Solanezumab trial fails

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The clinical trial of key Alzheimer’s drug solanezumab has failed, Eli Lilly has announced

But this is not the end for beta amyloid theory, one expert says.

Eli Lilly made the announcement yesterday that solanezumab did not slow down cognitive decline in patients with Alzheimer’s compared to those who took placebo.

Solanezumab targeted beta amyloid—the protein that forms clumps in the brains of Alzheimer’s patients—to clear the rogue proteins out, in the hope that this would lessen the symptoms and slow the progress of the disease.

In July 2015 it was announced that the initial results investigating the efficacy of the drug, while promising, were not conclusive and Eli Lilly arranged for larger-scale trials.

“This was a repeat of an earlier clinical trail of this drug, but this time they were testing it in patients with early-stage Alzheimer’s disease,” says Professor Bryce Vissel, The Roth Fellow and Director of Centre for Neuroscience and Regenerative Medicine at the University of Technology Sydney.

“The results were highly anticipated, not only because of hope for people with dementia, but also because, if the drug had succeeded, it would have demonstrated that beta amyloid contributes to the cause of Alzheimer’s disease, a major but recently controversial theory in the field.

“Importantly, this isn’t the end for beta amyloid theory. There’s a trial of another important drug for Alzheimer’s, aducanumab, being run by Biogen which has shown interesting and encouraging signs.”

There are numerous other trials in the pipeline of drugs which act in a variety of different ways to try to slow or reverse Alzheimer’s, he says.

“There’s good reason to have hope and optimism that a treatment will become available for this devastating disease in our lifetimes.”

Professor Roxana O’Carare, Professor of Clinical Neuroanatomy at the University of Southampton, says that it is “saddening” that the trial has failed, “but that may in part be because we need to deal with the problem of removing amyloid, not just breaking it down”.

“The brain is not equipped with lymph vessels as other organs have. Instead fluid and waste are eliminated from the brain along very narrow pathways that are embedded within the walls of blood vessels (perivascular pathways).

“These pathways change in composition and fail in their function with increasing age and with the risk factors for Alzheimer’s disease, resulting in the buildup of amyloid in the walls of blood vessels.

“When a vaccine such as solanezumab is administered, the sticky plaques of amyloid from the brain break down, but the excess waste and fluid (soluble amyloid) is unable to drain along the already compromised drainage pathways.

“In order for further immunisation trials to yield success, they need to be administered early, before the perivascular pathways are compromised.”

But Professor Peter Roberts, Emeritus Professor Pharmacology at the University of Bristol, says is he “not in the least surprised by the solanezemab data”.

“The problem, to my mind, is completely fundamental,” he says. “There is still no convincing evidence that shows a clear relationship between amyloid deposition and deficits in cognition in humans.

“All we really know is that evidence of amyloid deposition begins up to maybe 20 years before the onset of Alzheimer’s disease. This might be a good indicator, but does not prove causality.”

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