Amyloid-β precursor protein processing and oxidative stress are altered in human iPSC-derived neuron and astrocyte co-cultures carrying presenillin-1 gene mutations following spontaneous differentiation.

Abstract excerpt

INTRODUCTION: Presenilin-1 (PSEN1) gene mutations are the most common cause of familial Alzheimer's disease (fAD) and are known to interfere with activity of the membrane imbedded γ-secretase complex. PSEN1 mutations have been shown to shift Amyloid-β precursor protein (AβPP) processing toward amyloid-β (Aβ) 1-42 production. However, less is known about whether PSEN1 mutations may alter the activity of enzymes...

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