At the end of last month, a scientific journal pulled a research paper on Alzheimer’s disease.
The retraction came from Neurobiology of Aging, which removed a 2011 paper claiming to show that a version of a protein called amyloid-β was responsible for memory loss in Alzheimer’s disease. On its own, that might not seem notable; bad papers can make it through peer review and are only caught after publication.
But this wasn’t an isolated case. Over the past few years, multiple studies arguing that amyloid-β is the central driver of Alzheimer’s disease have been retracted. Some scientists have even been indicted for fraud over the issue. All the while, none of the drugs targeting this protein and its pathway have had any real clinical effect.
Why does this keep happening?
Plaques and tangles
The medical condition we currently call Alzheimer’s disease was first identified in 1906, after a neuropathologist named Alois Alzheimer examined brain tissue from the autopsy of Auguste Deter, a dementia patient he had been treating. Deter was just 55 when she died, much younger than most dementia patients. Alzheimer noted that her brain tissue contained plaques, which had previously been seen in other dementia patients, as well as tangles of nerve fibers, which had not.
For the next 80 years, that was about as much as we knew about this condition that robs sufferers of their memories, skills, and personalities. And until very recently, it was only possible to diagnose it post-mortem by examining the brain for those plaques and tangles. The advent of PET scanners and the discovery of biomarkers in blood have changed that.
