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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

Oxidative damage is the earliest event in Alzheimer disease.

TL;DR: The observations indicate that increased oxidative damage is an early event in AD that decreases with disease progression and lesion formation and suggest that AD is associated with compensatory changes that reduce damage from reactive oxygen.
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Statins and the risk of dementia.

TL;DR: Individuals of 50 years and older who were prescribed statins had a substantially lowered risk of developing dementia, independent of the presence or absence of untreated hyperlipidaemia, or exposure to nonstatin LLAs.
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Aging, energy, and oxidative stress in neurodegenerative diseases.

TL;DR: Potential therapeutic approaches include glutamate release inhibitors, excitatory amino acid antagonists, strategies to improve mitochondrial function, free radical scavengers, and trophic factors, which appear promising in experimental studies and are now being applied to human studies.
Journal ArticleDOI

A68: a major subunit of paired helical filaments and derivatized forms of normal Tau

TL;DR: The major subunits of a class of PHFs are A68 proteins and the excessive or inappropriate phosphorylation of normal tau may change its apparent Mr, thus transforming tau into A68.
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