Rudolf Jaenisch of the Whitehead Institute of Biomedical
Research in Cambridge, MA reports in the April 6, 2004 online
issue of the Proceedings of the National Academy of Sciences
that introduction of the MeCP2 protein into post-mitotic nerve
cells of MeCP2 mutant mice rescues the symptoms of Rett
Syndrome. This raises the possibility that neurons are
functionally normal in a newborn child and that neural
dysfunction manifests itself only later due to prolonged MeCP2
deficiency. If correct, therapeutic strategies aimed at
preventing the onset of Rett symptoms could be initiated at
birth. This project was funded by the Rett Syndrome Research
Foundation (RSRF) and the National Institutes of Health (NIH).
Rett Syndrome (RTT) is a severe neurological disorder diagnosed
almost exclusively in girls. Children with RTT appear to develop
normally until 6 to 18 months of age, when they enter a period
of regression, losing speech and motor skills. Most develop
repetitive hand movements, irregular breathing patterns, sei