After one year of treatment, practically no beta-amyloid plaques could be detected in the patients who received the highest dose of the antibody.
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Higher antibody doses and greater amyloid beta plaque reductions were also associated with slower cognitive decline.
“These early studies of aducanumab show its effectiveness in removing amyloid plaque from the brain as well as its potential effect on the slowing of cognitive decline in patients suffering from Alzheimer’s disease”, Dr. Alfred Sandrock, executive vice president and chief medical officer at Biogen Inc., the drug’s manufacturer, said in a press release. In a paper published Wednesday in the journal Nature, a trial to evaluate the drug’s safety and tolerability showed positive results.
Researchers from the University of Zurich (UZH) 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. There was little change in the brains of those who received the placebo.
The participants were divided into two groups, where the first one was to be given monthly infusions of the new drug and the other one was to be given only a placebo for 54 weeks. Many researchers argue that these protein blobs are the cause of Alzheimer’s symptoms, but we don’t know enough to say for sure-the tangles themselves could also be a symptom. “That is a very striking and encouraging finding and a major advance”. The plaques prevent brain cells from communicating, causing irreversible memory loss and cognitive decline.
“Now is the time to find out”.
And while experts believe the key to stopping Alzheimer’s will ultimately require a combination of approaches, “right now we need one good one, a new one”.
Funded by the Alzheimer’s Society, the group of researchers from Cardiff University, King’s College London and the University of Oxford studied blood from 292 individuals with the earliest signs of memory impairment and found a set of biomarkers (indicators of disease) that predicted whether or not a given individual would develop Alzheimer’s disease.
Dr Tara Spires-Jones, from the University of Edinburgh’s Centre for Cognitive and Neural Systems, said: “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”.
In a transgenic mouse model, the authors show that aducanumab can enter the brain and dose-dependently reduce soluble and insoluble amyloid beta.
“In the high dose group the amyloid has nearly completely disappeared”.
“At this point, I would not be so concerned that I would advise people not to participate in the trials of the drug”, says James Hendrix, director of global science initiatives at the Alzheimer’s Association.
The ENGAGE and EMERGE phase 3 clinical trials for aducanumab are now recruiting patients and are expected to be concluded in early 2022.
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However Gordon Wilcock, emeritus professor of geratology at Oxford University, was somewhat downbeat about the findings. Pharmaceutical companies have sunk billions of dollars into drugs aimed at preventing or reducing the disease’s hallmark plaques, abnormal brain deposits of a protein fragment called β amyloid, but a long list of failed clinical trials has led many to question that strategy.
