Study Pinpoints Potential “Master Regulator” of Age-Related Cognitive Decline

Upping a gene’s expression in rat brains made them better learners and normalized the activity of hundreds of other genes to resemble the brains of younger animals.

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A rat hippocampusWIKIMEDIA, BLACKNICKFor more than three decades, Philip Landfield has been chipping away at a central question, namely, “why the electrophysiology of hippocampal connections is impaired in aged animals,” as the University of Kentucky neuroscientist puts it. It’s far from an esoteric problem, given that electrical impulses sent across neuronal connections strengthens synapses over time, forming the physical basis of learning and memory—meaning that less-efficient electrical transmissions are linked to cognitive decline.

With a study published today (December 18) in the Journal of Neuroscience, Landfield says he thinks his team is now close to finally getting to the bottom of the phenomenon that caught his attention in the late 1970s. The answer, according to the new study, involves a family of genes known as FKBP and its regulation of calcium release within neurons. What they found was that increasing expression of one of the genes enhanced the rats’ learning ability and altered the expression levels of hundreds of other genes normally affected by aging, bringing them back to activities typical of younger animals.

“We’re . . . fascinated by the fact that just restoring this one molecule can reverse so many aspects of brain aging,” Landfield says.

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Meet the Author

  • Shawna Williams

    Shawna was an editor at The Scientist from 2017 through 2022. She holds a bachelor's degree in biochemistry from Colorado College and a graduate certificate and science communication from the University of California, Santa Cruz.
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