English (United Kingdom)

https://curated-unify.zendy.io/wp-json/zendy-region/v1/featured_content/oa?rat=en

https://curated-unify.zendy.io/wp-json/zendy-region/v1/highlighted_journal/

Global: Zendy Plus annual

Presents the access of premium content as premium feature

Premium Content

Presents the keyphrase highlighting as premium feature

Keyphrase Highlighting

Presents the summarisation as premium feature

Summarisation

Insights

Presents the pdf analysis as premium feature

PDF Analysis

Presents the zaia usage as premium feature

ZAIA

Global: Zendy Plus monthly

Global: Zendy Tools annual

Global: Zendy Tools monthly

Global: Zendy Free Plan

Background  Recently, inflammatory cascades have been suggested as a target for epilepsy therapy. Positron emission tomography (PET) imaging offers the unique possibility to evaluate brain inflammation longitudinally in a non-invasive translational manner. This study investigated brain inflammation during early epileptogenesis in the post-kainic acid-induced  status epilepticus  (KASE) model with  post - mortem  histology and  in vivo  with [ 18 F]-PBR111 PET.    Methods   Status epilepticus  (SE) was induced ( N  = 13) by low-dose injections of KA, while controls ( N  = 9) received saline. Translocator protein (TSPO) expression and microglia activation were assessed with [ 125 I]-CLINDE autoradiography and OX-42 immunohistochemistry, respectively, 7 days post-SE. In a subgroup of rats, [ 18 F]-PBR111 PET imaging with metabolite-corrected input function was performed before  post - mortem  evaluation. [ 18 F]-PBR111 volume of distribution ( V  t ) in volume of interests (VOIs) was quantified by means of kinetic modelling and a VOI/metabolite-corrected plasma activity ratio.    Results  Animals with substantial SE showed huge overexpression of TSPO  in vitro  in relevant brain regions such as the hippocampus and amygdala ( P  < 0.001), while animals with mild symptoms displayed a smaller increase in TSPO in amygdala only ( P  < 0.001). TSPO expression was associated with OX-42 signal but without obvious cell loss. Similar  in vivo  [ 18 F]-PBR111 increases in  V  t  and the simplified ratio were found in key regions such as the hippocampus ( P  < 0.05) and amygdala ( P  < 0.01).    Conclusion  Both  post - mortem  and  in vivo  methods substantiate that the brain regions important in seizure generation display significant brain inflammation during epileptogenesis in the KASE model. This work enables future longitudinal investigation of the role of brain inflammation during epileptogenesis and evaluation of anti-inflammatory treatments.

PET imaging of brain inflammation during early epileptogenesis in a rat model of temporal lobe epilepsy