Deposits of the beta-amyloid peptide are abundant in the brains of Alzheimer's patients and many researchers believe they are responsible for the massive neuronal death that these patients suffer.
In today's issue of Neuron, Cherny et al. report that clioquinol, which binds copper and zinc ions, reduces these plaques in a transgenic mouse model of Alzheimer's disease.
Previous work has shown that the beta-amyloid peptide can bind copper and zinc ions and that both are concentrated in the senile plaques in Alzheimer patients' brains.
Cherny et al. have managed to inhibit and possibly reverse the accumulation of the peptide deposits in the brains of the transgenic mice with clioquinol. The general health of the treated mice was significantly improved.
As Gouras and Beal write in an accompanying Preview of the paper, "This is an exciting time in Alzheimer's disease research since therapies that can directly address the beta-amyloid hypothesis are now available. A number of these have reached the clinic, including Abeta immunotherapy, gamma-secretase inhibitors, anti-inflammatory agents, cholesterol-lowering drugs, and now clioquinol."
In addition to contributing to a basic understanding of the pathology of Alzheimer's disease, the results of Cherny et al. support a new therapeutic approach to treating Alzheimer's disease using metal chelators.
Clioquinol is currently in Phase II of a clinical trial in Australia, which should be complete in early 2002.
[Contact: Ashley I. Bush]