Scientists have developed an antibody that can completely clear the harmful plaques linked to Alzheimer’s, as well as slow cognitive decline in people suffering from the neurodegenerative disease.
Although the causes of Alzheimer’s disease are still unknown, it is clear that the disease commences with progressive amyloid deposition in the brains of affected persons between ten and fifteen years before the emergence of initial clinical symptoms such as memory loss.
Researchers from the University of Zurich (UZH) in Switzerland have now been able to show that Aducanumab, a human monoclonal antibody, selectively binds brain amyloid plaques, thus enabling microglial cells to remove the plaques.
A one-year treatment with the antibody resulted in almost complete clearance of the brain amyloid plaques in the study group patients.
“The results of this clinical study make us optimistic that we can potentially make a great step forward in treating Alzheimer’s disease,” said Roger M Nitsch, professor at UZH.
“The effect of the antibody is very impressive. And the outcome is dependent on the dosage and length of treatment,” Nitsch said.
“After one year of treatment, practically no beta-amyloid plaques could be detected in the patients who received the highest dose of the antibody,” he said. The antibody was developed with the help of a technology platform from “Neurimmune.”
Using blood collected from elderly persons aged up to 100 years and demonstrating no cognitive impairment, researchers isolated immune cells whose antibodies are able to identify toxic beta-amyloid plaques.
As many 165 as patients with early-stage Alzheimer’s disease were treated in the clinical trial. The results encouraged researchers to additionally investigate how the treatment affected the symptoms of disease.
This was evaluated via standardised questionnaires to assess the cognitive abilities and everyday activities of the patients.
While patients in the placebo group exhibited significant cognitive decline, cognitive ability remained distinctly more stable in patients receiving the antibody,” Nitsch said. Some of the trial participants temporarily suffered from amyloid-related imaging abnormality (ARIA), an adverse effect that can be detected via magnetic resonance imaging.
In a minority of cases, this was accompanied by temporary mild to moderate headaches. The UZH researchers believe that ARIA is a measurable biological effect of amyloid clearance.
The research was published in the journal Nature.