An experimental drug that failed to stop mental decline in Alzheimer's patients also showed some potential benefit, fuller results of two major studies now 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 (bap-ih-NOOZ-uh-mab), made by Pfizer Inc. and Johnson & Johnson. The new results suggest it might work if given earlier in the course of the disease, 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 centre 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 "that we were doing something to the biology of the disease" by giving the drug, she said.
"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 to 20 per cent 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.
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.
Two studies of more than 1,000 patients each in the United States and Canada tested bapineuzumab in people with mild to moderate Alzheimer's. 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 Sweden.
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