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2012;12 Suppl 1:S37-51

The deficiencies in GABA receptor expression and GABA receptor-mediated inhibition have been demonstrated in fragile X animal models, linking GABA receptors to fragile X phenotypes and leading to the hypothesis that fragile X syndrome may result from an imbalance between excitation and inhibition, and increasing inhibition may ameliorate some fragile X pathophysiologies, including dysregulated protein synthesis (DHulst et al., 2006, 2009

Measurement of the selected biochemical markers, including oxidative stress biomarkers [glutathione-S-transferase (GST), catalase, lipid peroxide, glutathione (GSH) and vitamin C] and EAAT2, KCC2, KNCC1, GABA, VD3, glutamate and GABRA5 in the brain homogenates of the study groups was performed using a spectrophotometric and Enzyme-Linked Immunoassay (ELISA)

Medical guidance is safer than self-administering research chemicals

A stepwise model development workflow was used: A newly developed model for endogenous ACTH and cortisol was merged with a refined hydrocortisone pharmacokinetic model

Altered gut microbiome composition in children with refractory epilepsy after ketogenic diet