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Oxidative Stress Induces Intralysosomal Accumulation of Alzheimer Amyloid β-Protein in Cultured Neuroblastoma Cells
Linköping University, Department of Neuroscience and Locomotion, Geriatrics. Linköping University, Faculty of Health Sciences.
Linköping University, Department of Neuroscience and Locomotion, Oto-Rhiono-Laryngology and Head & Neck Surgery. Linköping University, Faculty of Health Sciences.
Linköping University, Department of Clinical and Experimental Medicine, Experimental Pathology. Linköping University, Faculty of Health Sciences.
Linköping University, Department of Neuroscience and Locomotion, Geriatrics. Linköping University, Faculty of Health Sciences.
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2006 (English)In: Annals of the New York Academy of Sciences, ISSN 0077-8923, E-ISSN 1749-6632, Vol. 1067, 248-251 p.Article in journal (Refereed) Published
Abstract [en]

Oxidative stress is considered important for the pathogenesis of Alzheimer's disease (AD), which is characterized by the formation of extracellular senile plaques, mainly composed of amyloid β-protein (Aβ). Aβ also accumulates within AD neurons and is believed to exert cellular toxicity through lysosomal labilization. We report that the exposure of human neuroblastoma cells to hyperoxia (40% vs. 8% ambient oxygen) induced the accumulation of large (over 1 μM) Aβ-containing lysosomes, which were not typical of control cells, showing a distinct localization of Aβ and lysosomal markers. An inhibitor of autophagy, 3-methyladenine, suppressed the effect of hyperoxia. The results suggest a link between the involvement of oxidative stress and lysosomes in AD.

Place, publisher, year, edition, pages
2006. Vol. 1067, 248-251 p.
Keyword [en]
Alzheimer disease; amyloid beta-protein; autophagy; lysosomes; oxidative stress
National Category
Medical and Health Sciences
Identifiers
URN: urn:nbn:se:liu:diva-35998DOI: 10.1196/annals.1354.032Local ID: 29306OAI: oai:DiVA.org:liu-35998DiVA: diva2:256846
Available from: 2009-10-10 Created: 2009-10-10 Last updated: 2017-12-13Bibliographically approved

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Zheng, LinRoberg, KarinJerhammar, FredrikMarcusson, JanTerman, Alexei

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Annals of the New York Academy of Sciences
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