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Explained: Why a decade-long trial to prevent Alzheimer’s failed, and what that means

The decade-long effort was the first time that a clinical trial for the disease focused on people who were genetically predisposed to Alzheimer’s, but did not have any symptoms yet.

Affecting almost 55 million people globally, Alzheimer’s is the most common form of dementia. (Photo: Pixabay)

An experimental Alzheimer’s drug aimed at slowing or preventing cognitive decline in people has failed a clinical trial, landing a blow to efforts to find a solution to fight back against the neurodegenerative disease. What was the trial, why is the failure a significant blow?

Why was the trial closely watched?

The decade-long effort was the first time that a clinical trial for the disease focused on people who were genetically predisposed to Alzheimer’s, but did not have any symptoms yet. The study, according to the New York Times, involved people from an extended family in Columbia. Around 1,200 members of this extended family of 6,000 had a specific gene mutation that is a guarantee of developing the diseases. The drug on test was crenezumab, made by Roche group’s Genentech.

How did the trial work?

The aim was to start therapy early and to keep this type of Alzheimer’s – driven by a single gene mutation – in check. So, around 169 members of the family with the gene mutation were given the trial drug ‘crenezumab’ or a placebo, while 83 who had no gene mutation were just given the placebo. But after the lengthy trial, drug maker Roche announced on Thursday that the results were disappointing and did not show “significant clinical benefits”.

Why is this a major setback?

Affecting almost 55 million people globally, Alzheimer’s is the most common form of dementia. According to WHO, dementia is currently the seventh leading cause of death among all diseases and one of the major causes of disability and dependency among older people globally. A drug to treat the memory-robbing disease has proved elusive for years.

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The US FDA’s approval for Biogen’s Alzheimer’s drug – aduhelm — last year was greeted with much fanfare that was followed by a debate over its trial data actually proving that it can slow cognitive decline.

The latest failure has also called into question the approach that targeting toxic protein plaque called “beta-amyloid” in the brain is the right way to fight the disease and its progression. Majority studies for Alzheimer’s treatment focus on the amyloid theory that backs preventing the toxic protein from becoming sticky, toxic plaque that leads to cognitive decline.

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