Amyloid & Alzheimer’s: the cause-and-effect question that some stories still miss

The announcement by Johnson & Johnson and Pfizer that they were pulling the plug on clinical testing of the Alzheimer’s drug Bapineuzumab after two failed clinical trials, got a lot of mainstream news media coverage – as it should have to balance some of the earlier breathless hype about the drug’s potential.

But not many stories that we saw got at a core issue.  Bloomberg News did a good job when it reported:

While companies have focused on developing drugs to hinder the amyloid deposits, scientists aren’t certain whether the clumps cause or are a minor contributor to the disease or merely a consequence. 

“Alzheimer’s is a tough nut for any drug company to crack,” said Erik Gordon, a professor at the University of Michigan’s Ross School of Business, in an e-mail. “We don’t know for sure what causes it or even what it really is. There will be more failures before we see a success.”

…

Numerous reasons may account for the bapineuzumab trial failures, said Lon Schneider, director of the University of Southern California Alzheimer’s Disease Research and Clinical Center in Los Angeles. It could be that intervening earlier in the disease process is necessary, or that researchers need to attack amyloid in a different way, he said.

“My wish is that the investor and scientific community doesn’t interpret this as something to the effect that the amyloid hypothesis for treatment is invalid or dead,” Schneider said in a telephone interview. “That’s not the way I’m interpreting it.”

The New York Times reported that the drug “targets beta amyloid, a protein that has toxic effects on the brain and is believed to be a cause of the disease,” and with its failure, “some have called that theory into question.”

Reuters at least included this – but we wish the perspective had come from a scientist in the field, not just an analyst:

“Disappointingly for patients and investors, the future of the beta amyloid approach to treatment of AD (Alzheimer’s disease) now lies in the balance,” said Deutsche Bank analyst Richard Parkes.

The Associated Press story didn’t offer that context.  Neither did the Wall Street Journal story that only danced around the topic:

 Bapineuzumab aimed to attack a sticky substance that builds up in the brains of Alzheimer’s patients. While the drug appeared to succeed at removing these so-called amyloid plaques, the trial results suggest that wasn’t enough to provide a therapeutic benefit, at least in patients who have had the disease for long enough to be classified as mild or moderate.

“Targeting amyloid we still believe is very important. The main question is going to be how early do you need to do that” and how to identify patients soon enough, said Husseini Manji, who heads neuroscience research at J&J. He called the results “a terrific disappointment and a setback,” but said lessons could be learned that would drive further drug R&D.

Right now amyloid is a surrogate marker.  Journalists who build up hope over experimental drugs – and then report on drug failures – need to keep that in mind and should help readers understand the core issue as well. And, yes, we know that some of the stories above are “business” stories, but as we’ve written in the past, online news surfers find business stories just as they find consumer health news stories and the differentiation is almost irrelevant online.

See our primer on surrogate markers.

(Photo credit:  Jensflorian [CC-BY-SA-3.0] via Wikimedia Commons)

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