Evidence of tumor necrosis factor receptor 1 signaling in human temporal lobe epilepsy

Elevated p53 and lower MDM2 expression in hippocampus from patients with intractable temporal lobe epilepsy

“…Finally, p53 may also have roles in signalling unrelated to cell death. Indeed, while only a subset of p53 target genes have been studied to date in human TLE, expressional differences were not found for apoptosis-associated death receptor 5 or Bid Yamamoto et al, 2006b). Of particular interest in the setting of intractable epilepsy might be p53-mediated regulation of neurite growth and expression of genes involved in axon guidance (Arakawa, 2005).…”

“…Simulated post mortem delay experiments were undertaken as previously described (Yamamoto et al, 2006b). Animal procedures were approved by the Research Ethics Committee of the Royal College of Surgeons in Ireland.…”

Temporal Lobe Epilepsy: Cell Death and Molecular Targets

“…The importance of the Bcl-2 family in human epilepsy has been studied extensively. Elevated Bcl-w, reduced Bim and normal levels of Bcl-xl, Bax, Bad and Bid have been reported in the hippocampus obtained from patients with intractable seizures (Murphy et al, 2007;Shinoda et al, 2004, Yamamoto et al, 2006a. Serum analysis has also provided indirect evidence for the modulation of Bcl-2 in patients with epilepsy (El-Hodhod et al, 2006).…”

“…The secondary role of the extrinsic pathway in cell death during seizures was demonstrated by the presence of caspase-8 cleavage in the early stages following the seizures (Henshall et al, 2001). The cleavage of a select group of caspases (-3, -7, -8 and -9) was detected in the hippocampus of rats after repeated electroshock seizures, indicating that the progression of apoptosis signaling may occur (Yamamoto et al, 2006b, Yamamoto et al, 2006c. In addition, activated TNFR1 and DISC were detected in a seizure-damaged hippocampus from rats Shinoda et al, 2003), and patients with TLE (Yamamoto et al, 2006).…”

Insights into inflammation and epilepsy from the basic and clinical sciences

“…33,35 Patients with treatment-resistant (or refractory) epilepsy also display a highly pro-inflammatory cytokine profile in the circulation, including high IL-6, low IL-1Ra and low IL-1Ra/IL-1b ratio. 62 Liimatainen et al 34 found increased serum levels of IL-6 in patients with refractory epilepsy and higher levels in patients with temporal lobe epilepsy (TLE) when compared to patients with extra-TLE, suggesting a chronic immune mechanism in refractory epilepsy and the influence of clinical parameters in cytokine overproduction.…”