Scientists have discovered a key molecular mechanism behind reminiscence linking. They’ve additionally found a technique to restore this mind perform in middle-aged mice – and an FDA-approved drug already exists that achieves the identical factor.
Scientists Identify How the Brain Links Memories
HIV drug may fight middle-aged reminiscence loss, analysis suggests.
Our brains seldom report single recollections—as an alternative, they retailer recollections into teams in order that the recollection of 1 vital reminiscence triggers the recall of others related by time. However, as we age, our brains progressively lose this capability to hyperlink associated recollections.
Now University of California, Los Angeles (UCLA) researchers have found a key molecular mechanism behind reminiscence linking. They’ve additionally recognized a technique to restore this mind perform in middle-aged mice – and an FDA-approved drug that achieves the identical factor.
Published right this moment (May 25, 2022) within the journal Nature, the findings recommend a brand new technique for strengthening human reminiscence in center age and a attainable early intervention for dementia.
“Our memories are a huge part of who we are,” defined Alcino Silva, a distinguished professor of neurobiology and psychiatry on 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.”
A little bit of Biology 101: cells are studded with receptors. To enter a cell, a molecule should latch onto its matching receptor, which operates like a doorknob to offer entry inside.
The UCLA group targeted on a gene referred to as CCR5 that encodes the CCR5 receptor—the identical one which HIV hitches a experience on to contaminate the mind cell and trigger reminiscence loss in AIDS sufferers.
Silva’s lab demonstrated in earlier analysis that CCR5 expression diminished reminiscence recall.
In the present examine, Silva and his colleagues found a central mechanism underlying mice’s capability to hyperlink their recollections of two completely different cages. A tiny microscope opened a window into the animals’ brains, enabling the scientists to look at neurons firing and creating new recollections.
Boosting CCR5 gene expression within the brains of middle-aged mice interfered with reminiscence linking. The animals forgot the connection between the 2 cages.
When the scientists deleted the CCR5 gene within the animals, the mice had been in a position to hyperlink recollections that standard mice couldn’t.
Silva had beforehand studied the drug, maraviroc, which the U.S. Food and Drug Administration accredited in 2007 for the remedy of HIV an infection. His lab found that maraviroc additionally suppressed CCR5 within the brains of mice.
“When we gave maraviroc to older mice, the drug duplicated the impact 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.”
The finding suggests that maraviroc could be used off-label to help restore middle-aged memory loss, as well as reverse the cognitive deficits caused by HIV infection.
“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.”
Which begs the question: why does the brain need a gene that interferes with its ability to link memories?
“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.”
Reference: “CCR5 closes the temporal window for memory linking” 25 May 2022, Nature.
DOI: 10.1038/s41586-022-04783-1
The National Institute on Aging funded the research. UCLA postdoctoral researchers Yang Shen and Miou Zhou, now an assistant professor at Western University, coauthored the study.
