Endogenous oxidative stress in sporadic Alzheimer’s disease neuronal cybrids reduces viability by increasing apoptosis through pro-death signaling pathways and is mimicked by oxidant exposure of control cybrids

Onyango, Isaac G.; Bennett, James P.; Tuttle, Jeremy B.

doi:10.1016/j.nbd.2005.01.026

Cited by 56Alzheimer's disease research and treatmentsMitochondrial Function and PathologyCell death mechanisms and regulation

Endogenous oxidative stress in sporadic Alzheimer’s disease neuronal cybrids reduces viability by increasing apoptosis through pro-death signaling pathways and is mimicked by oxidant exposure of control cybrids

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Onyango, Isaac G., Bennett, James P., Tuttle, Jeremy B.·2005·Neurobiology of Disease

DOI 10.1016/j.nbd.2005.01.026

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Abstract

Although oxidative stress and mitochondrial dysfunction have been linked to neurodegenerative diseases such as Alzheimer's disease (AD), it is not fully understood how mitochondrial oxidative stress may induce neuronal death. We used mitochondrial transgenic neuronal cell cybrid models of sporadic AD (SAD) to investigate the effects of endogenously generated reactive oxygen species (ROS) on viability and cell death mechanisms. Compared to control (CTL) cybrids, SAD cybrids have increased accumulation of oxidative stress markers and increased apoptosis that is blocked by N-acetylcysteine (NAC) and zVAD.fmk. SAD cybrids also have increased basal activation of the MAPKs, Akt, and NF-kappa B. NF-kappa B activation and cybrid viability are enhanced by NAC. Inhibiting the activity of the PI3K pathway or NF-kappa B aggravates neuronal death. Exposure of CTL cybrids to H2O2 decreased viability and activated in a NAC-sensitive manner, the same intracellular signaling pathways active under basal conditions in SAD cybrids.

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“Oxidative stress associated with Aβ pathology plays an important role in the death of neurons in the AD brain [82,83,84,85].”
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Authors: Onyango, I. G., Bennett, J. P., & Tuttle, J. B.
Affiliations: University of Virginia Medical Center (US)
University of Virginia (US)
Corresponding author: Onyango, Isaac G.
ORCID: Onyango, Isaac G.
Bennett, James P.
Venue: Neurobiology of Disease
Publisher: Elsevier BV
Published: 2005-06
Volume: 19
Issue: 1-2
Pages: 312-322
ISSN: 0969-9961 (ISSN-L)
DOI: 10.1016/j.nbd.2005.01.026
OpenAlex: W2008782167
Cited by: 56
References: 79
Citations by year: 2025: 1 · 2024: 1 · 2023: 1 · 2022: 3 · 2020: 2 · 2019: 1 · 2018: 2 · 2017: 4 · 2016: 2 · 2015: 3 · 2014: 3 · 2013: 4 · 2012: 5
FWCI: 3.61
Type: journal article
Language: en
Open access: green
doaj.org
Licence: cc-by-sa
www.elsevier.com/tdm/userlicense/1.0/ (tdm)
Locations: Neurobiology of Disease (publishedVersion)
PubMed (publishedVersion)
DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
Funders: National Institutes of Health (5r01ns039005-04)
National Institute on Aging (AG 14373, P01AG014373)
National Institute of Neurological Disorders and Stroke (NS39788, P50NS039788, NS39005)
Topics: Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Mitochondrial Function and Pathology
Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Cell death mechanisms and regulation
Keywords: sporadic Alzheimer's disease, oxidative stress, mitochondrial dysfunction, neuronal apoptosis, reactive oxygen species, MAPK signaling, Akt signaling, NF-κB, PI3K signaling, N-acetylcysteine, hydrogen peroxide, neuronal viability, neurodegeneration
MeSH terms: Aged, Alzheimer Disease, Cell Survival, Humans, Neurons, Signal Transduction, Cerebral Amyloid Angiopathy, Oxidants, Cell Death, Apoptosis, Oxidative Stress, Cell Line, Tumor

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Endogenous oxidative stress in sporadic Alzheimer’s disease neuronal cybrids reduces viability by increasing apoptosis through pro-death signaling pathways and is mimicked by oxidant exposure of control cybrids

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