(ran SP, CI editions)
Thinking and memory among Alzheimer's patients may decline more slowly if metals are removed from the toxic plaques that accumulate in their brains.
For years, scientists have experimented with ways to inhibit the production and accumulation of the protein beta-amyloid in the plaques associated with Alzheimer's disease.
Excessive amounts of copper and zinc have been observed in the plaques, so researchers from the University of Melbourne in Australia tried a novel approach called chelation therapy. (Unlike chelation therapy used to draw toxic metals, such as mercury, out of the blood, this type can penetrate into the brain.)
In a preliminary experiment, they gave patients the antibiotic clioquinol, which they hypothesized could remove zinc and copper from the beta-amyloid and help dissolve the protein.
In a 36-week study of 36 patients with moderate to severe Alzheimer's, half received twice-daily doses of clioquinol and half received a placebo. All underwent periodic tests of thinking and memory, along with blood measurements of beta-amyloid.
Beta-amyloid levels dropped among those who got the drug but increased among placebo recipients. The treated group scored higher on cognitive tests than the placebo group, but disease progression was slowed only in the most severely affected Alzheimer's patients.
The study appeared in the December issue of the Archives of Neurology.
In an accompanying editorial, Dr. Roger N. Rosenberg, the journal editor, said zinc-copper chelation "offers promise as a new therapeutic strategy" and merits further study in larger clinical trials.
A U.S. trial is being planned, but researchers must prove they can protect patients from several nerve-damaging illnesses that led to the withdrawal of oral clioquinol from the U.S. market in the 1970s, when it was predominantly used for intestinal infections. It's still used topically.