Deletion of Abi3/Gngt2 influences age-progressive amyloid β and tau pathologies in distinctive ways.

ABSTRACT:

Background

The S209F variant of Abelson Interactor Protein 3 (ABI3) increases risk for Alzheimer's disease (AD), but little is known about its function in relation to AD pathogenesis.

Methods

Here, we use a mouse model that is deficient in Abi3 locus to study how the loss of function of Abi3 impacts two cardinal neuropathological hallmarks of AD-amyloid β plaques and tau pathology. Our study employs extensive neuropathological and transcriptomic characterization using transgenic mouse models and adeno-associated virus-mediated gene targeting strategies.

Results

Analysis of bulk RNAseq data confirmed age-progressive increase in Abi3 levels in rodent models of AD-type amyloidosis and upregulation in AD patients relative to healthy controls. Using RNAscope in situ hybrid

SUBMITTER: Ibanez KR 

PROVIDER: S-EPMC9327202 | biostudies-literature | 2022 Jul

REPOSITORIES: biostudies-literature