Treatment with a Copper-Zinc Chelator Markedly and Rapidly Inhibits β-Amyloid Accumulation in Alzheimer's Disease Transgenic Mice

By R. Cherny, C. Atwood, M. Xilinas, D. Gray, Walton D. Jones, C. Mclean, K. Barnham, I. Volitakis, F. Fraser, Young-Seon Kim and 9 more. 2001

1,403 citations recorded by the source corpus.

Subfields: Nutrition and Dietetics, Physiology, Plant Science

View Paper: https://www.semanticscholar.org/paper/45c4207cba406225ab7860a62fb702f5a9911e52

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Citations in the corpus

Copper homeostasis and cuproptosis in health and disease (2022, background): “have shown that the chelator clioquinol could decrease Aβ deposits and improve the capacities in both learning and memory.(101) Moreover, several phase II trials have shown that clioquinol is capable of reducing Aβ aggregation and improving cognitive function, but fail to provide sufficient evidence”
Oxidative stress in neurodegenerative diseases (2012, background): “[108] Cherny RA, Atwood CS, Xilinas ME, et al.”
Paradigm shifts in Alzheimer's disease and other neurodegenerative disorders: The emerging role of oligomeric assemblies (2002, positive): “This paradigm has provided the theoretical basis for recent therapeutic approaches demonstrating promise for amyloid elimination (Schenk et al., 2000; Cherny et al., 2001; DeMattos et al., 2001).”
Zinc in the physiology and pathology of the CNS (2009, background): “Treatment of Tg2576 mice with oral clioquinol resulted in a 49% reduction of cortical amyloid burde”
Zinc and human health: an update (2011, positive): “Furthermore , zinc chelating agents, such as clioquinol (CQ) and DP-109, that modulate brain zinc levels can inhibit the formation of amyloid plaques (Cherny et al. 2001; Bush 2002; Lee et al. 2004).”
Accumulation of Amyloid Precursor Protein in the Mitochondrial Import Channels of Human Alzheimer’s Disease Brain Is Associated with Mitochondrial Dysfunction (2006, background): “Treatment with Clioquinol (a metal chelator) has been shown to reduce the accumulation of A species in transgenic mouse models (Cherny et al., 2001).”
Unfolding the role of protein misfolding in neurodegenerative diseases (2003, background): “Strategies for the specific removal of amyloid-P components, proteoglycans and metal ions have shown the best results in models of AD and systemic amyloidosi”
Rapid restoration of cognition in Alzheimer's transgenic mice with 8-hydroxy quinoline analogs is associated with decreased interstitial Abeta. (2008, positive): “PBT2 Is a Superior Ionophore to CQ Since recent findings suggest that increasing intracellular Cu or Zn may lower As production (Bayer et al., 2003; Borchardt et al., 1999; Cater et al., 2008; Phinney et al., 2003; White et al., 2006), we appraised PBT2 and CQ for their ionophoric ability to promo”
Metal-protein attenuation with iodochlorhydroxyquin (clioquinol) targeting Abeta amyloid deposition and toxicity in Alzheimer disease: a pilot phase 2 clinical trial. (2003, background): “One such MPAC lead compound, iodochlorhydroxyquin (an antiinfective agent also known as clioquinol) induces a rapid decrease in brain A deposition in a mouse model of AD.(5) Clioquinol also inhibits A toxicity in neuronal cell cultures, 6 possibly acting through an additional mechanism of preventing”