When a scientist has to work at “not getting too excited,” you know something big has just happened. The discovery of an antibody that has initially proved to completely clear all visible signs of Alzheimer’s disease in the human brain is now undergoing more clinical trials to verify the findings.
Clinical researchers performed brain scans of people under siege from this degenerative disease at the same moment they were being given a dose of a drug designed and structured into an antibody similar to immune cells taken from the bodies of elders of up to 100 years, who have virtually no signs of the disease.
After one year all of the disease-related “amyloid plaques” that predictably build up inside an Alzheimer patient’s brain were virtually non-existent in those who took the highest doses of this antibody.
The peer-reviewed journal Nature, published the paper which also showed that these same patients had shown clear signs that the progression of the disease had also slowed, significantly postponing any more cognitive decline.
Conclusions drawn by scientists studying the scans point to the plaque’s presence actually being a part of the cause of the disease and not simply a by-product of it, as they had predicted earlier.
Scientists are further predicting that if the results are confirmed by running larger clinical trials (which are already under way around the world), one scientist called it a “game-changer” for collective efforts designed to prevent the onset of Alzheimer’s disease. Prominent researcher, Professor Roger Nitsch, of Zurich University, where the tests were conducted, described what they found;
“One year later, the images of the placebo group are basically unchanged. In the three dose groups, a very clear reduction in amyloid plaques is shown – the higher the dose, the larger the degree of reduction,” he said.
According to Dr. Nitsch; “In the 10mg dose for the group of the drug called aducanumab, after one year you can see no red on the image. This meant that the amyloid has almost completely disappeared.
“Compared to other studies published in the past, the effect-size of this drug is unprecedented.”
Professor Eric Reiman, of The University of Arizona, also wrote: “If these preliminary cognitive findings are confirmed in larger and more-definitive clinical trials, which are now under way, it would provide a shot in the arm in the fight against Alzheimer’s disease. He also said; “although the authors’ additional cognitive findings are encouraging, they are not definitive. It would be prudent to withhold judgement about aducanumab’s cognitive benefit until results from the larger trials are in. But then he added: “Confirmation that an anti-amyloid plaque treatment slows cognitive decline would be a game-changer for how we understand, treat and prevent Alzheimer’s disease.”
The study was led by scientists from pharmaceutical companies such as Biogen and Neurimmune.
Dr. Tara Spires-Jones, interim director of Edinburgh University’s Centre for Cognitive and Neural Systems, reported that the research showed the antibody “robustly reduced amyloid pathology in a small group of people in very early stages of the disease.”
“I am cautiously optimistic about this treatment, but trying not to get too excited because many drugs make it through this early stage of testing then go on to fail in larger trials,” she said.
Researchers did find some side-effects, such as headaches, also reminding everyone that the initial trial had not been designed to measure whether the drug slowed the decline in memory and thinking.
The larger trials are now under way, including in the UK, and are due to finish in 2020.
For more information, or to make a donation to the Alzheimer’s Association of Northern California and Northern Nevada, go to www.alz.org/norcal
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