New alzheimer's drug reduce plaques in brain, slows dementia in early trial

The long, discouraging quest for a medication that works to treat alzheimer’s reached a potentially promising milestone on Wednesday. For the first time in a large clinical trial, a drug was able to both reduce the plaques in the brains of patients and slow the progression of dementia.
 
More extensive trials will be needed to know if the new drug is truly effective, but if the results, presented Wednesday at the Alzheimer’s Association International Conference in Chicago, are borne out, the drug may be the first to successfully attack both the brain changes and the symptoms of alzheimer’s.
 

“This trial shows you can both clear plaque and change cognition,” said Reisa Sperling, director of the Center for Alzheimer Research and Treatment at Brigham and Women’s Hospital in Boston, who was not involved in the study. “I don’t know that we’ve hit a home run yet. It’s important not to over-conclude on the data. But as a proof of concept, I feel like this is very encouraging.”
 

Aside from a couple of medications that can slow memory decline for a few months, there is no effective treatment for alzheimer’s, which affects about 44 million people worldwide, including 5.5 million Americans. It is estimated that those numbers will triple by 2050.

 
The trial involved 856 patients from the United States, Europe and Japan with early symptoms of cognitive decline. They were diagnosed with either mild cognitive impairment or mild alzheimer’s dementia, and all had significant accumulations of the amyloid protein that clumps into plaques in people with the disease, said Lynn Kramer, chief medical officer of Eisai, a Japan-based company that developed the drug, known as BAN2401, along with Biogen, based in Cambridge, Mass.
 
Many other drugs have managed to reduce amyloid levels but they did not ease memory decline or other cognitive difficulties. In the data presented Wednesday, the highest of the five doses of the new drug — an injection every two weeks of 10 milligrams per kilogram of a patient’s weight — both reduced amyloid levels and slowed cognitive decline when compared to patients who received placebo.

 
Of the 161 patients in the group taking the highest dose, 81 percent showed such significant drops in amyloid levels that they “converted from amyloid positive to amyloid negative,” Kramer said in an interview, meaning that the patients’ amyloid levels dropped from being considered high enough to correlate to dementia to a level below that dementia threshold.
 
And on a battery of cognitive and functional tests measuring memory and skills like planning and reasoning, the performance of the high-dose group declined at a rate that was 30 percent slower than the rate of decline in the placebo group.

 
Sperling, who briefly advised Eisai last year on a different drug, called the reductions in amyloid “dramatic,” but said the cognitive results were less momentous. Still, she said, “If you could really slow decline by 30 percent for people who are still normal or very mildly impaired, that would be clinically important.”
 
Samuel Gandy, associate director of the Mount Sinai Alzheimer’s Disease Research Center, said that for the drug to really be effective, it would have to allow patients to function longer independently without needing caregivers to help them with basic daily activities. That kind of practical application was not reflected in the data presented Wednesday.

 
“I wouldn’t say this is a quantum leap,” he said. “It is a convincing moving of the needle. But it’s not clear that the needle has moved far enough to make a difference in people’s lives.”
 
Kramer said the results were statistically significant 18 months after patients began taking the drug, but improvement began to be noticed after about six months.