Alzheimer’s researchers have for decades focused much of their study on the amyloid plaques thought to cause the Disease. That has largely been a mistake, according to Dr. Karl Herrup.

Herrup, who is a professor and investigator with the University of Pittsburgh’s Alzheimer’s Disease Research Center, thinks this is an issue that began back in 1906 when the first hypothesis regarding the disease was made.

“To pursue it doggedly now, all these years later, and to use it as a rationale to try … to suppress the pursuit of other forms of research that might have looked for other causes, I think is where we’ve gone substantially wrong,” Herrup told Memory Care Business.

Herrup has long studied what he considers flaws in the research and treatment of Alzheimer’s disease. It was the topic of his 2021 book, “How Not to Study a Disease: The Story of Alzheimer’s.” He also recently spoke about the issue on a University of Chicago podcast.

To Herrup, “the best way to study Alzheimer’s disease is not to study Alzheimer’s disease,” as he recently said on the podcast. By that, he means researchers have been too focused on Alzheimer’s supposed amyloid plaque origins, and not on its potentially deeper, more nuanced origins.

According to Herrup, a cross-section of older adults after death likely would reveal that many had high levels of plaque in their brains that would otherwise indicate Alzheimer’s disease, without ever having symptoms while they were alive. That is a curious result and worth more study and examination, he said.

“We’re still spending an inordinate amount of time pursuing the amyloid basis of Alzheimer’s disease, and that’s just holding us back,” Herrup said.

Instead, he is coming around to the notion that Alzheimer’s is a disease with many different smaller origins, inflammation being a big one.

Research has shown benefits in lowering the risk for Alzheimer’s disease through lifestyle changes including managing blood pressure, mental and physical exercise and keeping blood sugar under control.

“For both scientists and pharmaceutical people, I’m afraid we’ve got to deal with the complexity that none of us would have hoped for in the beginning,” he said. “For the public … it’s a complicated calculation to make, and it’s not remunerative for the industry.”

Despite the issues he has noted, Herrup added the industry as a whole is starting to move in a “broader strategy” with how it is approaching the disease, specifically highlighting there is more interest in inflammation control and “many other potential causes.”

An additional frustration Herrup noted is that when other research projects are funded, such as looking at DNA damage or aging and the impact of Alzheimer’s, amyloid plaque deposition is used “as a readout” to measure the success of the approach if the pathological markers are reduced. In doing so, it’s a “classic case of circular logic.”

However, despite these frustrations, Herrup said he is optimistic about the future of Alzheimer’s disease research, and there is more traction these days for a non-amyloid approach. Additionally, he added there needs to be a better understanding of the biology of aging.

“The future of Alzheimer’s research I think is still governed to a large extent by the orthodoxy,” he said. “So we will see a lot of studies about using anti-amyloid therapies in combination with other approaches.”

He added: I’m speaking as a basic scientist, not not as a clinician, or as a drug development person, where there’s a certain urgency in bringing a product to market … I think we’re seriously underinvesting in improving our understanding of the biology of aging.”

The solution can’t be a simple one, he noted, and it will be unlikely to be so.

“Alzheimer’s is a hugely complicated disease,” Herrup said. “What we need from people is the patience to stay the course and let us keep banging away at this problem. I do think progress is happening. I do think it’s possible to really make an impact. I would change the way we go about it, but I remain optimistic.”

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