Mitochondrial Alterations in Neurons Derived from the Murine AppNL-F Knock-In Model of Alzheimer's Disease.

ABSTRACT:

Background

Alzheimer's disease (AD) research has relied on mouse models overexpressing human mutant A βPP; however, newer generation knock-in models allow for physiological expression of amyloid-β protein precursor (AβPP) containing familial AD mutations where murine AβPP is edited with a humanized amyloid-β (Aβ) sequence. The AppNL-F mouse model has shown substantial similarities to AD brains developing late onset cognitive impairment.

Objective

In this study, we aimed to characterize mature primary cortical neurons derived from homozygous AppNL-F embryos, especially to identify early mitochondrial alterations in this model.

Methods

Primary cultures of AppNL-F neurons kept in culture for 12-15 days were used to measure Aβ levels, secretase activity, mitochondrial fun

SUBMITTER: Dentoni G 

PROVIDER: S-EPMC9697055 | biostudies-literature | 2022

REPOSITORIES: biostudies-literature