On Wednesday, the search for a drug to treat Alzheimer’s reached a hopeful crossroads. For the first time in a large clinical trial, a new drug both reduced plaques in brains of sufferers with Alzheimer’s and slowed the progression of dementia.
These results were presented on Wednesday at the Alzheimer’s Association International Conference in Chicago. More trials are needed if the drug is to be considered truly effective, but for the first time there is hope on the horizon for the 44 million people worldwide suffering from Alzheimer’s.
In an article published by The New York Times, Dr. 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 said,“This trial shows you can both clear plaque and change cognition. 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 promising.”
As reported in The Times, the trial involved 856 patients from the U.S., Europe and Japan who showed early symptoms of cognitive decline. They received a diagnosis of either mild cognitive impairment or mild Alzheimer’s dementia, and all had brain scans revealing significant accumulations of the amyloid protein that clumps into plaques in people with the disease, reported Dr. 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.
There have been other drugs that have been able to reduce amyloid levels but they didn’t alleviate memory decline or other cognitive deficits. The data presented on Wednesday revealed that 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 — reduced amyloid levels and slowed cognitive decline when compared to patients who received placebo.
Out of the 856 patients involved in the study, 161 patients in the group took the highest dose. Eighty-one percent of these patients showed such significant drops in amyloid levels that they “converted from amyloid positive to amyloid negative,” Dr. Kramer said in an interview. Translated, this means that patients’ amyloid levels dropped from being high enough to be considered dementia to a level below the dementia threshold.
Additionally, during a battery of cognitive and functional tests measuring memory and skills that involve planning and reasoning, the high-dose group’s performace declined at a rate that was 30 percent slower than the rate of decline in the placebo group.
In The Times interview, Dr. Sperling, who was an advisor to Eisai last year, called the reductions in amyloid “dramatic,” but said the cognitive results were less momentous. Still, she expressed, “If you could really slow decline by 30 percent for people who are still normal or very mildly impaired, that would be clinically important.”
More research and further tests are needed to determine if the drug has the capability to be effective long-term, but it’s definitely a move in the right direction.
Source:The New York Times