In what could potentially be a major breakthrough, scientists believe they may have found the first drug that could slow down the rate at which Alzheimer’s disease breaks down the brain by as much as 34 percent.
The drug itself is called solanezumab and is manufactured by the US-based company Eli Lilly. While researchers cautioned that it is not a cure by any means, data from their clinical trials seemed to show that the drug did reduce the brain’s decline in patients with mild Alzheimer’s – something that has never before been recorded.
“This is the first evidence of something genuinely modifying the disease process,” said Dr. Eric Karran of Alzheimer’s Research UK to the Guardian. “It’s a breakthrough in my mind. The history of medicine suggests that once you get through that door you can explore further therapeutic opportunities much more aggressively. It makes us less helpless.”
Generally, Alzheimer’s disease damages and destroys brain cells. Many scientists believe the illness could be caused by proteins called amyloids, which clump onto brain cells and kill them.
While solanezumab was designed to target these proteins and get rid of them, the initial 2012 clinical trial ended in what was roundly seen as failure. During this trial, half of the patients with mild or moderate Alzheimer’s were given solanezumab and the other half was given a placebo.
Despite initially recording disappointing results, researchers at Eli Lilly then went back and poured over their data to discover that the advance of Alzheimers in patients with mild forms of the disease looked like it had slowed down by as much as 34 percent when taking solanezumab, the BBC reported. This raised the possibility that if the drug is prescribed in early stages, it could be beneficial.
As a result, the company went back to all the patients with mild Alzheimer’s – including those originally in the placebo group – and gave them all solanezumab for another two years. Scientists were concerned that what originally looked like a slowing Alzheimer’s could have simply been the drug treating symptoms, not the cause of the disease.
If that was the case, then even though the placebo group was taking solanezumab much longer than the first group, both groups would have roughly the same cognitive abilities by the time the two year extension was over.
Significantly, that was not the case. Instead, the group that had been taking solanezumab ever since the beginning of the first clinical trial managed to retain better cognitive functions compared to the group that had most recently started the drug. This indicated that the drug really was keeping brain cells alive longer and not just treating symptoms.
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“Today’s findings strongly suggest that targeting people in the earliest stages of Alzheimer’s disease with these antibody treatments is the best way to slow or stop Alzheimer’s disease,” said Dr. Doug Brown of the Alzheimer’s Society to the Guardian. “These drugs are able to reduce the sticky plaques of amyloid that build up in the brain, and now we have seen the first hints that doing this early enough may slow disease progression.”
Still, scientists said the results would need to be repeated before they could say this drug signals a breakthrough. Additionally, there were no details on “efficacy” or on the drug’s impact on amyloids in the brain, University of Southern California professor Dr. Lon Schneider told the New York Times.
A third clinical trial has been initiated by Eli Lilly that will test the drug only on patients with mild forms of Alzheimer’s, and those results should be available in 2017.