://biologyinsights.com/the-mice-mating-process-and-thei...
Fascinating, really.
Deleted Comment
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
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] https://www.nature.com/articles/s43587-025-00940-z
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.
I wonder if they could run tests on regular blood donors as well for those with iron sensitivity and not.