GSK-3β and ERK1/2 incongruously act in tau hyperphosphorylation in SPS-induced PTSD rats.

ABSTRACT: Post-traumatic stress disorder (PTSD) manifests in neurocognitive deficits in association with increased tau deposition, which mainly consist of phosphorylated tau in Alzheimer disease (AD) brain. However, the exact mechanism of PTSD inducing tau hyperphosphorylation remains unclear and therefore no effective treatment options are currently available. We here show that employing single prolonged stress (SPS), as a consensus PTSD model, induced a typical anxiety and abnormal hyperphosphorylation of tau at Ser202/Thr205 (AT8) and Ser404 but not at Ser199 and Ser396 in the hippocampus compared to the control rats. Furthermore, there was a decrease in the level of inactivated phosphorylated GSK-3β at Ser9, an increase in the level of activated phosphorylated GSK-3β at Thr216 and an obvious dec

SUBMITTER: Wei Z 

PROVIDER: S-EPMC6782009 | biostudies-literature | 2019 Sep

REPOSITORIES: biostudies-literature