Objective: We aimed to study whether A beta O-42-induced mtDNA damage is involved in the regulation of stem cell differentiation.

Background: Amyloid-beta(42) oligomers (A beta O-42), the proximate effectors of neurotoxicity observed in Alzheimer's disease (AD), can induce mitochondrial oxidative stress and impair mitochondrial function besides causing mitochondrial DNA (mtDNA) damage. A beta O-42 also regulate the proliferative and differentiative properties of stem cells.

Amyloid-beta Oligomers-induced Mitochondrial DNA Repair Impairment Contributes to Altered Human Neural Stem Cell Differentiation

Mollinari Cristiana;
2019

Abstract

Background: Amyloid-beta(42) oligomers (A beta O-42), the proximate effectors of neurotoxicity observed in Alzheimer's disease (AD), can induce mitochondrial oxidative stress and impair mitochondrial function besides causing mitochondrial DNA (mtDNA) damage. A beta O-42 also regulate the proliferative and differentiative properties of stem cells.
2019
FARMACOLOGIA TRASLAZIONALE - IFT
Inglese
16
10
934
949
16
https://pubmed.ncbi.nlm.nih.gov/31642778/
Sì, ma tipo non specificato
Objective: We aimed to study whether A beta O-42-induced mtDNA damage is involved in the regulation of stem cell differentiation.
Amyloid-?; mitochondria; DNA damage; DNA repair; human neural stem cell; differentiation.
Amyloid-beta
mitochondria
DNA damage
DNA repair
human neural stem cell
differentiation
6
info:eu-repo/semantics/article
262
Lu, Jing; Li, Yi; Mollinari, Cristiana; Garaci, Enrico; Merlo, Daniela; Pei, Gang
01 Contributo su Rivista::01.01 Articolo in rivista
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/20.500.14243/366854
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