Abstract
Although oxidative stress and mitochondrial dysfunction have been linked to neurodegenerative diseases such as Alzheimers disease (AD), it remains unclear how mitochondrial oxidative stress may induce neuronal death. In a variety of tissues, cumulative oxidative stress, disrupted mitochondrial respiration, and mitochondrial damage are associated with, and may indeed promote cell death and degeneration. In this review, we examine current evidence supporting the involvement of mitochondria and mitochondrially generated stress signaling in AD and discuss potential implications for the mechanism of pathogenesis of this disease. Mitochondria are pivotal in controlling cell life and death not only by producing ATP, and sequestering calcium, but by also generating free radicals and serving as repositories for proteins which regulate the intrinsic apoptotic pathway. Perturbations in the physiological function of mitochondria inevitably disturb cell function, sensitize cells to neurotoxic insults and may initiate cell death, all significant phenomena in the pathogenesis of a number of neurodegenerative disorders including AD.
Keywords: Alzheimer's disease, oxidative stress, mitochondrial dysfunction, signal transduction, stress activated protein kinases, eactive oxygen species, presenilin, amyloid precursor protein, cybrids, apoptosis
Current Alzheimer Research
Title: Oxidative Stress, Mitochondrial Dysfunction, and Stress Signaling in Alzheimers Disease
Volume: 3 Issue: 4
Author(s): Isaac G. Onyango and Shaharyar M. Khan
Affiliation:
Keywords: Alzheimer's disease, oxidative stress, mitochondrial dysfunction, signal transduction, stress activated protein kinases, eactive oxygen species, presenilin, amyloid precursor protein, cybrids, apoptosis
Abstract: Although oxidative stress and mitochondrial dysfunction have been linked to neurodegenerative diseases such as Alzheimers disease (AD), it remains unclear how mitochondrial oxidative stress may induce neuronal death. In a variety of tissues, cumulative oxidative stress, disrupted mitochondrial respiration, and mitochondrial damage are associated with, and may indeed promote cell death and degeneration. In this review, we examine current evidence supporting the involvement of mitochondria and mitochondrially generated stress signaling in AD and discuss potential implications for the mechanism of pathogenesis of this disease. Mitochondria are pivotal in controlling cell life and death not only by producing ATP, and sequestering calcium, but by also generating free radicals and serving as repositories for proteins which regulate the intrinsic apoptotic pathway. Perturbations in the physiological function of mitochondria inevitably disturb cell function, sensitize cells to neurotoxic insults and may initiate cell death, all significant phenomena in the pathogenesis of a number of neurodegenerative disorders including AD.
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Cite this article as:
Onyango G. Isaac and Khan M. Shaharyar, Oxidative Stress, Mitochondrial Dysfunction, and Stress Signaling in Alzheimers Disease, Current Alzheimer Research 2006; 3 (4) . https://dx.doi.org/10.2174/156720506778249489
DOI https://dx.doi.org/10.2174/156720506778249489 |
Print ISSN 1567-2050 |
Publisher Name Bentham Science Publisher |
Online ISSN 1875-5828 |
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