An experimental drug that failed to stop mental decline in Alzheimer’s patients also signaled potential benefit that suggests it might help if given earlier, fuller results of two major studies show.
Some patients on the drug had stable levels of brain plaque and less evidence of nerve damage compared to others who were given a dummy treatment, researchers reported Tuesday.
The drug is called bapineuzumab, made by Pfizer Inc. and Johnson & Johnson. The new results suggest it might work if given sooner, before so much damage and memory loss have occurred that it might not be possible to reverse, experts say.
“We’re very disappointed that we were not able to come up with a treatment to provide to our dementia patients in the near term,” said Dr. Reisa Sperling, director of the Alzheimer’s center at Brigham and Women’s Hospital in Boston and leader of one of the studies.
But brain imaging and spinal fluid tests are “very encouraging” and suggest the drug was “doing something to the biology of the disease.”
“We’ve got a path forward” now to test it in people with mild mental impairment or those who show plaque on brain imaging but have not yet developed symptoms of dementia, Sperling said.
Of people with mild cognitive impairment, about 15 percent to 20 percent a year will develop Alzheimer’s disease.
About 35 million people worldwide have dementia, and Alzheimer’s is the most common type. In the U.S., about 5 million have Alzheimer’s. Current medicines such as Aricept and Namenda just temporarily ease symptoms. There is no known cure.
This year researchers had been hopeful of major progress in treating the disease, but study after study has proved disappointing, including results reported earlier on bapineuzumab. The drug failed to slow mental decline or improve activities of daily living for patients with mild to moderate Alzheimer’s in two studies in the United States and Canada.
Bapineuzumab is designed to attach to and help clear amyloid, the stuff that makes up the sticky plaque that clogs patients’ brains, harming nerve cells and impairing memory and thought. Doctors don’t know whether amyloid is a cause or just a symptom of Alzheimer’s, but many companies are testing drugs to try to remove it.
Sperling’s study involved people with a gene that raises the risk of developing the disease. Dr. Stephen Salloway, a neurologist at Brown Medical School in Providence, R.I., led the other study of people without the gene. Both researchers have consulted for the companies that make the drug and presented results Tuesday at a neurology conference in Stockholm.