Thorase deficiency causes both Aβ accumulation and tau hyperphosphorylation in mouse brain.

ABSTRACT:

Introduction

The pathogenesis of two major pathogenic characters-amyloid beta (Aβ) accumulation and hyperphosphorylated tau protein-in the brains of patients with Alzheimer's disease (AD) remains unclear.

Methods

Western blot and immunofluorescence staining were performed to detect the proteins in the brains of Thorase conditional knockout/transgenic mice and their littermates. A co-immunoprecipitation assay was applied to examine the Thorase-interacting proteins.

Results

Genetic deletion of Thorase resulted in tau hyperphosphorylation and promoted Aβ accumulation in the mouse brain. Conversely, Thorase overexpression alleviated the pathogenesis of AD. Thorase regulated the phosphorylation of tau by targeting specific kinases and theprotein phosphatase 2B (PP2B). Thor

SUBMITTER: Zhang H 

PROVIDER: S-EPMC11667493 | biostudies-literature | 2024 Dec

REPOSITORIES: biostudies-literature