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Drew SC. The Case for Abandoning Therapeutic Chelation of Copper Ions in Alzheimer's Disease. Front Neurosci. 2017;11:317doi: 10.3389/fnins.2017.00317.
Drew, S. C. (2017). The Case for Abandoning Therapeutic Chelation of Copper Ions in Alzheimer's Disease. Frontiers in neuroscience, 11317. https://doi.org/10.3389/fnins.2017.00317
Drew, Simon C. "The Case for Abandoning Therapeutic Chelation of Copper Ions in Alzheimer's Disease." Frontiers in neuroscience vol. 11 (2017): 317. doi: https://doi.org/10.3389/fnins.2017.00317
Drew SC. The Case for Abandoning Therapeutic Chelation of Copper Ions in Alzheimer's Disease. Front Neurosci. 2017 Jun 02;11:317. doi: 10.3389/fnins.2017.00317. eCollection 2017. PMID: 28626387; PMCID: PMC5455140.
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Front Neurosci. 2017 Jun 02;11:317. doi: 10.3389/fnins.2017.00317. eCollection 2017.

The Case for Abandoning Therapeutic Chelation of Copper Ions in Alzheimer's Disease.

Frontiers in neuroscience

Simon C Drew

Affiliations

  1. Department of Medicine, Royal Melbourne Hospital, University of MelbourneMelbourne, VIC, Australia.

PMID: 28626387 PMCID: PMC5455140 DOI: 10.3389/fnins.2017.00317

Abstract

The "therapeutic chelation" approach to treating Alzheimer's disease (AD) evolved from the metals hypothesis, with the premise that small molecules can be designed to prevent transition metal-induced amyloid deposition and oxidative stress within the AD brain. Over more than 20 years, countless

Keywords: Alzheimer's disease; N-truncation; bioinorganic chemistry; chelator; copper; metal homeostasis; metals hypothesis; β-amyloid

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