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A role for glia in the progression of Rett syndrome
Date:6/29/2011

f MeCP2's presence in glia, Rett Syndrome was thought to be caused exclusively by MeCP2 deficiencies in neurons.

Mandel and Ballas and colleagues now show that in a mouse model of Rett Syndrome, re-expression of MeCP2 solely in astrocytes, in male mice at 4 weeks of age and in female mice between the ages of 5 to 7 months, rescues the lifespan, breathing, anxiety, and locomotor activities associated with the global knockout mice.

Mandel states: "The RTT plot now thickenswe need to think about contributions from multiple cell types to this disease. The idea that neurons and glia might serve different roles in Rett Syndrome, in initiation and progression of symptoms, is reminiscent of the situation in another neurological disorder, an inherited form of ALS. Thus, a role for glia may turn out to be a more common theme in many neurological diseases. It will be important to determine if other glial types play roles in RTT, and to further investigate how normal neurons and astrocytes interact, a currently active but controversial area".

First author Daniel Lioy (Howard Hughes Medical Institute, OHSU) comments, "Future studies will focus on trying to identify the key molecules in astrocytes that might mediate the rescue. These molecules may provide new avenues for targeted pharmacological intervention for Rett."

"This new and unexpected result by the Mandel lab reveals important clues regarding the function of MeCP2 and how its absence causes devastation. The Rett Syndrome Research Trust will continue to support high-level exploration with the conviction that understanding how this protein works will open new doors to treatment approaches," said Monica Coenraads, Executive Director of RSRT and mother to a daughter with Rett Syndrome.


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Contact: Monica Coenraads
monica@rsrt.org
203-445-0041
Rett Syndrome Research Trust
Source:Eurekalert

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