HAL (France)
open access
Mitochondrial Alterations in Neurons Derived from the Murine AppNL-F Knock-In Model of Alzheimer’s Disease
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
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