Our brains remember a collective storage of memories rather than single recollections, according to a new study from the University of California – Los Angeles Health Sciences. As a result, recalling one meaningful memory may prompt an individual to recall others that are linked in time. As we become older, our brains lose the ability to connect memories together.
UCLA scientists have now found a critical chemical process that underpins memory linkage. They’ve also discovered a means to restore this brain function in middle-aged rats, as well as an FDA-approved medicine to do it. The findings, which were published in Nature, reveal a novel strategy for improving human memory in middle age and a possible early intervention for dementia.
“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.”
A quick reminder of Biology 101: cells are densely packed with receptors. A chemical must latch onto its corresponding receptor to get entry to a cell, which works like a doorknob.
The UCLA researchers focused on a gene called CCR5, which codes for the CCR5 receptor, which HIV uses to infect brain cells and cause memory loss in AIDS patients.
CCR5 expression was shown to impair memory recall in Silva’s lab’s previous research.
Silva and his colleagues uncovered a crucial mechanism behind mice’s capacity to connect memories from two distinct cages in the current investigation. The scientists were able to observe neurons firing and creating new memories thanks to a tiny microscope that provided a window into the animals’ brains.
Memory linking was disrupted when CCR5 gene expression was increased in the brains of middle-aged mice. The animals had forgotten that the two cages were connected.
When the CCR5 gene was removed from the mice, they were able to associate memories that normal mice couldn’t.
“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.”
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.”
The study was financed by the National Institute on Aging. The paper was co-authored by UCLA postdoctoral researchers Yang Shen and Miou Zhou, who are now assistant professors at Western University.
