Literature: A-K ; L-Z ; subject area
Compiled by: Julian Thorpe
Oxidative Stress
|
Please Note: Due to time constraints, the text part of this page has not been updated for some time. However, references are added reasonably frequently. |
General
 | The fact that aging is an obvious risk factor leads naturally to a hypothesis that free radicals may be involved. Neurons are extremely sensitive to the effects of free radicals. |
| AD has been linked to effects upon cytochrome-c oxidase in mitochondria which may bring about an abnormal production of free radicals. These latter can effect oxidative stress which is damaging to neurons. |
| Gibson et al. (2000) have used cultured fibroblasts to study a-ketoglutarate dehydrogenase complex (KGDHC; a key mitochondrial enzyme whose activity is reduced in AD brain). KGDHC was shown to be sensitive to oxidative stress (in cells, purified mitochondria and as an isolated protein) and their results were suggested to be indicative of the enzyme's involvement in critical events related to oxidative stress-induced selective neuronal loss. |
| Hsu et al. (2000) suggest that abnormal accumulations of
the pre-synaptic protein alpha-synuclein may have an effect on mitochondria
which results in oxidative stress and, eventually, cell death. |
| Apolipoprotein E is susceptible to free radicals, but may also act as a free radical scavenger. |
| The e4 allele of ApoE
has the poorest anti-oxidant potential (e.g. Ihara et al., 2000
). |
| Gibson et al. (2000) suggest that mitochondrial/oxidative
damage may be more important for the cognitive dysfunction in AD patients
with the ApoE4
allele. |
| Cedazo-Minguez and Cowburn (2001) have reviewed the involvement
of ApoE
in AD, including oxidative stress. |
| The presence of beta-amyloid plaques may contribute to elevated free radical levels. |
| Varadarajan et al. (2000) propose an 'amyloid beta-peptide-associated
oxidative stress model' for neurotoxicity in AD. They suggest that
aggregated peptide (soluble and fibrillar) initiates oxidative damage
with resultant cellular dysfunction leading to calcium ion accumulation
and cell death. |
| Ray et al. (2000) have used PC12 cells to show that the
upregulation of calpain (a Ca2+-dependent cysteine protease) by oxidative
stress and calcium influx, resulted in NF-L degradation (and apoptosis). |
| Leutner et al. (2000) used transgenic mice with human PS1 mutations to show evidence of a reduction in the activity of two antioxidant enzymes (Cu/Zn superoxide dismutase and glutathione reductase). |
(These journals include: Neurology, Neurobiology of Disease, Journal of Neurochemistry, Alzheimer's Disease Review)
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