Study: Antibiotic may help Alzheimer's disease

NEW ORLEANS - An antibiotic tested on mice genetically designed to mimic the effects of Alzheimer's disease reduced and even eliminated protein deposits that are a major feature of the disease, a researcher says.

Clioquinoline was approved as a human drug decades ago and is now being tested on 50 Alzheimer's patients, said Dr. Ashley Bush of Massachusetts General Hospital and Harvard Medical School.

The drug was last used in the 1970s, when it was linked to a rare neurological disorder, Bush said during a Society for Neuroscience news conference Sunday. Bush is a consultant, scientific adviser and shareholder in Prana Biotechnology Ltd., which makes the drug.

The drug was effective in the mice experiments not because it kills germs but because it binds two metals, Bush said. The mice used in the initial experiments were genetically programmed to overproduce beta-amyloid, which creates the sticky plaques that are a major feature of Alzheimer's.

Copper and zinc ''decorate'' those plaques - and mice given clioquinoline, which marries those metals, showed a 51 percent reduction in the plaques compared to untreated mice from the same strain, Bush said.

In one-third of the younger animals, it eliminated the plaques, even though the animals continued to overproduce beta-amyloid, he said. He said he believes this indicates that ''the brain can heal, can clear out the mess, if you get the plaque out of the way.''

The mice also got healthier and did better on a test of general behavior than untreated mice. Bush said he had not tested their ability to learn.

All of the patients testing the drug are being carefully monitored for any possible side effects, Bush said. They have mild to moderate Alzheimer's, and researchers expect to bring in more patients before the study is done a year from now.

The study is exciting, said David Morgan of the University of South Florida. ''It's very powerful data.''

However, he noted when discussing his own research that mice are an imperfect model of Alzheimer's disease because they do not lose large numbers of neurons, as people do.

Morgan described tests on mice treated with a possible vaccine produced by Elan Pharmaceuticals, an experiment which proved his own hypothesis wrong.

Morgan had expected the vaccine to hurt the animals' ability to learn, because it causes inflammation in the brain.

Instead, he confirmed that there was a slight plaque reduction and confounded his predictions about learning: The treated mice did much better than untreated mice in a water maze.

The maze's six arms radiate from a circle in the middle. One arm has an underwater platform on which a mouse can stand. The platform was in a different arm each day; mice swam through it five times a day.

''It's sort of like remembering where you parked your car that day,'' Morgan said.

By the fourth or fifth time through, 15-month-old treated mice remembered where to swim. Untreated 15-month-old mice did not.

Morgan said the magazine Nature plans to publish his results, but gave him permission to release them at this meeting.

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On the Net:

Society for Neuroscience: http://www.sfn.org

Alzheimer's Association: http://www.alz.org