Our brains don’t usually store a single memory. Instead, they retain memories in groups so that the recall of one key memory prompts the recall of others that are chronologically associated. However, as we become older, our brains lose the ability to link memories together.

UCLA scientists have now found a critical chemical mechanism that underpins memory linkage. They’ve also discovered a means to genetically restore this brain function in aging rats, as well as an FDA-approved medicine that does the same thing.

The findings, which were published in the journal Nature, point to a new strategy for improving human memory in middle age as well as a potential early dementia intervention.

“Our memories are a huge part of who we aree,” noted Alcino Silva, one of the study’s authors. “The ability to link related experiences teaches us how to stay safe and operate successfully in the world.”

A quick refresher on biology: brain cells are densely packed with receptors. A chemical must latch onto a certain receptor to get entry to a cell, which functions similarly to a doorknob. The UCLA researchers focused on a gene that codes for a CCR5 molecular receptor, which is the same receptor that HIV uses to infect brain cells and cause memory loss in AIDS patients.

The amount of CCR5 expressed in the brain increases with age, and higher CCR5 gene expression impairs memory recall, as Silva’s lab has shown in previous study.

In the current work, Silva and his colleagues identified a critical mechanism behind the ability of mice to integrate memories of encounters in two distinct cages. The scientists were able to witness neurons activating and establishing new memories thanks to a tiny microscope that provided a window into the animals’ brains.

The researchers discovered that increasing CCR5 gene expression in mice’s brains interfered with memory linkage. The animals had forgotten that the two cages were connected. When the CCR5 gene was removed from the mice, the mice were able to associate memories that normal mice couldn’t.

Silva had already looked into the drug maraviroc, which is used to treat HIV infection and was approved by the U.S. Food and Drug Administration in 2007. In his lab, they discovered that maraviroc also stopped CCR5 from working in the brains of mice.

“When we gave maraviroc to older mice, the drug duplicated the effect of genetically deleting CCR5 from their DNA,” adds the author. “The older animals were able to link memories again.”

The findings imply that, in addition to treating HIV-related cognitive deficiencies, maraviroc could also be utilized to help recover middle-aged 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,” says Silva, adding  “Once we fully understand how memory declines, we’ll possess the potential to slow down the process.”

Consequently, this prompts the question: why does the brain require a gene that impedes its capacity to associate memories?

“Life would be impossible if we remembered everything,” Silva says. “We suspect that CCR5 enables the brain to connect meaningful experiences by filtering out insignificant details.”

Image Credit: Getty

You were reading: Scientists Find A New Way To Restore Lost Memories In Middle Age People