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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.
Neurobiol Dis. 2005 Jun-Jul; 19(1-2):312-22.ND

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.

Authors+Show Affiliations

Center for the Study of Neurodegenerative Diseases, University of Virginia School of Medicine, Charlottesville, VA 22908, USA. Onyango@virginia.eduNo affiliation info availableNo affiliation info available

Pub Type(s)

Comparative Study
Journal Article
Research Support, N.I.H., Extramural
Research Support, U.S. Gov't, P.H.S.

Language

eng

PubMed ID

15837587

Citation

Onyango, Isaac G., et al. "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." Neurobiology of Disease, vol. 19, no. 1-2, 2005, pp. 312-22.
Onyango IG, Bennett JP, Tuttle JB. 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. Neurobiol Dis. 2005;19(1-2):312-22.
Onyango, I. G., Bennett, J. P., & Tuttle, J. B. (2005). 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. Neurobiology of Disease, 19(1-2), 312-22.
Onyango IG, Bennett JP, Tuttle JB. 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. Neurobiol Dis. 2005 Jun-Jul;19(1-2):312-22. PubMed PMID: 15837587.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - 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. AU - Onyango,Isaac G, AU - Bennett,James P,Jr AU - Tuttle,Jeremy B, PY - 2004/10/15/received PY - 2004/12/27/revised PY - 2005/01/12/accepted PY - 2005/4/20/pubmed PY - 2005/7/13/medline PY - 2005/4/20/entrez SP - 312 EP - 22 JF - Neurobiology of disease JO - Neurobiol Dis VL - 19 IS - 1-2 N2 - 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. SN - 0969-9961 UR - https://www.unboundmedicine.com/medline/citation/15837587/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_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0969-9961(05)00024-0 DB - PRIME DP - Unbound Medicine ER -