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Journal ArticleDOI

Oxidative stress in Alzheimer's disease

Ved Chauhan, +1 more
- 01 Aug 2006 - 
- Vol. 13, Iss: 3, pp 195-208
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TLDR
This review discusses free radical-mediated damage to the biochemical components involved in the pathology and clinical symptoms of Alzheimer's disease and explains how amyloid beta-protein, microtubule-associated protein tau, presenilins, apolipoprotein E, mitochondria and proteases play a role in increasing oxidative stress in AD.
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This article is published in Pathophysiology.The article was published on 2006-08-01. It has received 318 citations till now. The article focuses on the topics: Oxidative stress & Neurofibrillary tangle.

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Citations
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Oxidative Stress, Synaptic Dysfunction, and Alzheimer’s Disease

TL;DR: The role of oxidative stress in synaptic dysfunction in AD, innovative therapeutic strategies evolved based on a better understanding of the complexity of molecular mechanisms of AD, and the dual role ROS play in health and disease are discussed.
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Brain oxidative stress in a triple-transgenic mouse model of Alzheimer disease.

TL;DR: In this article, the authors investigated the role of oxidative stress in the early stages of Alzheimer's disease in a triple-transgenic mouse model and showed that the levels of antioxidants, namely, reduced glutathione and vitamin E, are decreased and the extent of lipid peroxidation is increased.
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Antioxidant activities and phenolics content of eight species of seaweeds from north Borneo

TL;DR: There was a strong correlation between the reducing power and the total phenolic content of the seaweeds methanolic dry extracts and these seaweeds could be potential rich sources of natural antioxidants.
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Intrahippocampal injection of a lentiviral vector expressing Nrf2 improves spatial learning in a mouse model of Alzheimer's disease

TL;DR: The data indicate that significant reductions in spatial learning deficits of aged APP/PS1 mice in a Morris Water Maze can be achieved by modulating levels of NRF2 in the brain and suggest that the Nrf2-ARE pathway may represent a potential therapeutic strategy to pursue in AD in humans, particularly in view of the multiple mechanisms by which Nrf1 can exert its protective effects.
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Resveratrol prevents memory deficits and the increase in acetylcholinesterase activity in streptozotocin-induced diabetic rats.

TL;DR: It is shown that treatment with resveratrol prevents the increase in AChE activity and consequently memory impairment in diabetic rats, demonstrating that this compound can modulate cholinergic neurotransmission and consequently improve cognition.
References
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Journal ArticleDOI

Superoxide dismutase activity in Alzheimer's disease: possible mechanism for paired helical filament formation☆

TL;DR: The elevation in SOD-1 activity observed in the familial Alzheimer's patients supports the theory that paired helical filaments are synthesized in Alzheimer's disease by free radical hydroxylation of proline residues in paired helicals filament precursor protein(s).
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Amyloid precursor proteins inhibit heme oxygenase activity and augment neurotoxicity in Alzheimer's disease.

TL;DR: It is reported that APP and APLP bind to heme oxygenase (HO), an enzyme whose product, bilirubin, is antioxidant and neuroprotective, indicating that augmented neurotoxicity caused by APP-HO interactions may contribute to neuronal cell death in Alzheimer's disease.
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β-Amyloid protein-dependent nitric oxide production from microglial cells and neurotoxicity

TL;DR: It is likely that A beta-induced NO production by microglial cells is one mechanism of the neuronal death in AD.
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The Ginkgo biloba extract EGb 761 rescues the PC12 neuronal cells from β-amyloid-induced cell death by inhibiting the formation of β-amyloid-derived diffusible neurotoxic ligands

TL;DR: Results indicate that the terpenoid and flavonoid constituents of EGb 761, acting probably in combination with components present in HE 208, are responsible for rescuing the neuronal cells from Aβ-induced apoptosis and cell death; their mechanism of action being distinct of their antioxidant properties.
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Brain Regional Quantification of F-Ring and D-/E-Ring Isoprostanes and Neuroprostanes in Alzheimer’s Disease

TL;DR: Results from in situ techniques are extended by quantifying significantly greater free radical damage to the DHA-containing compartments in cerebrum in AD patients than controls, and suggest that one mechanism of increased oxidative stress may be diminished reducing capacity in DHA.
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