The metallobiology of Alzheimer's disease.

By Ashley I. Bush. Trends in Neurosciences, 2003

1,181 citations recorded by the source corpus.

Subfields: Health, Toxicology and Mutagenesis, Nutrition and Dietetics, Physiology

View Paper: https://www.semanticscholar.org/paper/17eac7164527a89fefbb4fe28ad38aeccfb13a66

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In Health, Toxicology and Mutagenesis

In Nutrition and Dietetics

In Physiology

Citations in the corpus

Neurodegenerative diseases and oxidative stress (2004, background): “The brain is an organ that concentrates metal ions and recent evidence suggests that a breakdown in metal homeostasis is a key factor in a variety of age-related neurodegenerative disease”
The neurobiology of zinc in health and disease (2005, background): “198 ) becomes hypermetallated with age, and is abnormally oxidized during the physiological processing of coppe”
A Review of the Antioxidant Mechanisms of Polyphenol Compounds Related to Iron Binding (2009, background): “APP can be converted to Ab in the presence of divalent metal ions (such as Fe and Cu), generating neurotoxic amyloid fibrils [225].”
Mitochondria in health and disease: perspectives on a new mitochondrial biology. (2004, background): “The channel is apparently blocked by zinc, although the action of zinc is confusing, as it can also complex with Ab, prevent aggregation and so prevent insertion into the membrane or prevent pore formation rather than blocking the formed channel (see Arispe et al., 1996; Rhee et al., 1998; Bush, 200”
Metals, oxidative stress and neurodegenerative disorders (2010, neutral): “The central tenet of Ab toxicity is linked with the presence of redox metals, mainly copper and non-redox zinc [ 3 , 11, 23].”
Free radicals and antioxidants in normal physiological functions and human disease. (2007, background): “The exact mechanisms of the protective effect of zinc against A toxicity is unclear, however a reason might be cytoprotection through blockage of the membrane calcium channel pore formed by A (1-40) (Bush, 2003).”