More research questioning aducanumab
A new study gives evidence that amyloid plaques is not the driving factor in Alzheimers disease, but it is rather a consequence of the disease. It shows evidence that Alzheimers may develope as a result of the decline in amyloid-beta peptides. Therefore removing amyloid plaques, which the newly approved aducanumab effectively does, is not going to slow down Alzheimers. According to the study, an effective treatment would lie in normalizing the levels of amyloid-beta peptides.
Removing amyloid plagues has never been shown to be an effective treatment in humans, although Biogen has shown it is really effective with genetically altered mice. Biogen has been given nine years to prove their theory, but this drug needs to be re-evaluated before Medicare starts paying out billions for this experimental drug.
I suspect scientists who do the research for Biogen already know this drug is ineffective, but they don't run Biogen. It is the corporate executives that make the decisions based on profit, and they are going to use every tool possible to squeeze money out of Medicare. If aducanumab fails to be effective, they can always apologize later.
Researchers question prevailing Alzheimer's theory with new discovery https://medicalxpress.com/news/2021-06-prevailing-alzheimer-theory-discovery.html
Comments
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here it is as a hotlink
https://medicalxpress.com/news/2021-06-prevailing-alzheimer-theory-discovery.html
another review of the same article
https://neurosciencenews.com/amyloid-peptide-theory-alzheimers-18822/
“The key discovery from our analysis is that Alzheimer’s disease symptoms seem dependent on the depletion of the normal protein, which is in a soluble state, instead of when it aggregates into plaques,” says co-author Kariem Ezzat from the Karolinska Institute.
The article itself is a very difficult read
https://www.thelancet.com/pdfs/journals/eclinm/PIIS2589-5370(21)00268-6.pdf
The authors disclose that they have recently cofounded REGAIN Therapeutics, owner of a patent application that covers synthetic soluble non-aggregating peptide analogues as replacement treatment in proteinopathies.
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Here is more from the University of Cincinnati. As reported recently, Lecanemab showed a small decrease in Alzheimers progression. Dr Esay in an article this month stated that this may not be due to removing amyloid plaques but rather due to increasing amyloid-beta peptides (soluble amyloid-beta). Increasing soluble amyloid-beta appears to be a better target than decreasing amyloid plaques.
Dr Espay in the article says "Interestingly, lecanemab, the anti-amyloid drug recently reported as beneficial, does something that most other anti-amyloid treatments don't do in addition to reducing amyloid: It increases the levels of the soluble amyloid-beta".
Study: Decreased proteins, not amyloid plaques, are tied to Alzheimer's disease https://medicalxpress.com/news/2022-10-decreased-proteins-amyloid-plaques-tied.html
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Hotlink
file:///C:/Users/Owner/Downloads/2022-10-decreased-proteins-amyloid-plaques-tied.pdf
Hotlink to the study itselfhttps://content.iospress.com/articles/journal-of-alzheimers-disease/jad220808
note this research is on an extremely young population
Of 534 subjects participating in the DIAN study (mean age, 38±11.1 years), 232 mutation carriers met eligibility criteria (mean age, 38.3±11 years). Among them, 191 had available PiB-PET data at baseline (mean SUVR, 1.9±1.0), of whom 108 were PiB-PET-positive (mean SUVR, 2.5±1.0) (Table 1). These subjects were followed for a mean of 3.3±2.0 years (range = 1,
Why they used the mean age is unclear
Further they use predicted instead of correlated or associated
Conversely, cognitive deterioration was strongly predicted by lower levels of soluble Aβ42 but not by increases in SUVR, t-tau, or p-tau.
The conclusion is fairly stated
Brain toxicity in AD may be predominantly mediated by a reduction of the soluble protein pool, its functional fraction, rather than its accrual into amyloids.
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Crushed, the first hotlink for my second post is not working on my android phone. Thanks for the help.0
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Now it is working. Maybe it was my internet connection.0
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