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NY Times Corrects Gina Kolata Re: Alzheimer's Print E-mail
Thursday, 16 September 2010
Five weeks after publishing a grossly dis-informative front-page report by Gina Kolata about Alzheimer's research,The New York Times published a lengthy three paragraph correction.

Today, five weeks after publishing a grossly dis-informative front-page report by Gina Kolata, "Spinal-Fluid Test Finds Proteins Identified With Memory Loss," Aug. 10, The New York Times published a lengthy three paragraph correction: identifying not one, not two, but three MAJOR mistakes in this single report.

Kolata's article implied that a screening test to identify Alzheimer's was 100% accurate--there is no such test. Furthermore, it was tested in about 50 people. Furthermore, much like psychiatric screens for depression, schizophrenia, etc., the test is poor in  specifically identifying who will develop Alzheimer's. Instead, it would misidentify far more people--"false positives"-- who will never develop Alzheimer's, but they would be at risk of being exposed to experimental "preventiion" treatments.

Unvalidated medical screens are a market expansion tool--but do not lead to good health outcomes.

Commercially-driven drug research does not appear likely to succeed in discovering effective treatments for complex diseases which may be triggered by a variety of multiple causes, rather than a single biological cause. Alzheimer's is an example of failed, commercial, drug-focused research.

The stream of consistently negative results for experimental Alzheimer's drugs require a reassessment of the theoretical UNPROVEN assumption that beta amyloid plaque is the cause of this debilitating catastrophic neurotoxic disease.

Notwithstanding the facts, a series of articles by Gina Kolata (many on the front page) of The New York Times, under the heading The Vanishing Mind, purport to examine worldwide struggle to find answers about Alzheimer's disease. However, the articles were written as if the Times was in the business of promoting dubious commercial screens and tests and hype about unproven therapies.

The series has been a disservice to the public--and particularly to families struggling with the care of a loved one suffering from this devastating disease--or cluster of diseases--no one knows for sure, as there is no fail-safe test to confirm the presence of Alzheimer's.

On July 19, we criticized Kolata's promotional articles:
"Drug Trials Test Bold Plan to Slow Alzheimer’s," July 16, 2010 
and "Rules Seek to Expand Diagnosis of Alzheimer’s," July 14, 2010.

On Aug. 10, Kolata again misinformed the public with her article gross misrepresentation of the facts in a front page article, "Spinal-Fluid Test Finds Proteins Identified With Memory Loss."

READERS BEWARE: as the Times own correction confirms, Gina Kolata is NOT a reliable source for medical-scientific information about Alzheimer's. 

On Aug. 17, 2010,  Duff Willson of The Times reported that Eli Lilly had suspended two late stage clinical trials testing semagacestat, a drug that was designed to remove plaque from the brain, because, the company acknowledged, not only did the drug fail to improve patients' functioning, but patients taking the drug "actually showed worse cognitive functioning and less ability to perform daily living tasks than patients who had taken a placebo."

Furthermore, patients taking semagacestat had an increased risk of skin cancer.

To gain true insight with reliable informative reports about the theoretical problems involved in Alzheimer's research, we recommend a highly informative continuing series of reports by Robert Langreth of FORBES magazine.

"Alzheimer's disease is a bit like a murder mystery with numerous possible culprits and only a few vague clues. For years the prime suspect has been a protein fragment called beta-amyloid, which forms clumps inside the brains of dementia patients. Big drug companies since the 1990s have bet heavily on the concept that amyloid poisons brain cells and that blocking it will halt a patient's devastating decline.
But even as their drugs move into final human trials, the evidence implicating amyloid is starting to look a little shaky."
See also
:
Notwithstanding Eli Lilly's contention that the failure of its Alzheimer's drug, semagacestat, worsened patients' condition, was "a completely unexpected result,” some scientists contend that the Alzheimer’s field has it backwards.
"Far from being harmful, amyloid is “actually a response to injury that the brain secretes to protect itself, like a scar,” argues Mark Smith, a neuroscientist at Case Western Reserve University. By removing it, “you will make the disease worse.” Amyloid deposits are often found near cerebral blood vessels, hinting that amyloid may act as a sealant for damaged blood vesselsscientists actually predicted the outcome."
Langreth writes: "Nobody knows whether his theory is right. But it seems compatible with the basic facts known about Alzheimer’s disease...."
See: "The Man Who Predicted Eli Lilly’s Alzheimer Failure"


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THE NEW YORK TIMES
Correction : September 16, 2010

An article on Aug. 10 about spinal fluid tests in Alzheimer’s research left the incorrect impression that the test can predict the disease with 100 percent accuracy in all patients. (That impression was reinforced by the headline.) In fact, the test was found to be as much as 100 percent accurate in identifying a signature level of abnormal proteins in patients with memory loss who went on to develop Alzheimer’s — not in identifying patients who “are on their way” to developing the disease.

The article also misinterpreted an element of the researchers’ findings. Among a group of patients who had memory loss and developed Alzheimer’s within five years, every one had protein levels associated with the disease five years before; it was not the case that “every one of those patients with the proteins developed Alzheimer’s within five years.”

And the article misstated the source from which the finding of 100 percent accuracy was drawn. It came from a separate set of patients that the researchers examined to validate the protein signature they had identified in an initial group. (In the initial group, as the article noted, nearly every person with Alzheimer’s had the signature protein levels.)
 
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