Inflammatory mechanisms contribute to the neurological manifestations of tuberous sclerosis complex.

ABSTRACT: Epilepsy and other neurological deficits are common, disabling manifestations of the genetic disorder, tuberous sclerosis complex (TSC). Brain inflammation has been implicated in contributing to epileptogenesis in acquired epilepsy due to brain injury, but the potential role of inflammatory mechanisms in genetic epilepsies is relatively unexplored. In this study, we investigated activation of inflammatory mediators and tested the effects of anti-inflammatory treatment on epilepsy in the Tsc1-GFAP conditional knock-out mouse model of TSC (Tsc1(GFAP)CKO mice). Real-time quantitative RT-PCR, immunohistochemistry, and Western blotting demonstrated increased expression of specific cytokines and chemokines, particularly IL-1β and CXCL10, in the neocortex and hippocampus of Tsc1(GFAP)CKO mice, wh

SUBMITTER: Zhang B 

PROVIDER: S-EPMC4468035 | biostudies-literature | 2015 Aug

REPOSITORIES: biostudies-literature