Novel antibody shows hope for Alzheimer's patients

London: Researchers have developed a new antibody that has the potential to completely remove the harmful beta-amyloid plaques -- protein deposits -- in the brain of patients with early-stage Alzheimer's disease.

The findings of an early stage clinical study showed that mental decline could be significantly slowed in patients who were treated with antibody Aducanumab -- a human monoclonal antibody -- for a year as opposed to the placebo group.

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, the researchers said. 

"While patients in the placebo group exhibited significant cognitive decline, cognitive ability remained distinctly more stable in patients receiving the antibody," said Roger M. Nitsch, Professor at the University of Zurich in Switzerland.

Aducanumab selectively binds brain amyloid plaques, thus enabling microglial cells to remove the plaques. 

After one year of treatment, practically no beta-amyloid plaques could be detected in the patients who received the highest dose of the antibody, the researchers noted.

In the phase 1b clinical trial, 165 patients with early-stage Alzheimer's disease were treated with Aducanumab.

Aducanumab also showed positive effects on clinical symptoms the cognitive abilities and everyday activities of the patients. 

Using blood collected from elderly persons aged up to one hundred and demonstrating no cognitive impairment, the researchers isolated precisely those immune cells whose antibodies are able to identify toxic beta-amyloid plaques but not the amyloid precursor protein that is present throughout the human body and that presumably plays an important role in the growth of nerve cells. 

The good safety profile of Aducanumab in patients may well be attributed to the antibody's specific capacity to bond with the abnormally folded beta-amyloid protein fragment as well as the fact that the antibody is of human origin.

"The effect of the antibody is very impressive. And the outcome is dependent on the dosage and length of treatment," Nitsch added, in the paper published in the journal Nature.

However, 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 results of this clinical study make us optimistic that we can potentially make a great step forward in treating Alzheimer's disease," Nitsch concluded.