P47^phox deficiency improves cognitive impairment and attenuates tau hyperphosphorylation in mouse models of AD.

ABSTRACT:

Background

Alzheimer's disease (AD) is characterized by progressive memory loss and cognitive impairment. The aggregation of amyloid β (Aβ) and hyperphosphorylated tau protein are two major pathological features of AD. Nicotinamide adenine dinucleotide phosphate oxidase (NADPH oxidase, NOX) has been indicated in Aβ pathology; however, whether and how it affects tau pathology are not yet clear.

Methods

The role of NOX2 in cognitive function, amyloid plaque formation, and tau hyperphosphorylation were examined in APP/PS1 transgenic mice mated with p47^phox-deficient mice (with deletion of the gene of neutrophil cytosolic factor 1, Ncf1) and/or in p47^phox-deficient mice receiving intracerebroventricular (ICV) injection of streptozotocin (STZ). The cognitive

SUBMITTER: Gong P 

PROVIDER: S-EPMC7659091 | biostudies-literature | 2020 Nov

REPOSITORIES: biostudies-literature