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dc.contributor.authorKahanovitch, Uri
dc.contributor.authorPatterson, Kelsey C.
dc.contributor.authorHernandez, Raymundo
dc.contributor.authorOlsen, Michelle L.
dc.date.accessioned2019-08-09T12:25:58Z
dc.date.available2019-08-09T12:25:58Z
dc.date.issued2019-08-05
dc.identifier.citationKahanovitch, U.; Patterson, K.C.; Hernandez, R.; Olsen, M.L. Glial Dysfunction in MeCP2 Deficiency Models: Implications for Rett Syndrome. Int. J. Mol. Sci. 2019, 20, 3813.
dc.identifier.urihttp://hdl.handle.net/10919/93016
dc.description.abstractRett syndrome (RTT) is a rare, X-linked neurodevelopmental disorder typically affecting females, resulting in a range of symptoms including autistic features, intellectual impairment, motor deterioration, and autonomic abnormalities. RTT is primarily caused by the genetic mutation of the Mecp2 gene. Initially considered a neuronal disease, recent research shows that glial dysfunction contributes to the RTT disease phenotype. In the following manuscript, we review the evidence regarding glial dysfunction and its effects on disease etiology.en_US
dc.format.mimetypeapplication/pdf
dc.language.isoen
dc.publisherMDPI
dc.rightsCreative Commons Attribution 4.0 Internationalen
dc.rights.urihttp://creativecommons.org/licenses/by/4.0/en
dc.titleGlial Dysfunction in MeCP2 Deficiency Models: Implications for Rett Syndromeen_US
dc.typeArticle - Refereed
dc.date.updated2019-08-09T08:01:55Z
dc.contributor.departmentSchool of Neuroscienceen_US
dc.title.serialInternational Journal of Molecular Science
dc.identifier.doihttps://doi.org/10.3390/ijms20153813
dc.type.dcmitypeText


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Creative Commons Attribution 4.0 International
License: Creative Commons Attribution 4.0 International