A role for glia in the progression of Rett’s syndrome

Daniel T. Lioy, Saurabh K. Garg, Caitlin E. Monaghan, Jacob Raber, Kevin D. Foust, Brian K. Kaspar, Petra G. Hirrlinger, Frank Kirchhoff, John M. Bissonnette, Nurit Ballas and Gail Mandel ()
Additional contact information
Daniel T. Lioy: Vollum Institute, Oregon Health and Science University
Saurabh K. Garg: Vollum Institute, Oregon Health and Science University
Caitlin E. Monaghan: Vollum Institute, Oregon Health and Science University
Jacob Raber: Oregon Health and Science University
Kevin D. Foust: The Ohio State University, Center for Gene Therapy, Nationwide Children’s Hospital
Brian K. Kaspar: The Ohio State University, Center for Gene Therapy, Nationwide Children’s Hospital
Petra G. Hirrlinger: Paul-Flechsig-Institute for Brain Research
Frank Kirchhoff: Max Planck Institute of Experimental Medicine
John M. Bissonnette: Oregon Health and Science University
Nurit Ballas: State University of New York
Gail Mandel: Vollum Institute, Oregon Health and Science University

Nature, 2011, vol. 475, issue 7357, 497-500

Abstract: Astrocytes targeted in Rett's syndrome Rett's syndrome, a disorder caused by loss of function of methyl CpG-binding protein 2 (MeCP2), is associated with various neurological symptoms on the autism spectrum. Although impaired neurons are the underlying cause of nervous system failure in Rett's syndrome, experiments in a mouse model show that the genetic correction of MeCP2 expression in glial cells — principally in astrocytes — can reverse three hallmark behaviour abnormalities of the neurological disorder. Neuronal morphology and neurotransmitter markers are also rescued, suggesting an interactive mechanism between glial and neuronal cells in Rett's syndrome initiation and progression.

Date: 2011
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DOI: 10.1038/nature10214

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