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Introduction of the 'Rett protein' in post-mitotic neurons rescues Rett Syndrome in mice

riment to determine the point at which nerve cells become dysfunctional in "Rett mice". Early in embryonic development precursor neuronal cells divide rapidly. As the brain cells mature they stop dividing and become post-mitotic. Dr. Jaenisch hooked the MECP2 gene to the Tau gene which is expressed only in post-mitotic neurons. Mutant Mecp2 mice that also expressed the Tau/Mecp2 transgene never manifested any of the Rett-like symptoms and developed normally.

The experiments also showed that introducing too much MeCP2, 4-6 fold, caused severe motor deficits. This will be an important issue as treatments are developed.

"These experiments lay the groundwork for the next key project: determining whether Rett Syndrome is reversible and if so identifying the appropriate time frame for MeCP2 re-introduction." shared Dr. Jaenisch.

"The announcement by Dr. Jaenisch and his colleagues is an important step towards realizing our mission of accelerating treatments and cures for Rett Syndrome. RSRF has financially supported Dr. Jaenisch's work since our inception and we are encouraged by the contributions he is making to the field", stated Gordy Rich, Chairman of the RSRF Board of Trustees.


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Contact: Monica Coenraads
monica@rsrf.org
203-445-9233
Rett Syndrome Research Foundation
7-Apr-2004


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