As we age, our brains slowly lose the ability to learn, remember, adapt and heal from injury. This flexibility is known as brain plasticity, and it explains why youngsters can soak up information like sponges and adapt to their surroundings, while the more mature of us tend to forget things and struggle to learn new skills. Scientists have long sought an uncover the mechanisms behind this reduction in brain plasticity, and a team at the University of Utah has uncovered a possible key piece in the plasticity puzzle with the discovery of a single gene that can rejuvenate plasticity in the brains of adult mice.

Several processes that potentially control brain plasticity have been discovered in recent years. One team at Yale found that the Nogo Receptor 1 gene played a significant role in brain maturation, while researchers from UC Irvine discovered they could restore youthful plasticity to a mouse brain by transplanting a certain type of embryonic neuron.

This latest discovery hones in on a gene called Arc. In an earlier study, the research team discovered that when a young mouse temporarily closed one of its eyes, there was a noticeable neuronal change to the animal's electrophysiological response. This demonstrated the animal's youthful brain plasticity through its ability to adapt to changes in its visual experience. It was also noticed that young mice without the Arc gene were unable to effectively make this adaptation to the visual interruption.

"Given our previous studies, we wondered whether Arc is essential for controlling the critical period of plasticity during normal brain development," says lead investigator on the study Jason Shepherd.

In search of an answer, the researchers first looked at the correlation between the activation of the Arc gene in the visual cortex, and the visual plasticity of the brain. A parallel was indeed observed between the two factors – both peaking in teen mice and falling by middle-age. After extending the availability of the Arc gene in a sample of middle aged mice, the window of plasticity was shown to remain open for longer.

The most surprising part of the study came when the researchers used viruses to deliver the Arc gene to older mice whose plasticity had markedly begun to reduce. These mice started to dynamically respond to altered visual stimulation in the same way as younger mice.

"It was incredible to see that in adult mice, who have gone through normal development and aging, simply overexpressing Arc with a virus restored plasticity," says co-first author Kyle Jenks.

How exactly the gene restores brain plasticity is one of the key questions the researchers will be looking to now answer. It is generally understood that brain plasticity declines as we age because our inhibitory neurons become stronger and more mature. The discovery that the Arc gene can drastically alter, and even reverse this process, offers scientists an entirely new insight into how to potentially stop age-related cognitive decline.

Much still needs to be discovered regarding the function of the Arc gene, and the team still don't know if this effect can be translated into human studies or whether Arc regulates the plasticity of other neurological functions, such as memory or repair. Still, this is another compelling study giving hope for the development of treatments that could repair or reverse age-related cognitive decline.

The study was published in the journal Proceedings of the National Academy of Sciences (PNAS).

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