As more experimental drugs fail to stop Alzheimer’s from destroying human memory, experts now wonder whether research into the devastating brain disease has been marching in the wrong direction.
In recent weeks, a pair of high-profile disappointments have been reported, including one just announced on a trial of the Eli Lily drug solanezumab.
Now, researchers are trying to figure out what might have been missed in the search for an Alzheimer’s cure.
Did errors occur in the clinical trials of these drugs, creating the failure of potentially promising therapies? Or has there been a fundamental misunderstanding of the complex nature of Alzheimer’s disease?
Until now, research has focused mainly on treating or preventing Alzheimer’s by attacking the clumps of amyloid beta protein that form in patients’ brains, potentially blocking signals sent between brain synapses. Amyloid plaques are one of the hallmarks of the disease.
“The overriding hypothesis for many years has been the amyloid hypothesis — the idea if you can stop, slow or clear the formation of amyloid plaques from the brain you will be able to treat the disease and see marked improvements in cognition,” said James Hendrix, director of global science initiatives for the Alzheimer’s Association. “So far, that hasn’t worked out.”
Solanezumab binds with amyloid beta, and was intended to help the body flush the protein out of the brain before it could form damaging plaques.
But the drug failed to significantly slow thinking declines, Columbia University researchers reported in the Jan. 25 issue of the New England Journal of Medicine.
Those results came on the heels of a trio of failed trials of the drug idalopirdine, which was intended to help treat Alzheimer’s by promoting production of serotonin and other essential brain chemicals. A team of researchers reported in the Journal of the American Medical Association earlier this month that the drug failed to improve thinking or memory in Alzheimer’s patients.
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