Topic: epileptogenic networks

Temporal lobe epilepsy (TLE) is one of the most common forms of drug-resistant epilepsy and its precise etiology is still unknown making it imperative to understand the molecular pathways contributing to the disease. It is, therefore, crucial to study the therapeutic targets and signalling pathways involved in the treatment of this disease. Pyk2 has previously been shown to be activated in stress-mediated pathways in the brain. Consequently, we hypothesized that Pyk2 activation might contribute to the pathogenesis of the disease. A pilocarpine model of TLE was used to examine p-Pyk2Tyr402 prot

Temporal lobe epilepsy (TLE) is a neurological disorder associated with spontaneously recurrent seizures with about 30% of the patients exhibiting pharmacoresistant. Thus, it is imperative to understand the molecular mechanisms underlying the pathogenesis of TLE to develop an effective treatment strategy. Several neurological disorders are associated with Histone deacetylase 4 (HDAC4) dysregulation, but its specific molecular substrates and the precise mechanism by which it contributes to TLE are unknown. Thus, in our study, we used the lithium-pilocarpine model of TLE and samples resected fro

Tuberous sclerosis complex (TSC) is a genetic disorder where many patients affected by the disease suffer from refractive epilepsy. To alleviate related symptoms, the patients must undergo surgery to resect the epileptogenic lesion. Obtaining this tissue and instantly flash freeze it provides a unique opportunity to gain insight to the pathogenesis of TSC.Thus, we embarked on an in-depth unbiased characterization of the transcriptomic landscape, cellular identify, and potential epileptogenic networks of frontal cortical tubers of pediatric TSC using snRNA-seq on resected epileptic tissue and c