Do you ever find yourself heading to the fridge only to forget why you went there in the first place? That’s a common occurrence as we age and our memory worsens.
Now, there could be a new treatment for middle-aged memory loss on the horizon and it comes in the shape of an HIV drug. University of California, Los Angeles (UCLA) researchers have discovered a key molecular mechanism behind memory linking and found a way to restore this brain function in middle-aged mice through an FDA-approved drug, according to a press release published by the institution on Wednesday.
Strengthening human memory in middle age
“Our memories are a huge part of who we are,” explained Alcino Silva, a distinguished professor of neurobiology and psychiatry at the David Geffen School of Medicine at UCLA. “The ability to link related experiences teaches how to stay safe and operate successfully in the world.”
The new research offers the possibility of finding a new method for strengthening human memory in middle age and preventing dementia. It all has to do with a gene called CCR5.
Silva’s lab had found in earlier research that CCR5 expression reduced memory recall. Essentially, in the experiments, it messed with the central mechanism underlying mice’s ability to link their memories of two different cages.
The researchers amplified CCR5 gene expression in the brains of middle-aged mice to see the effect and found that it did indeed interfere with memory linking. When lots of CCR5 was present, the animals forgot the connection between the two cages.
To confirm this hypothesis, the scientists then proceeded to delete the CCR5 gene in the animals. Once that was done, the mice were then able to link memories that normal mice could not.
Using an HIV drug for memory boosting
So, where does the HIV drug come into the picture?
Silva and his team had conducted previous experiments with the drug maraviroc, which the U.S. Food and Drug Administration approved in 2007 for the treatment of HIV. The researchers found that maraviroc also successfully suppressed CCR5 in the brains of mice.
“When we gave maraviroc to older mice, the drug duplicated the effect of genetically deleting CCR5 from their DNA,” said Silva, a member of the UCLA Brain Research Institute. “The older animals were able to link memories again.”
But why does the brain produce a gene that interferes with memory in the first place? Silva said it could be to keep us sane by forgetting what is no longer useful or relevant to us.
“Life would be impossible if we remembered everything,” said Silva. “We suspect that CCR5 enables the brain to connect meaningful experiences by filtering out less significant details.”
Now, Silva hopes to undertake clinical trials to test maraviroc’s effectiveness in preventing and reversing memory loss.
“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,” said Silva. “Once we fully understand how memory declines, we possess the potential to slow down the process.”
Could this HIV drug be the key to effective memory loss prevention and reversal?