This was published 1 year ago
Alleged Alzheimer’s research fraud won’t derail search for cure
By Stuart Layt
Australian experts say revelations that data from a major Alzheimer’s study may have been falsified is a wake-up call for the field, but it is not the fatal blow to current treatments that it appears to be.
A news report in Science went public late last week claiming to have found significant problems with the findings presented in a research paper on the causes of Alzheimer’s.
Alzheimer’s researchers have played down the discovery that key research from 16 years ago appears to have been flawed.Credit: Getty
That paper, published in the journal Nature in 2006, was a highly cited piece of evidence for the amyloid theory – that the degenerative neurological disease is caused by the build-up of plaques in the brain that disrupt the neurons.
An investigation by Science has now revealed that many of the images used by the researchers to show how a particular plaque, designated Aβ*56, accumulates in the brain appear to have been manipulated.
Multiple investigations are now underway into the accusations, but in the meantime, the scientific world has been left to grapple with what this means for Alzheimer’s research.
Potentially, 16 years of research, as well as billions of dollars spent in the US alone to develop treatments targeting amyloid beta proteins, could have been futile, as it was chasing a target that did not exist.
The initial uneasy consensus, however, appears to be that while unfortunate, the apparent falsification of data in the earlier paper does not invalidate the research that has followed.
Professor Colin Masters, a neuropathologist at the Florey Institute and the University of Melbourne, is a world-leading Alzheimer’s researcher whose work was the first in the world to define the key molecular and genetic pathways that produce amyloid plaques.
He said the initial reporting on the implications of the apparent falsification of data was “overblown” because the paper in question only dealt with a very specific protein that was not widely used as a research or drug target any more.
“It’s never been an issue for us in the field because we tried to reproduce those results at the time and we couldn’t, so we just got on and did other things,” he said.
“We never relied on this information, and we never took much notice of it [in subsequent research].”
Masters, who freely discloses that he is on the scientific advisory board of Acumen, which is developing anti-Aβ oligomer therapies, said he did not think any time or money had been wasted by investigating that avenue of research for potential treatments.
Professor Bryce Vissel, director of neuroscience and regenerative medicine at the University of Technology Sydney, is a noted sceptic of the amyloid theory, but he agrees with Masters that the Nature paper’s influence waned in subsequent years.
However, he believes it demonstrates the danger of becoming beholden to one scientific theory at the expense of others.
“In the Alzheimer’s field, there are several broad ideas [of the cause of the disease], and the dominant idea is that amyloid causes Azheimer’s,” he said.
“There’s been enormous failure in trying to treat the disease based on that theory, but the proponents for that theory point out that there are different forms of amyloid.”
Dementia is the leading cause of death for women in Australia, and the second leading cause of death overall, according to the Australian Bureau of Statistics, with Alzheimer’s specifically making up more than 70 per cent of all dementia cases in Australia.
Vissel said that fact, plus the billions of dollars poured into research for potential treatments and even a cure for the condition, meant there was “a lot at stake” when it came to research targets.
“The community want to see a solution for this, and on the other side of things, there’s the potential for some people to profit if we find the right solution,” he said.
“I think the majority of people working on this do not fall prey to that sort of pressure, but some people may do the wrong thing, and that is extremely disappointing and wrong.”
Vissel is convinced that while amyloids may play some part in the expression of Alzheimer’s, they are not the underlying cause, and continuing to target them with therapies is counterproductive.
But Masters says “you’ve got to go where the science is telling you to go”.
“And the genetics, which doesn’t lie, is pushing us strongly in the direction of amyloid-beta.”