Eli Lilly and Co. suffered a delay in its effort to bring an Alzheimer’s drug to market this month, but it also published new research that the pharmaceutical company thinks confirms it is on the right track.

Indianapolis-based Lilly announced on Dec. 12 that it will conduct another Phase 3 trial of the drug solanezumab to show that the drug slows the progression of Alzheimer’s disease. In October, scientists detailed clinical trial results that showed the drug moderately slowed the decline in mental abilities in patients with mild forms of the memory-sapping disease.

But a week before that announcement, the journal Neuron published a paper by a team of 13 Alzheimer’s researchers at Lilly, which they think proves the science behind solanezumab is sound.

That could be significant because Lilly, which is losing patent protection on its older neuroscience blockbusters Zyprexa and Cymbalta, has staked enormous resources on bringing an Alzheimer’s drug to market. If successful, it could reap billions of dollars per year in sales.

“We learned a lot from solanezumab and that was the key point for how we figured out how to attack this,” said Ron DeMattos, Lilly’s lead biologist on solanezumab and the lead author of the new study.

The Neuron study tested a new drug’s ability to reduce the buildup of plaques in the brain that are a key marker of Alzheimer’s disease and, according to some theories, the cause of its damage.

These plaques are formed by the clumping and tangling of chunks of a brain protein called amyloid-beta. It is produced in every person’s brain but reaches excess levels in the brains of Alzheimer’s patients.

Removing amyloid or slowing its production are the goals of nearly all the experimental Alzheimer’s drugs being tested now by major pharmaceutical companies. Alzheimer’s disease is getting such attention because there is no effective treatment for it currently and the costs of caring for Alzheimer’s patients are estimated to be $180 billion per year in the United States alone.

Lilly’s scientists designed solanezumab to attach to free-floating pieces of amyloid and carry them out of the brain tissue into the spinal fluid or the bloodstream.

Solanezumab does not attach to amyloid plaques. But Lilly’s scientists reasoned that, as solanezumab reduced the levels of free-floating amyloid that hover around the amyloid plaques like a cloud, more of the amyloid pieces clumped up in plaques would be able to jump off and float away.

In its latest study, Lilly scientists designed a new drug, called mE8, that attaches only to amyloid plaques, but not to the free-floating pieces of amyloid surrounding the plaques.

Lilly’s drug, which is known as mE8, showed a better ability to remove plaque than the mouse version of a competing drug called bapineuzumab. That drug, which was developed by Ireland-based Elan Corp. and tested by New York-based Pfizer Inc. and New Jersey-based Johnson & Johnson, failed in a Phase 3 clinical trial this summer. Human studies of the drug were discontinued.

DeMattos attributed the differences to the fact that bapineuzumab attaches to both free-floating amyloid and to amyloid plaques. Much of the drug appears to have become clustered with free-floating amyloid before it could ever reach amyloid plaques in most parts of the brain.

He also noted that Lilly’s drug mE8 showed no bleeding in the brain, called microhemorrhaging. The mouse version of bapineuzumab did show some bleeding in mice brains.

“We’re really enthusiastic about this approach,” DeMattos said, noting that a humanized version of mE8 drug would be the next Alzheimer’s drug Lilly moves into clinical trials. In addition to solanezumab, Lilly already has one other drug in human trials.

DeMattos said it is likely that Alzheimer’s will be successfully treated through a combination of drugs, rather than just one. However, he said Lilly would need to thoroughly study both solanezumab and mE8 separately before it considers whether they could be used as a combination therapy.

“This has become a very hot topic among the academic clinicians,” DeMattos said of a combination therapy. “Lilly is uniquely positioned in that we have an antibody that targets the soluble [amyloid] beta and we have an antibody that targets the plaques specifically.”