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MIT Researchers Believe Targeting Treatments to This Brain Circuit May Reverse Memory Decline


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MIT Researchers Believe Targeting Treatments to This Brain Circuit May Reverse Memory Decline

As we age, the retention power of our memory often degrades. This makes performing everyday tasks difficult. It gets very difficult to remember things. For instance, elderly people could forget by afternoon what they ate for breakfast. They may even find it difficult to recall a conversation they had with someone. One key brain region linked to this type of memory is the anterior thalamus, which is primarily involved in the recollection of our surroundings and how to navigate them. The thalamus is an egg-shaped structure in the middle of the brain whose primary function is to relay incoming sensory information — such as hearing, taste, sight, and touch — from the body to the brain. However, it does not relay information related to smell.

In a recent study on mice, researchers have identified a circuit in the anterior thalamus that is key to remembering how to navigate a maze. They found that this circuit is usually impaired in older mice. But if this circuit’s activity is enhanced, it greatly improves the ability of the mice to run the maze correctly.

The researchers at the Massachusetts Institute of Technology (MIT) focussed on this region of the brain in their study,

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in the Proceedings of the National Academy of Sciences, and say this could be an ideal target for treatments to reverse memory loss in elderly people.

They say if a non-invasive or minimally invasive technology is developed to target treatments in this part of the human brain, it could offer a way to help prevent age-related memory loss.

Guoping Feng, senior author of the study,

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that instead of influencing the prefrontal cortex, which has many distinct roles, they want to uncover more specific and druggable targets in this area by studying how the thalamus affects the cortical output.

An advantage of targeting the thalamus for treatments is that it limits possible disturbances to other parts of the brain.

We can trigger anxiety-related behaviour by directly activating neurons in the medial prefrontal cortex, but this will not happen with AV (anteroventral) activation, said Ying Zhang, lead author of the study.


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