On May 3, 2021, Matt Price drove his 73-year-old father Stephen from their home in New Jersey at a medical center on the coast of Jersey, for his first injection of an experimental drug called Simufilam. Cassava Sciences, a Biofarma company in Texas, had developed Simufilam to treat (and probably curated) Alzheimer’s disease, the most common form of dementia that affects tens of millions of people all over the world.
When Matt, 27, heard for the first time about Simufilam, “this seemed exciting,” writes Charles Piller in his new book, “Doctally: Fraud, Arrogance and Tragedy in trying to cure Alzheimer’s.” Instead of simply calming the symptoms, Simuflam promised “to quench, stop or restore cognitive fall – or for people who have no symptoms, prevent them – attacking Alzheimer’s biochemical cause,” Piller writes.
It was based on a long -debated notion called “Amiloid Hypothesis”, which argued that Alzheimer’s was caused by the construction of amyloid protein in the brain. “If true, removing it would lead to a cure,” Piller writes. The discovery was shocking, especially given that it would have been introduced by a small biotechnical company that was previously specialized in opioid pain and “had never taken a drug to trade in its fifteen years of existence,” writes Piller. “Yet she claimed to have discovered a new molecule that stabbed the dark heart of the terrible illness.”
Even at the beginning, Matt Price, a Harvard -trained epidemiologist and global health specialist, had his doubts. Cassava’s theory, which had not yet been proven by independent scholars, “seemed weird and slightly thin,” Matt told the author.
His concerns are soon confirmed by a whistle who produced “persuasive evidence that laboratory studies at the heart of the prevailing hypothesis due to Alzheimer’s disease. The amyloid hypothesis was not written alone, but it received valuable resources away from other promising theories How to handle Alzheimer’s.
And it is not a limited problem only in Alzheimer’s research. Since this month, at least 55,000 medical and study studies have been withdrawn, according to the Watch Data Database from the Center for Scientific Integrity. And it is estimated that there may be about hundreds of thousands of fake studies that are still circulating and have not yet been identified. Even when they are exposed, magazines are often slow to attract false studies, if it happens at all. It is not just a matter of lost search dollars. “It makes people start not trusting the clinical research enterprise,” Price says.
Simufilam began as an experimental code named PTI-125 developed by neuroscientists Lindsay Burns and Hoau-Yan Wang. It was designed to target filaminine A, which becomes twisted in an abnormal form and causes inflammation in the brain, promoting the formation of myloid-beeta proteins. PTI-125, researchers suggested, can return those terrible effects.
The drug was renamed Simufilam in August 2020, and in preliminary studies, patients began to show improvement after only one month – “extraordinary for each Alzheimer’s trial,” Piller writes. Simufilam begins to look like a sacred grail, “the drug of dreams that generations of research had sought in vain,” the author writes. By the end of July 2021, the small company Biopharma, whose sample size for their experiments Simufilam was a fifty minuscule participants, with Suddden had a $ 5.4 billion market rating.
The victory was short -lived. In August. 18, 2021, just weeks after the company’s shares reached high record levels, two neuroscientists – Geoffrey Pitt of Weill Cornell Medical College and David Bredt, a former ecteal in drug manufacturers Eli Lilly and Johnson & Johnson – present a “Petition Citizen “for FDA, FDA, asking them to take a closer look at Simufilam. Their main concern was that drug development “contained scientific images manipulated,” Piller writes. “In short, they claimed, the job seemed to be a doctorate.”
To help test their doubts, they brought to Matthew Schrag, a neurologist and neuroscientist at Vanderbil University, who would become “the most important whistles in Alzheimer’s history”, writes Piller. When they sought Schrag’s help, “my answer was,“ You think I’m stupid enough to do it? “” Schrag told the author. “Apparently. I was.”
Using Imagej and Mipav, software developed and approved by NIH, Schrag carefully studied the images used in the Simufilam study. He had a “seasoned eye to detect digital manipulation with ordinary software programs,” Piller writes. Almost immediately, he noticed the test of manipulation. “Schrag without micrographs – enlargement of microscopic traits of brain tissue – that seemed clearly cloned,” Piller writes. “However they presented themselves as finding for different experimental conditions.”
Schrag worried that he was not just revealing evidence of research behavior, but something much bigger and more ominous. “How had those problems gone unnoticed for years or even decades?” Writes Piller. “[Schrag] Asked with nervousness: which other Alzheimer’s research should be skeptical -eyed? “
Schrag had an uphill battle, mainly because “opposing someone else’s experiment can be a desire of death in science,” Piller writes. Or as Schragut explained to the author, “The field is absolutely calibrated for the latest, more interesting, more intensive discovery. It detizes replication at every step.”
Piller shared Schrag’s findings with a dozen expert, including some senior Alzheimer’s scholars. While most were hexagons to go to the record saying anything negative about original research, some – like Donna Wilcock, an Alzheimer’s expert at the University of Kentucky who would later become Alzheimer’s & Dementia editor – accepted the signs of confusion.
But others, like Dennis Selkoe, a Harvard Professor of Neurological Diseases and a famous Alzheimer’s scholar, “punished” the author for his criticism of “objective evidence” that the reduction of amyloid in the human brain produces better cognitive results . “I’m on the right side of history,” argued Selkoe, who Piller accuses of being part of the “amyloid mafia”.
George Perry, a scientist at the University of Texas in San Antonio and the editor of the Alzheimer’s disease newspaper, agreed with Piller that many Alzheimer’s scholars are very strange to be accurate. “The main purpose of these people is to win – if it is not the Nobel Prize, it is the glory of God,” Perry the author told. “To admit that they really do something great. They do not want the amyloid hypothesis to die because they have no inheritance. “
Schrag held his Kasava file in NIH in 2021, providing “forensic loan” for research suspicion, writes Piller. Two years later, in 2023, a university panel found Haau-Yan guilty of “misconduct” because of his work for Cassava. Last September, the company agreed to pay $ 40m for the insurance and exchange commission (SEC) for fraudulent investors. And then in November, Cassava acknowledged that Simufilam failed to deliver the results they were waiting for in a clinical test of Phase 3, and the company would interrupt the research. Their shares decreased by more than 80% after the notice.
Schrag was not surprised by the result. “You can cheat to get a letter,” he told the author. “You can cheat to get a degree. You can cheat to get a grant. You can’t cheat to cure a disease. Biology doesn’t care. “
#greed #profit #failed #Alzheimers #failed
Image Source : nypost.com