TRAIL-R Deficient Mice Are Protected from Neurotoxic Effects of Amyloid-β.

ABSTRACT: TRAIL, a member of TNF superfamily, is a potent inducer of neuronal death. Neurotoxic effects of TRAIL appear mediated by its death receptor TRAIL-R2/DR5. To assess the role of TRAIL/TRAIL-R2 pathway in AD-related neurodegeneration, we studied the impact of the treatment with amyloid-β (Aβ) upon cell viability and inflammation in TRAIL-R-deficient mice (TRAIL-R^-/-). Here, we demonstrate that the lack of TRAIL-R2 protects from death cultured TRAIL-R^-/- mouse embryonic hippocampal cells after treatment with either Aβ1-42 or TRAIL. Consistently, stereotaxic injection of Aβ1-42 resulted in blunted caspase activation, as well as in reduction of JNK phosphorylation and increased AKT phosphorylation in TRAIL-R^-/- mice. Moreover, the lack of TRAIL-R2 was associated

SUBMITTER: Di Benedetto G 

PROVIDER: S-EPMC9569968 | biostudies-literature | 2022 Oct

REPOSITORIES: biostudies-literature