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Current Alzheimer Research

Editor-in-Chief

ISSN (Print): 1567-2050
ISSN (Online): 1875-5828

Amyloid Beta Peptide, 4-Hydroxynonenal and Apoptosis

Author(s): Mark A. Lovell and William R. Markesbery

Volume 3, Issue 4, 2006

Page: [359 - 364] Pages: 6

DOI: 10.2174/156720506778249506

Price: $65

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)


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