The failure of another drug that targets beta amyloid plaques in the brains of people with Alzheimer’s has revived doubts over whether plaque causes the disease
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[NewScientist] Key Alzheimer’s drug shows ‘virtually no chance of working’
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ImmInst
, Feb 16 2017 02:43 PM
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Posted 17 February 2017 - 08:13 AM
"Any hope left?
It may not be the end of the verubecestat story, however, because a parallel study of the drug continues. It might not have worked in people with mild or moderate Alzheimer’s because there was already too much amyloid plaque in the brain.
The parallel study is looking into the drug’s effect in people at a much earlier stage of the disease, when the hope is that they have so little plaque that stopping it in its tracks will prevent further symptoms.
Earlier trials with similar drugs that blocked amyloid production had to be halted because of severe side effects. Merck hoped that verubecestat could sidestep these by shutting off production exclusively in the brain, avoiding side effects caused by the disruption of amyloid elsewhere in the body.
Other drugs are now entering trials that work even more subtly, allowing amyloid production to continue in the brain, but shifting the type of amyloid plaques formed away from the most toxic, sticky forms that accumulate into plaques.
And there is one anti-amyloid drug that has already shown signs of having benefits. Called aducanumab and developed by Biogen, it targets and depletes pre-existing plaque. The company recently revealed scans showing that it reduces the amount of plaque in the brains of people with the disease, although we will have to wait until 2019 to find out whether by doing this, it also halts the progression of symptoms. Results of Merck’s second study into verubecestat will be ready the same year."
It may not be the end of the verubecestat story, however, because a parallel study of the drug continues. It might not have worked in people with mild or moderate Alzheimer’s because there was already too much amyloid plaque in the brain.
The parallel study is looking into the drug’s effect in people at a much earlier stage of the disease, when the hope is that they have so little plaque that stopping it in its tracks will prevent further symptoms.
Earlier trials with similar drugs that blocked amyloid production had to be halted because of severe side effects. Merck hoped that verubecestat could sidestep these by shutting off production exclusively in the brain, avoiding side effects caused by the disruption of amyloid elsewhere in the body.
Other drugs are now entering trials that work even more subtly, allowing amyloid production to continue in the brain, but shifting the type of amyloid plaques formed away from the most toxic, sticky forms that accumulate into plaques.
And there is one anti-amyloid drug that has already shown signs of having benefits. Called aducanumab and developed by Biogen, it targets and depletes pre-existing plaque. The company recently revealed scans showing that it reduces the amount of plaque in the brains of people with the disease, although we will have to wait until 2019 to find out whether by doing this, it also halts the progression of symptoms. Results of Merck’s second study into verubecestat will be ready the same year."
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