β-amyloid accumulation enhances microtubule associated protein tau pathology in an APP^NL-G-F/MAPT^P301S mouse model of Alzheimer's disease.

ABSTRACT:

Introduction

The study of the pathophysiology study of Alzheimer's disease (AD) has been hampered by lack animal models that recapitulate the major AD pathologies, including extracellular -amyloid (A) deposition, intracellular aggregation of microtubule associated protein tau (MAPT), inflammation and neurodegeneration.

Methods

The humanized APP^NL-G-F knock-in mouse line was crossed to the PS19 MAPT^P301S, over-expression mouse line to create the dual APPNL-G-F/PS19 MAPTP301S line. The resulting pathologies were characterized by immunochemical methods and PCR.

Results

We now report on a double transgenic APP^NL-G-F/PS19 MAPT^P301S mouse that at 6 months of age exhibits robust A plaque accumulation, intense MAPT pathology, strong

SUBMITTER: Jiang L 

PROVIDER: S-EPMC10987964 | biostudies-literature | 2024

REPOSITORIES: biostudies-literature