Involvement of Oxidative Stress in Alzheimer Disease
By A. Nunomura, R. Castellani, Xiongwei Zhu, P. Moreira, George Perry, Mark A. Smith. Journal of Neuropathology and Experimental Neurology, 2006
610 citations recorded by the source corpus.
Subfields: Molecular Biology, Pharmacology, Physiology
View Paper: https://www.semanticscholar.org/paper/d5081d074462a6bcb95029ed72a74b4efb20ba4b
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Citations in the corpus
- Phenolic Profile and Antioxidant Activity of Crude Extracts from Microalgae and Cyanobacteria Strains (2017, background): “Several studies on pharmacological research have evidenced that oxidative stress and increased amounts of free radicals are features of chronic diseases including cancer [2], aging, and neurodegenerative diseases such as Alzheimer’s and Parkinson’s [3, 4] and cardiovascular diseases such as atherosc”
- Amyloid-β overproduction causes abnormal mitochondrial dynamics via differential modulation of mitochondrial fission/fusion proteins (2008, background): “Persuasive evidence suggests that oxidative stress is one of the earliest changes and plays an important role in the pathological process in AD (3).”
- Oxidative Stress and the Pathogenesis of Alzheimer's Disease (2013, background): “These unexpected observations have led to the hypothesis that Abeta may potentially play a protective role against neuronal oxidative stress [64].”
- Long-term Air Pollution Exposure Is Associated with Neuroinflammation, an Altered Innate Immune Response, Disruption of the Blood-Brain Barrier, Ultrafine Particulate Deposition, and Accumulation of Amyloid β-42 and α-Synuclein in Children and Young Adults (2008, background): “Chronic oxidative stress is a major contributing factor in the pathogenesis of both Alzheimer’s and Parkinson’s diseases (Nunomura et al. 2006; Quilty et al. 2006).”
- Amyloid beta, mitochondrial dysfunction and synaptic damage: implications for cognitive decline in aging and Alzheimer's disease. (2008, background): “AD is also associated with loss of neurons, synapses, and synaptic function, mitochondrial abnormalities, and inflammatory responses [7–13].”