Review: Alzheimer's amyloid beta-peptide-associated free radical oxidative stress and neurotoxicity.

By S. Varadarajan, S. Yatin, M. Aksenova, D. Allan Butterfield. Journal of Structural Biology, 2000

744 citations recorded by the source corpus.

View Paper: https://www.semanticscholar.org/paper/818f0b6db33a03455ec6b99063f0c32d6b85fdc9

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In Physiology

Citations in the corpus

Curcumin has potent anti‐amyloidogenic effects for Alzheimer's β‐amyloid fibrils in vitro (2004, background): “Many studies have demonstrated that oxidative damage is closely associated with the hallmark pathologies of AD and may play a critical role in the development of AD (Pratico and Delanty, 2000; Rottkamp et al., 2000; Smith et al., 2000; Varadarajan et al., 2000).”
Role of oxidative stress in Alzheimer's disease (2016, background): “This seems to be associated with the length of Aβ fragments, with Aβ (1-42) being more toxic than Aβ (1-40) and the most likely candidate to generate hydrogen peroxide and other ROS (54).”
Age-related myelin breakdown: a developmental model of cognitive decline and Alzheimer's disease. (2004, background): “Oligomeric A can also increase lipid peroxidation [229,244], which is increased in AD myelin [44] and disrupts its integrity [227].”
The Curry Spice Curcumin Reduces Oxidative Damage and Amyloid Pathology in an Alzheimer Transgenic Mouse (2001, background): “Extensive evidence of oxidative damage has been reported in AD (Conrad et al., 2000; Praticò and Delanty, 2000; Varadarajan et al., 2000) and results in lipid peroxidation products such as 4-hydroxynonenal and isoprostanes (Montine et al., 1998; Praticò et al., 1998).”
Antioxidant Activity of Proteins and Peptides (2008, background): “…has been suggested that the symptoms of Alzheimer’s disease is attributable to the accumulation of aggregated amyloid β-protein as neurofibrillary tangles in the brain resulting from oxidation reactions (Butterfield, 2002; Nunomura et al., 2001; Shringarpure et al., 2000; Varadarajan et al., 2000).”
Evidence that amyloid beta-peptide-induced lipid peroxidation and its sequelae in Alzheimer's disease brain contribute to neuronal death. (2002, background): “The centrality of the 42-amino acid form of this peptide, A (1–42), to the pathogenesis of AD was coupled to the extensive oxidative stress under which the AD brain exists in the A -associated free radical oxidative stress model for neurodegeneration in AD brain [14,96].”