American scientists have found that the accumulation of a special protein in the brain associated with iron metabolism can accelerate age-related memory decline. This is the protein FTL1 (ferritin light chain 1), the level of which in the hippocampus of old mice was significantly higher than in young ones. The more of this protein there was, the worse the animals performed on cognitive tests. The study was published in Nature Aging.
Imagine your brain is a big computer, and your memory is its hard drive. As we age, this “hard drive” starts to work slower, and we remember worse. Scientists have found one “microbalancer” in the brain, a special protein called FTL1. They noticed that in old mice, in the part of the brain that is responsible for memory (called the hippocampus – it's like your own personal “memory center”), there was significantly more of this protein FTL1 than in young mice. And the more FTL1 they saw, the worse the old mice did at various “memory games”. This suggests that FTL1 may be an “aging accelerator” for our memory, and it is also somehow connected to how the brain processes iron – an important element for its work.
The researchers artificially increased the level of FTL1 in young mice. As a result, their cognitive abilities deteriorated: synaptic plasticity decreased, the work of neurons was disrupted, and memory resembled the “senile” type. On the contrary, reducing the level of FTL1 in old animals led to improved synapse function and memory recovery.
To test whether FTL1 was actually causing memory problems, and not just being there, the scientists did the following. They took young mice that had normal memory and specifically increased the levels of FTL1 in their brains. And what happened? These young mice began to behave like old mice—their memory and learning abilities were significantly impaired. Imagine that your brain cells (neurons) communicate with each other through “wires” (synapses), which can change and learn new things (this is called “synaptic plasticity”). In these young mice, the “wires” became less flexible, and the communication between the cells deteriorated. But what if you did the opposite? The scientists reduced the levels of FTL1 in the old mice. And lo and behold! Their “wires” started working better again, and their memory was significantly restored. This is very strong evidence that FTL1 is not just a “witness”, but an active “criminal” in the matter of memory aging.
Molecular analysis showed that FTL1 affects iron metabolism in neurons and disrupts energy processes, primarily ATP synthesis. When the researchers injected mice with additional coenzyme NADH, metabolic and cognitive impairments were partially eliminated.
Okay, we know that FTL1 messes with memory. But how exactly does it do it? Scientists have looked inside brain cells (neurons) at the molecular level to understand the mechanism. They found that FTL1 interferes with how neurons manage iron (and iron is very important for cell health). But the main thing is that FTL1 disrupts the “power plant” of cells. Imagine that each of your cells has a little power plant that produces energy in the form of molecules called ATP. ATP is the “fuel” for all the processes in the cell, including thoughts and memory. FTL1 damages this power plant, so the cells don't get enough “fuel” and start to work poorly. Interestingly, when scientists gave mice a special “supplement” (coenzyme NADH) that helps produce energy, they were able to partially restore these energy processes and improve memory. It's like giving a rattling engine better fuel – it starts working better.
The authors emphasize that their work is the first to identify FTL1 as a key factor in cognitive aging and a potential target for therapy. If the results can be confirmed in humans, this could open up new approaches to preventing age-related memory decline and dementia.
The authors of the study are very excited because their work has clearly shown for the first time that FTL1 is not just some random protein, but a key “culprit” in the aging process of our memory. This is a huge discovery! And even more importantly, FTL1 could become a “target” for new drugs. Imagine that FTL1 is a button that you can press to turn off or reduce memory problems. If scientists can confirm the same in humans (because so far this study has only been done on mice), it will open up completely new possibilities! We will be able to develop new drugs or methods to prevent age-related memory decline or even treat serious diseases such as dementia (for example, Alzheimer's disease). This will give hope to millions of people to maintain their sharp minds in old age.
