#1

Aging is particularly harsh on the hippocampus - the brain region responsible for learning and memory.

Now, researchers at UC San Francisco have identified a protein that’s at the center of this decline.

They looked at how the genes and proteins in the hippocampus changed over time in mice and found just one that differed between old and young animals. It’s called FTL1.

Old mice had more FTL1, as well as fewer connections between brain cells in the hippocampus and diminished cognitive abilities.

When the researchers artificially increased FTL1 levels in young mice, their brains and behavior began to resemble that of old mice.

Open Access Paper:

Targeting iron-associated protein Ftl1 in the brain of old mice improves age-related cognitive impairment

https://www.nature.com/articles/s43587-025-00940-z

ChatGPT:

You’re asking whether there are any known compounds or chemicals that humans can consume to reduce levels of ferritin light chain 1 (FTL1) in the brain, based on the recent Nature Aging paper (published August 19, 2025) showing that neuronal FTL1 increases with age and contributes to cognitive decline in mice, while targeting it improves cognitive function (Nature).

What the Nature Aging Study Found

  • The study identified FTL1 as a pro-aging factor in neurons: aged mice had elevated hippocampal FTL1 levels that correlated with poorer cognition (Nature).
  • Overexpressing FTL1 in young mice caused aging-related neuronal changes, including altered iron oxidation states and cognitive deficits (Nature).
  • In aged mice, targeting neuronal FTL1 (presumably via gene-based or molecular interventions, though not via dietary compounds) improved synaptic markers and cognitive performance (Nature).
  • Interestingly, the study also found that NADH supplementation (i.e., boosting neuronal metabolic functions) mitigated the pro-aging effects of FTL1 on cognition (Nature).

Key takeaway: The beneficial intervention in the study was targeting neuronal FTL1 directly, and separately, metabolic boosting with NADH helped counteract FTL1’s effects—not that any substance directly lowered FTL1 levels.

Are There Human-Consumable Compounds That Reduce FTL1 Levels?

A current review of the literature reveals no known human-safe compounds that have been demonstrated to directly lower FTL1 levels in the brain. Here’s a breakdown of related findings:

  • Iron chelators, such as deferoxamine (DFX), reduced ferritin (both heavy and light chains) induction in rodent models of intracerebral hemorrhage—but this was in the context of acute injury, not age-related neuronal FTL1 expression (PMC). These results do not support a practical long-term therapeutic strategy for reducing FTL1 in normal aging.

  • Neuroferritinopathy (a rare genetic disorder caused by FTL gene mutation) is currently managed symptomatically; some research suggests deferiprone (another iron chelator) may help, but that’s under investigation in specific pathological contexts—not as a general FTL1-lowering strategy (Wikipedia).

  • The Nature Aging paper does not report any substances beyond NADH supplementation that affect neuronal FTL1.

Summary Table

Intervention Effect on FTL1 / Cognition Evidence & Notes
Targeting FTL1 directly Lowers neuronal FTL1, improves cognition Shown in aged mice; method likely molecular manipulation, not dietary/ingested (Nature)
NADH supplementation Mitigates FTL1-associated cognitive decline Observed in mice; not necessarily reducing FTL1, but offsets its negative impact (Nature)
Deferoxamine (DFX, iron chelator) Suppresses ferritin (light/heavy) upregulation post-injury Rodent ICH model; acute effect in injury context—not in normal aging (PMC)
Deferiprone & other chelators Potentially beneficial in neuroferritinopathy Experimental; not yet confirmed for general FTL1 reduction (Wikipedia)

So, in Human Terms…

To date, no known dietary or pharmaceutical compound consumed orally has been shown to specifically reduce brain FTL1 levels in humans—or even in normal aging animal models.

The Nature Aging study suggests:

  1. Targeting FTL1 expression can be beneficial, but this was done via research-grade molecular approaches in mice—not consumer substances.
  2. Boosting metabolic function with NADH may counteract FTL1’s detrimental effects—but again, this was a controlled lab intervention in mice.

What You Could Explore Next

  • NADH-related strategies: Although NADH showed promise in mice, its effectiveness and safety in humans for cognitive aging is unproven—more research is needed.
  • Clinical trials: Keep an eye on potential future studies exploring iron modulation, metabolic support, or gene-targeted therapies that affect FTL1 expression.
  • Mechanistic research: Understanding how FTL1 expression is regulated could lead to discovery of small-molecule modulators in the future.

Final Takeaway

At present, there are no compounds that humans can safely consume that are proven to lower neuronal FTL1 levels. The promising leads from the Nature Aging paper involve targeted intervention in mice (not applicable to humans yet) and NADH supplementation (a metabolic approach, but untested in people for this purpose).

Let me know if you’d like to explore mechanisms that regulate FTL1 expression, or the potential role of NADH in human aging—happy to dig deeper!

NADH: OTHER NAME(S): B-DPNH, BNADH, Coenzyme 1, Enada, NAD, Nicotinamide Adénine Dinucléotide, Nicotinamide Adenine Dinucleotide Hydrate, Reduced DPN, Reduced Nicotinamide Adenine Dinucleotide.

More info: Nicotinamide adenine dinucleotide - Wikipedia

1 Like