The researchers also measured neuronal signaling in the mice, and particularly long-term potentiation (LTP), which is thought to be the cellular basis for learning and memory.
In female experimental mice, the onset of symptoms coincided with a reduction in LTP, compared with wild-type mice, the researchers found. However, after treatment to restore the gene function, LTP in the experimental mice was indistinguishable from wild-type.
"Like many other people, we expected that giving MECP2 to mice that were already sick would not work," Dr. Bird said. "The idea that you could put back an essential component after the damage to the brain is done and recover an apparently normal mouse seemed farfetched."
Yet, he added, "the results are gratifyingly clear, and must give hope to those who are affected by this distressing disorder."