CHICAGO (Reuters) -
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 on
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)