An American team of scientists has determined how the brain associates memories and, in experiments in mice, showed that an anti-HIV drug can combat memory loss in middle age.

The human brain rarely records individual memories, but instead stores them in groups, so remembering one important memory triggers the recall of others linked to time.

However, as we age, the brain gradually loses its ability to link related memories together.

Now researchers at the University of California, Los Angeles (UCLA) have discovered an important molecular mechanism for linking memories.

They’ve also identified a way to restore this brain function in middle-aged mice, and a drug approved by the U.S. Food and Drug Administration (FDA) that will do the same.

results, published Natureproposes a new method for enhancing human memory in middle age and a possible early intervention for dementia, summarizes a university paper.

“Our memories are a crucial part of who we are,” explains Alcino Silva, professor of neurobiology and psychiatry at UCLA. “The ability to connect related experiences teaches us to stay safe and navigate the world successfully.”

Cells are packed with receptors, and in order to enter a cell, a molecule must latch onto its corresponding receptor, which works like a doorknob for easy access inside.

The UCLA team focused on a gene called CCR5, which encodes the CCR5 receptor that HIV uses to infect brain cells and cause memory loss in AIDS patients.

Silva’s lab has shown in previous research that CCR5 activity reduces recall.

In the current study, the scientists uncovered a central mechanism underlying the mice’s ability to link their memories and found that increased expression of this gene in the brains of middle-aged mice interfered with the binding of these memories (the animals forgot the connection). two cages).

When the scientists disabled the CCR5 gene in one group of animals, they were able to connect memories that other mice couldn’t.

Silva previously worked on the drug maraviroc, which the FDA approved in 2007 for the treatment of HIV infection; lab found that it also suppressed CCR5 in the brains of mice.

“When we gave maraviroc to old mice, the drug doubled the effect of genetically deleting CCR5 from their DNA,” he says. “Older animals were able to reconnect memories.”

The finding suggests that maraviroc could be used to help reverse midlife memory loss as well as cognitive deficits caused by HIV infection.

“Our next step will be to organize a clinical trial to check its effect on early memory loss for the purpose of early intervention,” says Silva, emphasizing: “Once we fully understand how memory declines, we have the potential to slow down the process.”