Another once-promising Alzheimer's drug has just been tossed on the pharmaceutical scrap heap.
This time it's a drug called bapineuzumab. Like several previous experimental drugs, it was designed to attack the plaques that build up in the brains of people with Alzheimer's.
And like those earlier drugs, it failed.
The drug company Pfizer issued a statement yesterday saying a study of about 1,300 patients with mild-to-moderate Alzheimer's disease found that bapineuzumab didn't help. Pfizer also announced it was discontinuing all studies of the intravenous form of the drug.
The failure of bapineuzumab is the latest evidence that treating Alzheimer's may not be as simple as going after plaques in the brain.
But scientists remain confident that treatments will need to target the major component of those plaques, a protein called amyloid beta or "A-beta."
"It all begins with A-beta," Robert Vassar, an Alzheimer's researcher at Northwestern University, tells Shots. "If we could limit the production of A-beta in the brain or enhance its clearance out of the brain then I think we could really make some headway in terms of preventing Alzheimer's disease and perhaps curing it."
The question is whether it makes sense to attack the A-beta in plaques that have already formed.
Recently, some scientists have suggested that the sticky plaques actually protect the brain by trapping bits of A-beta. These scientists suspect that it's free-floating particles of A-beta that actually damage brain cells.
If that's the case, drugs would have to eliminate free floating bits of A-beta, not just the A-beta in plaques.
One way to accomplish this may be to interrupt the process that forms A-beta in the first place, researchers say.
Several drugs designed to do this are in the pipeline. And their prospects are looking bright after a study found that people with a gene mutation that reduces A-beta production were much less likely to develop Alzheimer's.
The failure of plaque-attacking drugs may also be a sign that treatments need to begin well before people begin showing symptoms of Alzheimer's.
"My opinion and the opinion of many colleagues is that once the A-Beta begins to accumulate in the brain and a person actually has memory symptoms it may actually be too late," Vassar says.
And ultimately, treating Alzheimer's may require going after A-beta in several different ways, says William Mobley, chairman of the department of neurosciences at the University of California, San Diego. That could mean finding a way to both reduce production of A-beta and remove it from the brain, he says.
"Several shots on goal may be needed," Mobley says.