Oxidative Stress: Emerging Mitochondrial and Cellular Themes and Variations in Neuronal Injury

Gavin Clive Higgins, Philip M Beart, Yea Seul Shin, Minghui Jessica Chen, Nam Sang Cheung, Phillip Nagley

Research output: Contribution to journalArticleResearchpeer-review

94 Citations (Scopus)

Abstract

Oxidative stress plays a central role in neuronal injury and cell death in acute and chronic pathological conditions. The cellular responses to oxidative stress embrace changes in mitochondria and other organelles, notably endoplasmic reticulum, and can lead to a number of cell death paradigms, which cover a spectrum from apoptosis to necrosis and include autophagy. In Alzheimer s disease, and other pathologies including Parkinson s disease, protein aggregation provides further cellular stresses that can initiate or feed into the pathways to cell death engendered by oxidative stress. Specific attention is paid here to mitochondrial dysfunction and programmed cell death, and the diverse modes of cell death mediated by mitochondria under oxidative stress. Novel insights into cellular responses to neuronal oxidative stress from a range of different stressors can be gained by detailed transcriptomics analyses. Such studies at the cellular level provide the key for understanding the molecular and cellular pathways whereby neurons respond to oxidative stress and undergo injury and death. These considerations underpin the development of detailed knowledge in more complex integrated systems, up to the intact human bearing the neuropathology, facilitating therapeutic advances.
Original languageEnglish
Pages (from-to)453 - 473
Number of pages21
JournalJournal of Alzheimer's Disease
Volume20
Issue numberSuppl 2
DOIs
Publication statusPublished - 2010

Cite this

Higgins, Gavin Clive ; Beart, Philip M ; Shin, Yea Seul ; Chen, Minghui Jessica ; Sang Cheung, Nam ; Nagley, Phillip. / Oxidative Stress: Emerging Mitochondrial and Cellular Themes and Variations in Neuronal Injury. In: Journal of Alzheimer's Disease. 2010 ; Vol. 20, No. Suppl 2. pp. 453 - 473.
@article{8bd5dc5a2c1246e4bcb7eae3ceebe34f,
title = "Oxidative Stress: Emerging Mitochondrial and Cellular Themes and Variations in Neuronal Injury",
abstract = "Oxidative stress plays a central role in neuronal injury and cell death in acute and chronic pathological conditions. The cellular responses to oxidative stress embrace changes in mitochondria and other organelles, notably endoplasmic reticulum, and can lead to a number of cell death paradigms, which cover a spectrum from apoptosis to necrosis and include autophagy. In Alzheimer s disease, and other pathologies including Parkinson s disease, protein aggregation provides further cellular stresses that can initiate or feed into the pathways to cell death engendered by oxidative stress. Specific attention is paid here to mitochondrial dysfunction and programmed cell death, and the diverse modes of cell death mediated by mitochondria under oxidative stress. Novel insights into cellular responses to neuronal oxidative stress from a range of different stressors can be gained by detailed transcriptomics analyses. Such studies at the cellular level provide the key for understanding the molecular and cellular pathways whereby neurons respond to oxidative stress and undergo injury and death. These considerations underpin the development of detailed knowledge in more complex integrated systems, up to the intact human bearing the neuropathology, facilitating therapeutic advances.",
author = "Higgins, {Gavin Clive} and Beart, {Philip M} and Shin, {Yea Seul} and Chen, {Minghui Jessica} and {Sang Cheung}, Nam and Phillip Nagley",
year = "2010",
doi = "10.3233/JAD-2010-100321",
language = "English",
volume = "20",
pages = "453 -- 473",
journal = "Journal of Alzheimer's Disease",
issn = "1387-2877",
publisher = "IOS Press",
number = "Suppl 2",

}

Oxidative Stress: Emerging Mitochondrial and Cellular Themes and Variations in Neuronal Injury. / Higgins, Gavin Clive; Beart, Philip M; Shin, Yea Seul; Chen, Minghui Jessica; Sang Cheung, Nam; Nagley, Phillip.

In: Journal of Alzheimer's Disease, Vol. 20, No. Suppl 2, 2010, p. 453 - 473.

Research output: Contribution to journalArticleResearchpeer-review

TY - JOUR

T1 - Oxidative Stress: Emerging Mitochondrial and Cellular Themes and Variations in Neuronal Injury

AU - Higgins, Gavin Clive

AU - Beart, Philip M

AU - Shin, Yea Seul

AU - Chen, Minghui Jessica

AU - Sang Cheung, Nam

AU - Nagley, Phillip

PY - 2010

Y1 - 2010

N2 - Oxidative stress plays a central role in neuronal injury and cell death in acute and chronic pathological conditions. The cellular responses to oxidative stress embrace changes in mitochondria and other organelles, notably endoplasmic reticulum, and can lead to a number of cell death paradigms, which cover a spectrum from apoptosis to necrosis and include autophagy. In Alzheimer s disease, and other pathologies including Parkinson s disease, protein aggregation provides further cellular stresses that can initiate or feed into the pathways to cell death engendered by oxidative stress. Specific attention is paid here to mitochondrial dysfunction and programmed cell death, and the diverse modes of cell death mediated by mitochondria under oxidative stress. Novel insights into cellular responses to neuronal oxidative stress from a range of different stressors can be gained by detailed transcriptomics analyses. Such studies at the cellular level provide the key for understanding the molecular and cellular pathways whereby neurons respond to oxidative stress and undergo injury and death. These considerations underpin the development of detailed knowledge in more complex integrated systems, up to the intact human bearing the neuropathology, facilitating therapeutic advances.

AB - Oxidative stress plays a central role in neuronal injury and cell death in acute and chronic pathological conditions. The cellular responses to oxidative stress embrace changes in mitochondria and other organelles, notably endoplasmic reticulum, and can lead to a number of cell death paradigms, which cover a spectrum from apoptosis to necrosis and include autophagy. In Alzheimer s disease, and other pathologies including Parkinson s disease, protein aggregation provides further cellular stresses that can initiate or feed into the pathways to cell death engendered by oxidative stress. Specific attention is paid here to mitochondrial dysfunction and programmed cell death, and the diverse modes of cell death mediated by mitochondria under oxidative stress. Novel insights into cellular responses to neuronal oxidative stress from a range of different stressors can be gained by detailed transcriptomics analyses. Such studies at the cellular level provide the key for understanding the molecular and cellular pathways whereby neurons respond to oxidative stress and undergo injury and death. These considerations underpin the development of detailed knowledge in more complex integrated systems, up to the intact human bearing the neuropathology, facilitating therapeutic advances.

UR - http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=20463398

U2 - 10.3233/JAD-2010-100321

DO - 10.3233/JAD-2010-100321

M3 - Article

VL - 20

SP - 453

EP - 473

JO - Journal of Alzheimer's Disease

JF - Journal of Alzheimer's Disease

SN - 1387-2877

IS - Suppl 2

ER -