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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

  • Crushed
    Crushed Member Posts: 1,444
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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.

  • Larrytherunner
    Larrytherunner Member Posts: 83
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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

  • Crushed
    Crushed Member Posts: 1,444
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    Hotlink 

    file:///C:/Users/Owner/Downloads/2022-10-decreased-proteins-amyloid-plaques-tied.pdf 

    Hotlink to the study itself 

    https://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.
      

  • Larrytherunner
    Larrytherunner Member Posts: 83
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    Crushed, the first hotlink for my second post is not working on my android phone. Thanks for the help.
  • Larrytherunner
    Larrytherunner Member Posts: 83
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    Now it is working. Maybe it was my internet connection.

Commonly Used Abbreviations


DH = Dear Husband
DW= Dear Wife, Darling Wife
LO = Loved One
ES = Early Stage
EO = Early Onset
FTD = Frontotemporal Dementia
VD = Vascular Dementia
MC = Memory Care
AL = Assisted Living
POA = Power of Attorney
Read more