University of Minnesota researcher tries to back up Alzheimer’s findings amid image scandal, #University #Minnesota #researcher #seeks #sustain #Alzheimers #findings #image #scandal OLASMEDIA TV NEWSThis is what we have for you today:
Accusations of manipulated images and manipulated Alzheimer’s research may tarnish the University of Minnesota, but greater demand is looming in the race for a cure.
What about U Alzheimer’s historical discoveries that are still valid today?
Researchers who questioned whether images in U studies had been falsified said they could undermine an important 2006 discovery: a protein called abeta star 56, which independently caused amnesia in rats and looked like the long-awaited smoking gun behind Alzheimer’s disease. . The leader of the U study, Dr. Karen Ashe objected that a colleague, Sylvain Lesné, had edited the wrong photos, but she defended the discovery.
“While editing of selected images should not have taken place, the adjustments are immaterial, unimportant and do not affect the study results,” she said.
Investigations by the U and the National Institutes of Health — which funded much of the research — will assess misconduct by Lesné or other authors, while scientific journals determine whether the studies containing suspicious images require corrections or retractions.
Behind the controversy is a nasty neurological disease that affects 6 million Americans and is expected to grow with an aging population. The condition inhibits thinking cells, neurons, from performing cognitive or memory functions, or from transmitting signals that tell muscles and organs what to do.
Although several papers are involved, the 2006 study in the journal Nature gets the most attention because it has discovered abeta star 56 or Aβ*56. Some researchers have been dismissive of the effort to replicate the findings, but there’s little doubt about the study’s impact. The article has been cited thousands of times by scientists who have used it as the basis for further Alzheimer’s research.
“We wouldn’t be where we are today in terms of understanding,” said Maria Carrillo, chief science officer of the Alzheimer’s Association. However, as the organization prepared its convention in San Diego next week, she said: planned presentations were proof that the investigation has gone beyond this discovery.
However, rooting out academic improprieties remains important, she said. “We are self-monitoring. If we can’t count on that, everything will fall apart.”
The U paper built on the theory that the disease was related to amyloids, proteins that can build up abnormally as plaques and perhaps block neurons. The researchers focused on soluble forms, rather than hardened plaques, that could accumulate for years prior to the dementia symptoms that come with age.
U researchers found a link between Aβ*56 and cognitive problems in middle-aged mice that were genetically bred to produce amyloid plaques. They then purified the protein and injected it into young rats, which consequently showed memory problems based on their inability to navigate a water maze.
At the time, the discovery that “Aβ*56 impairs memory independent of plaques or neuronal loss” was hailed by nature as a “star suspect” in the search for treatments for Alzheimer’s disease. Today, the paper is tagged with a warning to handle the results with caution until the review of disputed images is complete.
Much attention is paid to Western blots, which use electrical charges to separate proteins and a chemical process to create visual representations of them. The size and thickness of the chemical bands produced on film correspond to the amount of protein and, by extension, whether it is involved in a disease.
A magnification of one spot in the Nature paper showed bands indicating the presence of Aβ*56 in rats exhibiting amnesia. dr. However, Matthew Schrag, an Alzheimer’s disease researcher in Tennessee, discovered linear discolorations around the bands, suggesting they may have been cut and pasted. Some bands also appeared duplicated. Another spot showed clusters of identical peripheral dots around the bands suggesting photo editing.
Schrag, who conducted the review outside of his work at Vanderbilt University, publicized his concerns about the PubPeer academic website and contributed to a study by Science magazine on Lesné in July. Expert reviewers confirmed the concerns.
“This is a very sad example of human vulnerability and crime,” said Dr. Dennis Selkoe, a neuroscientist at Harvard Medical School. The proponent of the amyloid link to Alzheimer’s agreed that some U images appeared to be manipulated.
The Science article suggested that Lesné had manipulated images before joining Ashe’s team in 2002 as a research assistant and being promoted to U assistant professor in 2009 with his own lab. A supervisor of Lesné’s doctoral training at the University of Caen Normandy in France told the magazine he withdrew a paper from publication because he questioned the images Lesné made.
Lesné did not respond to requests for comment on this story.
The U addressed this issue before and ordered a recall in 2008 from a milestone paper about adult stem cells after they discovered they contained manipulated images.
Schrag said he didn’t find any manipulated image studies in which Ashe was an author without Lesné, but the concerns extend beyond their 16-year paper. He found traces of manipulated images in a 2013 study in the journal Brain in which the U researchers confirmed their findings in human tissue about Aβ*56 as a precursor to Alzheimer’s disease. Images released this year as a correction look so different that Schrag wonders if they came from the same experiment.
Stains mean little to the untrained eye, but they are the essence of research, said Elisabeth Bik, a San Diego microbiologist turned forensic imaging consultant. She agreed that some of the images in Lesné’s papers appear to have been manipulated.
“A scientific paper is not like a children’s book, where the pictures are just there to clarify the whole story,” she said. “It’s different. The images are the data in my opinion.”
The now controversial Nature paper has influenced years of research. Federal funding increased for Alzheimer’s disease in general, but for studies focusing on amyloids in particular.
The research was needed because amyloids are part of the Alzheimer’s puzzle, but the increased focus delayed studies of other key pieces, said Dr. Ronald Petersen, director of the Mayo Clinic Alzheimer’s Disease Research Center. Immune reactions and cardiovascular disease also affect Alzheimer’s disease, along with tau, a protein that can build up abnormally in neurons.
The inequality is apparent from the development of medicines. Aduhelm received federal approval last year as a treatment for Alzheimer’s disease that breaks down amyloid plaques, although some doctors dispute whether it also slows cognitive decline. Three monoclonal antibody infusions are halfway through clinical trials; all target amyloids.
Trials of other compounds targeting amyloids have failed. Ashe said it’s unfair to label the controversial U papers for such errors, because they involved classes of amyloid proteins that were different and easier to replicate than Aβ*56.
Ashe said she expressed doubts that drugs targeting those proteins would work and that she is not married to amyloids as the primary cause of Alzheimer’s disease. Her research has explored tau and other possible causes.
Carrillo of the Alzheimer’s Association said limited funding years ago forced conservative judgments to support research in areas such as amyloids where there was early evidence. Increases have fostered bolder exploration, and she expects Alzheimer’s treatments targeting tau and inflammation to appear right behind the current wave targeting amyloids.
Aβ*56 has been “quite irrelevant” to current drug studies, she said, so the idea that the U controversy could undermine ongoing discoveries is “exaggerated and exaggerated.”