[BostonCard]

Back to MTL, he makes a cameo in this piece about fraud in Alzheimer's Disease research.

https://www.nytimes.com/2025/01/24/opini...74f24220a2

The characterization of MTL's role seems to take the University report at face value.  I think that's fair, but I think others might disagree and feel like he was much more complicit.

Marc Tessier-Lavigne, the former president of Stanford University, was known as a global leader in research on the brain’s circuitry in Alzheimer’s and other neurological conditions. He resigned in 2023 after an intrepid student journalist revealed numerous altered images in his research. Dr. Tessier-Lavigne didn’t personally falsify data or coerce junior colleagues to do so. But he failed to correct dubious results that came to his attention and may have provided inadequate oversight of his lab — allowing apparently doctored studies that helped build his reputation to remain on the scientific record, according to an investigation by a special committee appointed by the university’s board of trustees. In his resignation letter, Dr. Tessier-Lavigne denied that he had engaged in any unethical research but admitted that there were instances in which he “should have been more diligent in seeking corrections.”

Interesting (and sad) reading.  That being said, the author seems to underplay the effect of intervening on amyloid.  Here are the clinical trials of lecanemab and donanedab, the two monoclonal antibodies that target amyloid in the brain.

https://www.nejm.org/doi/full/10.1056/NEJMoa2212948
https://www.nejm.org/doi/full/10.1056/NEJMoa2100708

Over the course of 18 months, they slow down the progression of Alzheimer's disease by about a third (so that someone on the drug for 18 months progresses to the same extent as someone not on the drug for 12 months).  That's not revolutionary, but that does make amyloid targeting drugs the only drugs that have slowed the progression of the disease.  Whether that is so minute as to be imperceptible is a matter of opinion, and research has shown that the "minimally clinically important difference" (MCID) for the CDR-SB is about 1 point, which is more than the difference between treatment arms at 18 months (the length of the trial).  But the fact that intervening on amyloid produces any difference at all validates the hypothesis that amyloid plays a role in the pathophysiology of disease, despite the fact that the field is rife with misconduct.

Both things can be correct at once:
The field of AD (and especially the role of amyloid in it) is rife with fraud
Notwithstanding this, the fact that drugs which clear amyloid reduce the progression of disease is pretty direct evidence that amyloid is at least partially causative in the pathology of disease

BC
(disclosure: neither of the two drugs are made by my employer, though the company continues to pursue drugs that target amyloid; I'm not involved)

[BostonCard]

Back to MTL, he makes a cameo in this piece about fraud in Alzheimer's Disease research.

https://www.nytimes.com/2025/01/24/opini...74f24220a2

The characterization of MTL's role seems to take the University report at face value.  I think that's fair, but I think others might disagree and feel like he was much more complicit.

Marc Tessier-Lavigne, the former president of Stanford University, was known as a global leader in research on the brain’s circuitry in Alzheimer’s and other neurological conditions. He resigned in 2023 after an intrepid student journalist revealed numerous altered images in his research. Dr. Tessier-Lavigne didn’t personally falsify data or coerce junior colleagues to do so. But he failed to correct dubious results that came to his attention and may have provided inadequate oversight of his lab — allowing apparently doctored studies that helped build his reputation to remain on the scientific record, according to an investigation by a special committee appointed by the university’s board of trustees. In his resignation letter, Dr. Tessier-Lavigne denied that he had engaged in any unethical research but admitted that there were instances in which he “should have been more diligent in seeking corrections.”

Interesting (and sad) reading.  That being said, the author seems to underplay the effect of intervening on amyloid.  Here are the clinical trials of lecanemab and donanedab, the two monoclonal antibodies that target amyloid in the brain.

https://www.nejm.org/doi/full/10.1056/NEJMoa2212948
https://www.nejm.org/doi/full/10.1056/NEJMoa2100708

Over the course of 18 months, they slow down the progression of Alzheimer's disease by about a third (so that someone on the drug for 18 months progresses to the same extent as someone not on the drug for 12 months).  That's not revolutionary, but that does make amyloid targeting drugs the only drugs that have slowed the progression of the disease.  Whether that is so minute as to be imperceptible is a matter of opinion, and research has shown that the "minimally clinically important difference" (MCID) for the CDR-SB is about 1 point, which is more than the difference between treatment arms at 18 months (the length of the trial).  But the fact that intervening on amyloid produces any difference at all validates the hypothesis that amyloid plays a role in the pathophysiology of disease, despite the fact that the field is rife with misconduct.

Both things can be correct at once:
The field of AD (and especially the role of amyloid in it) is rife with fraud
Notwithstanding this, the fact that drugs which clear amyloid reduce the progression of disease is pretty direct evidence that amyloid is at least partially causative in the pathology of disease

BC
(disclosure: neither of the two drugs are made by my employer, though the company continues to pursue drugs that target amyloid; I'm not involved)