Alzheimer’s Disease: An Influential 2006 Study Containing False Images Leads Scientists To Reverse Previous Theories


The failure rate of drug development for Alzheimer’s is 99 percent according to a recent study. Since 1984 scientists have concentrated on developing treatments to prevent the formation of beta-amyloid clumps. Central to this theory is an influential paper published in 2006 in Science Magazine. The article has been cited thousands of times. Researchers refer to it as the “amyloid hypothesis.”

However, Science Magazine subsequently found evidence of the paper’s images on Aβ*56 that were doctored in order to promote the role of the Aβ*56 protein in Alzheimer’s.

A Neuroscientist Identified Altered Images

 A neuroscientist at Vanderbilt University, Matthew Schrag, was commissioned to examine suspect images in papers that involved Alzheimer’s disease. Dr. Schrag received a call from a colleague who wanted to introduce him to an attorney investigating a proposed Alzheimer’s disease called simufilam. The developer was Cassava Sciences who claimed that the drug improved cognition. The process was described as a partial repair of amyloid beta (Aβ) the hallmark of Alzheimer’s disease.

The attorney represented two neuroscientists who were short sellers, profiting when a company’s stock falls. The scientists engaged the attorney as they believed some research associated with simufilam had been false. A petition to this effect was filed with the FDA on their behalf.

Dr. Schrag, a 37-year-old junior professor, had already gained notoriety with his public criticism of the FDA’s controversial approval of the anti-Aβ drug Aduhelm. His own concern regarding patients who were participating in clinical trials investigating simufilam was their exposure to side effects without any benefit.

Dr. Schrag accepted the attorney’s offer to analyze published images of simufilam and received $18,000 for his efforts. He found seemingly altered images published in various journal articles. His findings were included in the FDA petition with copies sent to the NIH which had tens of millions of dollars invested in the simufilam studies.

Investments, in Terms of Dollars and Hours

Millions of dollars and countless hours have been spent on what now appears to be a falsified study. The NIH reports that looking at 2018 alone it spent $1.9 billion on research for Alzheimer’s disease.

It appears that scientists had been focusing almost exclusively on the often-cited 2006 study, ignoring or neglecting other possible explanations.

Based on current investigations surrounding the 2006 study, scientists are beginning to turn their focus away from amyloid plaque buildup as the cause of Alzheimer’s. They have found that older people with exceptional memories can have brain plaque but not dementia. There is also the premise that amyloid and tau may be a critical brain response to injury rather than the cause of the disease.

The Cause and Not the Result

New evidence may override old theories. The newly emerging theory is that bacteria found in the brain may not be a result of Alzheimer’s, but the cause.

Dementia cases have skyrocketed in lockstep with an aging population. There is substantial evidence that Alzheimer’s could be caused by bacterium associated with gum disease. One doctor cautioned that Alzheimer’s is a complex disease and not ‘one size fits all’. He believes that there are several ways to solve the mystery and said that we should be vigilant.

Going forward with any or all of these theories could lead to solving one of medicine’s biggest mysteries. Recent statistics show that Alzheimer’s is the world’s fifth leading cause of death.

Following Misleading Signals Since 1984

The leading hypothesis has been to follow the amyloid proteins as they accumulate in the brain. Researchers discovered that amyloid kills bacteria but still believed that Alzheimer’s is caused by inadequate control of amyloid and not caused by bacteria.

Porphyromonas gingivalis is considered to be the main bacterium in gum disease. It is known to be an Alzheimer’s risk factor, causing neural damage, brain inflammation, and amyloid plaques in healthy lab mice.

When Scientists Converge on a New Hypothesis

 Casey Lynch of the pharmaceutical firm Cortexyme in San Francisco noted the impact created by multiple laboratories converging on one solid theory. After heading in the wrong direction since 1984, scientists welcome opposing opinions such as those expressed by the UK’s Dr. David Reynolds. Dr. Reynolds explained his doubts about P. gingivalis causing Alzheimer’s due to evidence that shows a person’s genes are responsible.

As a compromise, we are to consider that the bacterial theory is not in conflict with genetic evidence. The primary genetic risk factor for Alzheimer’s is a variant of the gene that produces ApoE immune protein.

The key factor is how quickly the damage accumulates. Some people may harbor P. gingivalis in their mouths but only some will develop Alzheimer’s as it may take decades before Alzheimer’s symptoms are evident.


Rose Duesterwald

Rose Duesterwald

Rose became acquainted with Patient Worthy after her husband was diagnosed with Acute Myeloid Leukemia (AML) six years ago. During this period of partial remission, Rose researched investigational drugs to be prepared in the event of a relapse. Her husband died February 12, 2021 with a rare and unexplained occurrence of liver cancer possibly unrelated to AML.

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