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Prescription drug restores lost memories in mice

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Extracting memories and anecdotes from information can be difficult even at the best of times, and even more so when you’re sleep deprived.

But what if there was a way to reverse memory loss and restore those unreliable memories?

A new study in mice suggests that “forgotten” memories can be retrieved after a few days by activating certain brain cells or by using a drug commonly used in humans to treat chronic obstructive pulmonary disease (COPD), a group of diseases that affect the lungs and airways. including These include emphysema, chronic bronchitis and asthma.

And that may sound crazy, but it’s not that crazy when you consider how memory is somehow chemically encoded in brain cells.

While being able to replicate this in humans is somewhat fantastic, the study does reveal something about the new memories we thought we lost during our sleepless nights.

Previous research has shown how even short periods of sleep deprivation affect memory processes by altering protein levels and brain cell structure. But researchers are still unsure whether lack of sleep impairs information storage, making it harder to access it later.

This was the first question that University of Groningen neuroscientist Robert Hux and colleagues set out to answer, using rats that were deprived of sleep for 6 hours after examining a cage with several objects.

A few days later, the animals could not detect that the object had been moved to a new position, unless some neurons in the hippocampus, a sensitive area of ​​the brain that stores spatial information and consolidates memories, were activated by light.

This shows that mice can remember where the original objects are if the neurons in the hippocampus that encode this information are activated. “In reality, the information was stored in the brain, but it was difficult to retrieve it,” Hukix explains.

The findings suggest that memories thought to be “lost” may still exist in an inaccessible state that can only be recovered artificially, at least in mice.

But the technology used to do this, optogenetics, is an experimental approach that requires genetic modification (to make cells sensitive to light), and is therefore a long way from being used in humans.

To try more in mice with a less invasive approach, the researchers turned to a chronic obstructive pulmonary disease drug called roflumilast. Among its various pharmacological effects, the increase in the level of a specific cellular signaling molecule decreases when memory is impaired due to lack of sleep.

“When we gave roflumilast-trained sleep-deprived mice just before the second test, they remembered exactly the same as when they were directly stimulated with neurons,” says Hakix.

The memory recovery effect of roflumilast was evident 5 days after initial training and even longer when both drugs and photoactivation were used.

For centuries, scientists have speculated and then searched for networks of brain cells that they believed hold individual memories. The coherence and strength of these networks, called engrams, is considered the key to the storage of memories.

The existence of engrams as the basic unit of memory is sometimes questioned. But research on memory engrams has recently seen a resurgence when scientists have the right tool for manipulating individual populations of brain cells: optogenetics.

Using optogenetics, the researchers induced the fear-related “freeze” response in mice by reactivating a subset of hippocampal neurons that were active during the previous fear.

They also implanted a false memory that made mice fear being kicked in the absence of environmental cues, and even stimulated memory recovery in amnesic mice, which are a model for early Alzheimer’s disease.

While this is still only the field of animal research, the long-term goal of this type of research is to understand how information is acquired, stored, and reproduced in humans, and perhaps someday find a way to help humans.

The study is published in the journal Current Biology.

Source: Science Alert

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