3 ms·

This was written November 13, 2020. At that time, the majority of the community believed that amyloid plaques caused Alzheimers from a paper in 2006. Since th

by tleish 4y ago

This was written November 13, 2020. At that time, the majority of the community believed that amyloid plaques caused Alzheimers from a paper in 2006. Since the paper in 2006 drug companies that spent billions of dollars in a race for a drug to decrease amyloid plaques to slow down or prevent Alzheimer's. In the trials last year, they found that while the drugs did decrease amyloid plaques, they did not impact Alzheimer's symptoms. see: Evidence Mounts for Alternate Origins of Alzheimer’s Disease Plaques https://nyulangone.org/news/evidence-mounts-alternate-origins-alzheimers-disease-plaques https://nyulangone.org/news/evidence-mounts-alternate-origin... This led to the discovery that some of the data in the 2006 study was faked. see: Faked Beta-Amyloid Data. What Does It Mean? https://www.science.org/content/blog-post/faked-beta-amyloid-data-what-does-it-mean https://www.science.org/content/blog-post/faked-beta-amyloid... The latest theory is now on beta-amyloid proteins. see: Decreased proteins, not amyloid plaques, tied to Alzheimer's disease https://www.sciencedaily.com/releases/2022/10/221004151217.htm https://www.sciencedaily.com/releases/2022/10/221004151217.h... If the new theory of beta-amyloid proteins linked to Alzheimer's proves to be true then someone should look into if there's a link between gut and beta-amyloid proteins.

vaxman 4y ago
We can still infer dementia from the presence of excessive amyloid plaque even if removing the excessive amyloid plaque doesn’t resolve the dementia.
zosima 4y ago
No, the fact that amyloid-beta or at least its precursor protein APP is causative in Alzheimer's disease is based on very solid science, with a huge amount of genetic evidence behind it. Lecanemab an antibody that binds to amyloid-beta, is disease-modifying and slows down cognitive deterioration. The paper from 2006 carried no significance for any of this and it had only minor impact on Alzheimer's disease research. There has been discussion to whether the plaques of amyloid-beta protein are disease-causing or not. I, as probably most others, believe the plaques as such are non-causative, and that the damage from amyloid-beta happens when amyloid-beta is in a soluble state.

by tleish 4y ago

vaxman 4y ago

We can still infer dementia from the presence of excessive amyloid plaque even if removing the excessive amyloid plaque doesn’t resolve the dementia.

zosima 4y ago

No, the fact that amyloid-beta or at least its precursor protein APP is causative in Alzheimer's disease is based on very solid science, with a huge amount of genetic evidence behind it. Lecanemab an antibody that binds to amyloid-beta, is disease-modifying and slows down cognitive deterioration. The paper from 2006 carried no significance for any of this and it had only minor impact on Alzheimer's disease research. There has been discussion to whether the plaques of amyloid-beta protein are disease-causing or not. I, as probably most others, believe the plaques as such are non-causative, and that the damage from amyloid-beta happens when amyloid-beta is in a soluble state.