Open AccessIncreased expression of Fragile X mental retardation protein in malformative lesions of patients with focal cortical dysplasia
Author(s) -
Conner D. Reynolds,
Suzanne O. Nolan,
Gregory D. Smith,
Taylor S. Jefferson,
Samantha L. Hodges,
Amy L. Brewster,
Joaquín N. Lugo
Publication year - 2020
Publication title -
neuroreport/neuroreport
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.607
H-Index - 188
eISSN - 1473-558X
pISSN - 0959-4965
DOI - 10.1097/wnr.0000000000001517
Subject(s) - cortical dysplasia , wnt signaling pathway , pi3k/akt/mtor pathway , epilepsy , dysplasia , protein kinase b , biology , pathology , neuroscience , medicine , phosphorylation , signal transduction , microbiology and biotechnology
Focal cortical dysplasia (FCD) accounts for nearly half of all cases of medically refractory epilepsy in the pediatric and adult patient populations. This neurological disorder stems from localized malformations in cortical brain tissue due to impaired neuronal proliferation, differentiation, and migration patterns. Recent studies in animal models have highlighted the potential role of the Fragile X mental retardation protein (FMRP) levels in FCD. The purpose of this study was to investigate the status of FMRP activation in cortical brain tissues surgically resected from patients with FCD. In parallel, this study also investigated protein levels within the PI3K/AKT/mTOR and canonical Wnt signaling pathways.