Our brain usually stored memories into groups so that the recollection of one significant memory triggers the recall of others connected by time and they rarely record single memories. But, as we age our brains gradually lose this ability to link related memories.
In such, UCLA researchers have recently discovered a key molecular mechanism behind memory linking. They’ve also identified a way to restore this brain function in middle-aged mice – and an FDA-approved drug that achieves the same thing.
The findings, which are published in Nature, suggest a new method for strengthening human memory in middle age and a possible early intervention for dementia.
Alcino Silva, an author of the research and a distinguished professor of neurobiology and psychiatry at the David Geffen School of Medicine at UCLA said that our memories are a huge part of who we are and the ability to link related experiences teaches how to stay safe and operate successfully in the world.
According to the researchers, cells are studded with receptors. To enter a cell, a molecule must latch onto its matching receptor, which operates like a doorknob to provide access inside.
The UCLA team said they focused on a gene called CCR5 that encodes the CCR5 receptor – the same one that HIV hitches a ride on to infect the brain cell and cause memory loss in AIDS patients.
Silva’s lab demonstrated in earlier research that CCR5 expression reduced memory recall.
In the ongoing study, Silva and his workmates discovered a central mechanism underlying mice’s ability to link their memories of two different cages. A tiny microscope opened a window into the mice’s brain. This enabled the scientists to observe neurons firing and creating new memories.
The memory linking was interfered by boosting CCRS gene expression in the brains of middle-aged mice. The mice forgot the connection between the two cages.
When the scientists deleted the CCR5 gene in the animals, the mice were able to link memories that normal mice could not.
Silva had previously studied maraviroc (a drug). This drug was approved by the U.S. Food and Drug Administration in 2007 for the treatment of HIV infection. Silva’s lab discovered that maraviroc also suppressed CCR5 in the brains of mice.
Silva said, “When we gave maraviroc to older mice, the drug duplicated the effect of genetically deleting CCR5 from their DNA.” The older mice were able to link memories again.
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The finding suggests that maraviroc could be used off-label to help restore middle-aged memory loss, as well as undo the cognitive deficits caused by HIV infection.
He also states, “Our next step will be to organize a clinical trial to test maraviroc’s influence on early memory loss with the goal of early intervention.” “Once we fully understand how memory declines, we possess the potential to slow down the process.”
Which begs the question, why does the brain need a gene that interferes with its ability to link memories?