Abstract
| Original language | English |
|---|---|
| Pages (from-to) | 453 - 473 |
| Number of pages | 21 |
| Journal | Journal of Alzheimer's Disease |
| Volume | 20 |
| Issue number | Suppl 2 |
| DOIs | |
| Publication status | Published - 2010 |
Cite this
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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 journal › Article › Research › peer-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 -