Abstract
Considerable evidence suggests a role for oxidative stress in the pathogenesis of neuron degeneration in several neurodegenerative disorders including Alzheimers disease (AD). Although debated, increasing evidence suggests that oxidative stress/damage (amyloid beta peptide, iron/hydrogen peroxide) or neurotoxic by-products of lipid peroxidation (4-hydroxy-2-nonenal, acrolein) lead to cell death through apoptosis or programmed cell death in AD. This review discusses current evidence supporting the role of oxidative stress/damage mediated apoptosis in in vitro models of neurodegeneration.
Keywords: anti-apoptotic proteins, oxidative damage, permeability transition pore (PTP), sodium/potassium-transporting ATPase, dependent anion channel (VDAC)
Current Alzheimer Research
Title: Amyloid Beta Peptide, 4-Hydroxynonenal and Apoptosis
Volume: 3 Issue: 4
Author(s): Mark A. Lovell and William R. Markesbery
Affiliation:
Keywords: anti-apoptotic proteins, oxidative damage, permeability transition pore (PTP), sodium/potassium-transporting ATPase, dependent anion channel (VDAC)
Abstract: Considerable evidence suggests a role for oxidative stress in the pathogenesis of neuron degeneration in several neurodegenerative disorders including Alzheimers disease (AD). Although debated, increasing evidence suggests that oxidative stress/damage (amyloid beta peptide, iron/hydrogen peroxide) or neurotoxic by-products of lipid peroxidation (4-hydroxy-2-nonenal, acrolein) lead to cell death through apoptosis or programmed cell death in AD. This review discusses current evidence supporting the role of oxidative stress/damage mediated apoptosis in in vitro models of neurodegeneration.
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Cite this article as:
Lovell A. Mark and Markesbery R. William, Amyloid Beta Peptide, 4-Hydroxynonenal and Apoptosis, Current Alzheimer Research 2006; 3 (4) . https://dx.doi.org/10.2174/156720506778249506
DOI https://dx.doi.org/10.2174/156720506778249506 |
Print ISSN 1567-2050 |
Publisher Name Bentham Science Publisher |
Online ISSN 1875-5828 |
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