(Reuters) – Drugmaker Eli Lilly & Co said it may have found a way to remove plaque from the brains of forgetful, old mice using an experimental therapy it hopes someday will be used to treat Alzheimer’s disease in humans.
Previous animal studies have demonstrated that it is possible to prevent the formation of brain plaques, which are thought to be a hallmark of the progressive memory-robbing disease. But until now, researchers have not been able to remove pre-existing plaques, made of amyloid beta protein, once they have deposited into the brain, Lilly said.
These deposited plaques are insoluble, whereas soluble forms of amyloid beta are free-floating around the brain and have been easier to target.
Lilly researchers developed a genetically engineered antibody that selectively targets insoluble plaques and was able to cross the blood-brain barrier. The antibody was then able to bind itself to the deposited amyloid beta, and clear roughly 50 percent of pre-existing plaques in the mice without causing damage to tiny vessels in the brain.
“We’re very enthused about understanding the mechanism and science behind it,” lead researcher Ronald DeMattos said in a telephone interview. “We don’t know how it translates in humans until we test human antibodies in clinical trials.”
Indeed, there have been scores of mice that were cured of cancer and other diseases with experimental drugs that did not work in humans.
But Lilly is excited about this study because, at least in mice, a new therapeutic approach for Alzheimer’s disease appears to be viable.
DeMattos said the drugmaker, which is developing other Alzheimer’s drugs, is already engineering a human antibody that will target insoluble plaques. He said he expects the company to begin clinical trials using this antibody within a year.
Results of the study, entirely funded by Lilly, were published in the journal Neuron on Wednesday.
Lilly’s best known Alzheimer’s disease drug is solanezumab, a medicine given by infusion that attacks amyloid beta protein. In data presented in August, the drug failed in large clinical trials to arrest cognitive and physical declines among patients with mild to moderate Alzheimer’s. But it was shown to somewhat delay cognitive declines in patients with mild symptoms.
(Additional reporting Ransdell Pierson; Editing by Nick Zieminski)
(This story corrects timeline paragraph eight to start clinical trials to one year.)
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