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2006 Study: Alzheimer Community Remains Optimistic

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Concerns have been raised about the future of Alzheimer’s research after doubts were raised about a landmark 2006 study. Pamela Joe McFarlane/Getty Images
  • An investigative report has raised questions about the potential falsification of images in a landmark 2006 Alzheimer’s report.
  • The allegations have created concerns from some experts about the study’s conclusions that amyloid beta in the brain is a possible cause of Alzheimer’s.
  • However, experts told Healthline that even if the 2006 research is retracted there has been an abundance of research since then that has provided advancements in the search for a treatment and cure for the disease.
  • Officials at the Alzheimer’s Association say they remain optimistic about the current research in the field.

It’s news that has shaken up the Alzheimer’s world.

In a lengthy investigation published in the journal Science, a researcher has expressed concerns that a prominent 2006 Alzheimer’s disease study may have falsified images.

The new report states that images in the 2006 study, which identified a protein called amyloid beta as a possible cause of Alzheimer’s, may have been doctored by the study author, Sylvain Lesné, who at the time was a newly recognized PhD researcher at the University of Minnesota.

According to the report in Science, Lesné manipulated data images in multiple papers, casting doubt on the validity of hundreds of images in the research.

“Some look like ‘shockingly blatant’ examples of image tampering,” Donna Wilcock, Ph.D., an Alzheimer’s expert at the University of Kentucky, said in the Science story.

The revelation has left the Alzheimer’s community — researchers, doctors, patients, and family members — anxious and wondering how damaging this could be in terms of finding a treatment and possible cure for the disease.

However, experts interviewed by Healthline insist that the potential damage to Alzheimer’s research from this controversy has been overstated.

In Alzheimer’s disease, brain cells that process, store, and retrieve information degenerate and die.

Although scientists do not yet know the underlying cause of this process, they have identified several possible culprits, according to the Alzheimer’s Association.

One suspect is a microscopic brain protein fragment called beta-amyloid, a sticky compound that accumulates in the brain, disrupting communication between brain cells and eventually killing them.

Some researchers believe that flaws in the processes governing the production, accumulation, or disposal of beta-amyloid are the primary cause of Alzheimer’s.

Dr. Douglas Galasko, an emeritus professor in the department of neurosciences at the University of California San Diego, told Healthline that even if the 2006 research ends up being formally retracted, it will not negate years of research on amyloid aggregates and oligomers or substantially slow research.

Oligomers come in many sizes, Galasko explained, and are inherently difficult to characterize.

“Many other labs have made claims that other species of amyloid oligomers may play an important role in Alzheimer’s Disease,” he said.

“Whether oligomers are directly toxic or trigger abnormal signaling pathways or responses, or need to form fibrils or plaques for these pathological effects to emerge is still unclear. So the amyloid landscape is much larger than Abeta56*,” he added.

Dr. Karen Hsiao Ashe, a University of Minnesota professor and the senior author of the 2006 study, was not implicated in the alleged image fraud.

She took issue with parts of the Science story and said the repercussions will not be as profound as many believe.

“This Science article implied that my work has misled researchers in the Alzheimer’s field by encouraging the development of therapies targeting amyloid plaques, which most of us know are composed of Aβ. In fact, for over 20 years, I have consistently expressed concerns that drugs targeting plaques were likely to be ineffective,” Ashe wrote in the comments section of a column on Alzforum, an information site focused on Alzheimer’s and related disorders.

“There have been no clinical trials targeting the type 1 form of Aβ, the form which my research has suggested is more relevant to dementia. Mr. Piller erroneously conflated the two forms of Aβ,” she wrote.

“Having worked for decades to understand the cause of Alzheimer’s disease, so that better treatments can be found for patients, it is devastating to discover that a co-worker may have misled me and the scientific community through the doctoring of images,” she added. “It is, however, additionally distressing to find that a major scientific journal has flagrantly misrepresented the implications of my work.”

Maria Carrillo, Ph.D., the chief science officer at the Alzheimer’s Association, told Healthline that there is now great investment and diversity in Alzheimer’s and dementia research and she does not believe that will change.

“As we continue to move forward, it is important to note that this investigation is related only to a small segment of Alzheimer’s and dementia research, and does not reflect the full body or science in the field,” Carrillo said.

“As such, this should not influence the field’s accelerating pursuit of the initial causes and other contributors to Alzheimer’s disease and other dementia,” she added.

Carrillo added that there is no room for shortcuts based on dishonesty and deception.

“We owe that to all those who have been impacted by Alzheimer’s,” said Carrillo.

“If these accusations of falsification of images and data are true, there needs to be appropriate accountability for all responsible — including the scientists, their facility, the journals, and funders,” she said. “These include an admission of falsification, retraction of falsified images and data, funds should be returned, and those found responsible should be ineligible for future funding.”

Phil Gutis was diagnosed with younger-onset Alzheimer’s disease in 2016 at age 54.

He is currently enrolled in a clinical trial of aducanumab and writes for Being Patient, an advocacy organization for Alzheimer’s patients and caregivers.

“After reading the Science story, I certainly did not feel like they found the fraud of the century,” he said. “Fraud, yes, Bad, certainly. Story of the century? Not from this layman’s perspective, limited as it may be.”

As someone who continues to participate in trials of aducanumab, the anti-amyloid drug from Biogen that received controversial approval from the Food and Drug Administration last year, Gutis remains convinced that the drug has helped him.

“No alleged Photoshop fraud will change that perspective,” he said. “My read of the literature, with or without this one study, is that beta-amyloid remains one of several important factors in the pathogenesis of Alzheimer’s disease.”

New therapies for Alzheimer’s have been few and far between the past two decades, but are we getting closer to finding a treatment?

Dr. Edward Koo, an emeritus professor in the department of neurosciences at the University of California San Diego, said nobody knows for certain.

“It’s reasonable to hedge our bets by considering a variety of treatment approaches, as long as they have credible supporting evidence and drugs are used that engage defined targets and test hypotheses,” he told Healthline.

“If a drug does not work, we should be able to make clear conclusions from its clinical trial program and move on. We will know when the first unequivocal ‘win’ in [Alzheimer’s] treatment comes along and that will be very informative on where we went wrong previously, and how we can improve on future treatments. But it will have very little to do with the abeta*56 story, right or wrong,” Koo said.

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