Scientists just found a protein that reverses brain aging in mice (sciencedaily.com)

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

This feels like a headline that arrives in my parents' spam folder every two weeks or so for the past two decades.

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.

We should already have immortal mice

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.

Serious question: With all the advancements in mice medicine, are we theoretically able to create immortal mice?

Ketones Reverse Brain Aging During Midlife Critical Window 19 points by rhodescolossus 4 months - https://news.ycombinator.com/item?id=43506791

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

YES, I need this! I think ... I can't remember.

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...

Yet another reminder that there has never been a better time to be a lab rat with an awful disease.

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.

> 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

HN needs an automatically generated [in mice] suffix

Let's read "Flowers for Algernon" again.

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.