Authors
Craig W Ritchie, Ashley I Bush, Andrew Mackinnon, Steve Macfarlane, Maree Mastwyk, Lachlan MacGregor, Lyn Kiers, Robert Cherny, Qiao-Xin Li, Amanda Tammer, Darryl Carrington, Christine Mavros, Irene Volitakis, Michel Xilinas, David Ames, Stephen Davis, Konrad Beyreuther, Rudolph E Tanzi, Colin L Masters
Publication date
2003/12/1
Journal
Archives of neurology
Volume
60
Issue
12
Pages
1685-1691
Publisher
American Medical Association
Description
Background
Alzheimer disease (AD) may be caused by the toxic accumulation of β-amyloid (Aβ).
Objective
To test this theory, we developed a clinical intervention using clioquinol, a metal-protein–attenuating compound (MPAC) that inhibits zinc and copper ions from binding to Aβ, thereby promoting Aβ dissolution and diminishing its toxic properties.
Methods
A pilot phase 2 clinical trial in patients with moderately severe Alzheimer disease.
Results
Thirty-six subjects were randomized. The effect of treatment was significant in the more severely affected group (baseline cognitive subscale score of the Alzheimer's Disease Assessment Scale, ≥25), due to a substantial worsening of scores in those taking placebo compared with minimal deterioration for the clioquinol group. Plasma Aβ42levels declined in the clioquinol group and increased in the placebo group. Plasma zinc levels rose in the clioquinol-treated group. The …
Total citations
Scholar articles
CW Ritchie, AI Bush, A Mackinnon, S Macfarlane… - Archives of neurology, 2003