When University of California, San Francisco scientists introduced the mutation to mice, the animals required 31 minutes less sleep daily. The modified enzyme showed highest activity in brain synapses, suggesting it might support brain homeostasis — the resetting process thought to occur during sleep.
“These people, all these functions our bodies are doing while we are sleeping, they can just perform at a higher level than we can,” said Ying-Hui Fu, the study’s co-author. This marks the fifth mutation across four genes identified in naturally short sleepers. Fu’s team hopes these discoveries could eventually lead to treatments for sleep disorders by revealing how sleep regulation functions in humans.
