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The human brain stores memories into groups so that remembering one significant memory activates the recollection of others connected by time. As people age, their brains slowly fail to link interconnected memories.
Now UCLA researchers discovered a critical molecular agent behind memory linking. They pinpointed a way to revitalize this brain function in middle-aged mice with an approved FDA drug.
The discoveries published in the Nature science journal suggest a novel method for strengthening middle-aged human memory and possible early dementia intervention. Alcino Silva, a prominent psychiatrist, and neurobiologist at the UCLA David Geffen School of Medicine said:
The ability to link related experiences teaches how to stay safe and operate successfully in the world.
The UCLA team concentrated on a CCR5 gene—the same one that HIV hitches a ride to infect the AIDS patient’s brain cell and cause memory loss.
Silva’s lab demonstrated that CCR5 expression lessened memory recall in earlier research. Silva and his colleagues uncovered a central mechanism underlying the mice’s capability to connect their memories in the current study.
Elevating CCR5 gene expression in the middle-aged mice’s brain interrupted memory linking. When the CCR5 gene was deleted, the mice could link memories.
Silva had previously studied the maraviroc drug, which the U.S. FDA approved in 2007 for HIV infection treatment. His lab discovered that maraviroc suppressed CCR5 in the mice’s brains.
The result suggests that maraviroc could restore middle-aged memory loss and reverse the mental depletion caused by HIV infection.
Their next step is to test maraviroc’s influence on early intervention of memory loss. Sliva suspects that CCR5 enables the brain to filter less important details and only connect meaningful experiences.
The National Institute on Aging funded the research, and UCLA postdoctoral researchers Miou Zhou and Yang Shen coauthored the study.
Written by Janet Grace Ortigas
Edited by Sheena Robertson
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