The hippocampal GFAP, synaptophysin and mGluR3 expressions where upregulated in PTZ rats with PFS history when compared to PTZ rats alone.These findings indicated that PFS may increase the severity of epilepsy and alter brain expression of GFAP, synaptophysin and mGluR3 proteins.
The hippocampal GFAP, synaptophysin and mGluR3 expressions where upregulated in PTZ rats with PFS history when compared to PTZ rats alone.These findings indicated that PFS may increase the severity of epilepsy and alter brain expression of GFAP, synaptophysin and mGluR3 proteins.
The hippocampal GFAP, synaptophysin and mGluR3 expressions where upregulated in PTZ rats with PFS history when compared to PTZ rats alone.These findings indicated that PFS may increase the severity of epilepsy and alter brain expression of GFAP, synaptophysin and mGluR3 proteins.
Analysis revealed that serum concentrations (calculated from DBS) within the respective reference ranges were attained in only 52.9% of the 68 Nodding syndrome patients treated with valproic acid, in 21.4% of the 56 Ugandan epilepsy patients treated with carbamazepine, and in 65.7% of the 137 onchocerciasis-associated epilepsy patients from the DRC treated with phenobarbital.
Analysis revealed that serum concentrations (calculated from DBS) within the respective reference ranges were attained in only 52.9% of the 68 Nodding syndrome patients treated with valproic acid, in 21.4% of the 56 Ugandan epilepsy patients treated with carbamazepine, and in 65.7% of the 137 onchocerciasis-associated epilepsy patients from the DRC treated with phenobarbital.
Importantly, our analysis showed KCNMA1 as a common gene signature with a link to epilepsy, movement disorders and wide paroxysmal neurological presentations-with the greatest potential risk of being a disease gene in a paroxysmal or psychiatric disorder.
We suggest that a strategy of augmenting KCC2 activity by antagonizing its critical inhibitory phosphorylation sites may be a particularly efficacious method of facilitating Cl<sup>-</sup> extrusion and restoring GABA inhibition to treat medication-refractory epilepsy and other seizure disorders.
These results may explain conflicting findings from previous studies that have reported both preserved and decreased PV bouton densities and establish a new standard for quantitative assessment of interneuron boutons in epilepsy.
Use of the mixed reality tool "VSI Patient Education" for more comprehensible and imaginable patient educations before epilepsy surgery and stereotactic implantation of DBS or stereo-EEG electrodes.
Use of the mixed reality tool "VSI Patient Education" for more comprehensible and imaginable patient educations before epilepsy surgery and stereotactic implantation of DBS or stereo-EEG electrodes.
The main findings of our study were: (a) TRPM2-KO had a protective effect on epilepsy; (b) TRPM2-KO improved spatial memory deficits overtime during epilepsy, but it did not improve anxiety; (c) the protective effect probably occurred via the PARP1 downstream signaling pathway; (d) TRPM2-KO could ameliorate epilepsy-induced hippocampal pathological damages and weaken astrocyte activation.
The transient receptor potential melastatin type 2 channel (TRPM2) is a Ca<sup>2+</sup>-permeable cation channel that contributes to cell apoptosis; its possible signaling pathway is the PARP1/BNIP3/AIF/Endo G pathway that may be related to epilepsy.
The transient receptor potential melastatin type 2 channel (TRPM2) is a Ca<sup>2+</sup>-permeable cation channel that contributes to cell apoptosis; its possible signaling pathway is the PARP1/BNIP3/AIF/Endo G pathway that may be related to epilepsy.
The transient receptor potential melastatin type 2 channel (TRPM2) is a Ca<sup>2+</sup>-permeable cation channel that contributes to cell apoptosis; its possible signaling pathway is the PARP1/BNIP3/AIF/Endo G pathway that may be related to epilepsy.
The gene associated with retinoid-interferon-induced mortality-19 (GRIM-19) plays several significant roles in cellular processes, including ATP synthesis, reactive oxygen species formation, and the regulation of glycolytic enzyme activity, which are closely related to the pathophysiological mechanisms of epilepsy.
The gene associated with retinoid-interferon-induced mortality-19 (GRIM-19) plays several significant roles in cellular processes, including ATP synthesis, reactive oxygen species formation, and the regulation of glycolytic enzyme activity, which are closely related to the pathophysiological mechanisms of epilepsy.
Among the 816 probands suspected hereditary epilepsy whose initial report of trio-based whole exome sequencing (WES) were negative, 10 de novo pathogenic or likely pathogenic variants of CSNK2B in nine probands were identified after reanalysis of their raw Trio-WES data.
Variants in the SCN1A gene are associated with a wide range of disorders including genetic epilepsy with febrile seizures plus (GEFS+), familial hemiplegic migraine (FHM), and the severe childhood epilepsy Dravet syndrome (DS).