(Corrects timeline paragraph eight to start clinical trials to
By Debra Sherman
Dec 5 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