CHICAGO – Eli Lilly and Co's antibody drug for Alzheimer's disease was safe and appeared to be dissolving sticky brain plaques, but a three-month study was too short to show any improvement in memory, company researchers said Wednesday.

The infused therapy, known by the experimental name LY2062430, attempts to remove a brain-damaging protein called beta amyloid via antibodies that attach to individual, free-floating molecules of the protein before they can form clumps known as plaques.

“The safety profile for our antibody seems to be very, very good. We were not able to identify any side effects we could relate to the antibody,” Dr. Eric Siemers, medical director of Lilly's Alzheimer's disease research, said in an interview.

That may be significant.

People with Alzheimer's disease have too much beta amyloid plaque in the brain, and the prevailing theory is that removing the plaque may slow disease progression.

Rivals Elan Corp Plc and Wyeth, which are developing a drug with a similar approach, said on Tuesday that 12 people in a larger, longer study treated with their antibody developed vasogenic edema, a condition marked by a build-up of fluid in the brain, although the side effect appeared to be manageable.

Siemers said the Lilly drug may avoid damaging the brain because it does not attack plaque. “It binds to individual amyloid beta molecules,” he said.

FINDING THE TOXIN

“One of the big questions is what is really the toxic part of beta amyloid. There is good evidence that it is not the plaque itself,” said Siemers, who presented the findings at an Alzheimer's Association conference in Chicago.

Lilly's study involved 52 people with mild-to-moderate Alzheimer's disease and 16 healthy people who received 30-minute infusions of the drug or a placebo for 12 weeks.

The goal was to test for safety and to see if tests of blood and spinal fluid could detect changes in protein levels that would suggest it was working.

They found that after giving the antibody, more beta amyloid appeared in patients' blood and spinal fluid. The company sees this as a sign the antibody is clearing out the beta amyloid.

They used a type of brain imaging known as SPECT to measure plaque in the brains of 24 Alzheimer's patients and 13 healthy people.

In people who got the highest dose of the antibody, a type of beta amyloid typically found only in plaque appeared in their blood. “It appears the plaque started to dissolve around the edges,” Siemers said.

The study found no evidence that this made any difference at improving memory, but Siemers said researchers did not expect it would in such a short time.

Lilly will move to longer, larger studies next year to see if the treatment can alter mental decline. Siemers acknowledged that the larger studies may turn up side effects not seen in the smaller study.

Meanwhile, he said the company is pressing ahead with a drug using a completely different approach. It targets an enzyme called gamma secretase that is thought to be involved in making beta amyloid.

The aim of that drug is to interfere with the production of beta amyloid before it can build up in the brain.

Myriad Genetics Inc's Flurizan, also called tarenflurbil, targeted gamma secretase and showed promise in mid-stage trials but failed to show any benefit in a large study released last month.

(Editing by Maggie Fox/Jeffrey Benkoe)