Characterisation of NLRP3 pathway-related neuroinflammation in temporal lobe epilepsy.

ABSTRACT:

Objective

Inflammation of brain structures, in particular the hippocampal formation, can induce neuronal degeneration and be associated with increased excitability manifesting as propensity for repetitive seizures. An increase in the abundance of individual proinflammatory molecules including interleukin 1 beta has been observed in brain tissue samples of patients with pharmacoresistant temporal lobe epilepsy (TLE) and corresponding animal models. The NLRP3-inflammasome, a cytosolic protein complex, acts as a key regulator in proinflammatory innate immune signalling. Upon activation, it leads to the release of interleukin 1 beta and inflammation-mediated neurodegeneration. Transient brain insults, like status epilepticus (SE), can render hippocampi chronically hyperexcitable and in

SUBMITTER: Pohlentz MS 

PROVIDER: S-EPMC9380933 | biostudies-literature | 2022

REPOSITORIES: biostudies-literature