amyloid
Article
amyloid is a recurring concept in the Astral Codex Ten archive, appearing 2 times across 2 issues between August 20, 2021 and August 14, 2025. The archive places it in contexts such as “amyloid-reduction as a therapy”; “1: Amyloid The common entrypoint, typically at least 15 years before clinically detectable symptoms”; “1: Amyloid The common entrypoint … is accumulation of amyloid-β deposits”. It most often appears alongside aducanumab, aducanumab, Aduhelm.
Metadata
- Category: Concepts
- Mention count: 2
- Issue count: 2
- First seen: August 20, 2021
- Last seen: August 14, 2025
Appears In
Related Pages
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- aducanumab (2 shared issues)
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- aducanumab (2 shared issues)
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- Aduhelm (2 shared issues)
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- Biogen (2 shared issues)
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- Scott (2 shared issues)
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- Scott Alexander (2 shared issues)
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- A. Bejanin (1 shared issues)
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- A. de Calignon (1 shared issues)
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- A. Elobeid (1 shared issues)
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- A. J. Aschenbrenner (1 shared issues)
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- A. L. Woerman (1 shared issues)
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- A. M. Pooler (1 shared issues)
External Links
Source Context
Recovered passages from the original issue text. When the raw archive preserved outbound links inside the source passage, they are listed directly under the quote.
- Anecdotally, as someone who used to work in the Alzheimer's research space, nobody in the field seriously thinks the amyloid hypothesis is true. It's been tried, over and over again, every drug that's ever aimed at that mechanism has failed, it's busted.
Yesterday the FDA approved aducanumab, an anti-amyloid antibody developed by Biogen, for the treatment of Alzheimer’s disease. This was based on post hoc interpretation of clinical trials that were stopped early due to futility, and against the strong recommendation of the FDA’s own advisory committee. Aducanumab will be priced at $56,000 per patient per year. Since Alzheimer’s patients are usually covered by Medicare, this cost will be paid by the American public. I estimate that it could be over $100 billion per year.1 This is excluding indirect costs, such as those of monitoring for brain swelling that is a known effect of this drug.
Inline links: 1
Aducanumab is not only excellent at doing its direct job - removing amyloid plaques - but also pretty good at reducing secondary biomarkers like amyloid PET signals and ARIAs (small hemorrhages and edemas that show up in an MRI). The problem is with the final proof of slowing cognitive decline, where most cognitive tests in the different trials failed to show statistically significant difference from placebo.
The “amyloid hypothesis” says that Alzheimer’s is caused by accumulation of the peptide amyloid-β. It’s the leading model in academia, but a favorite target for science journalists, contrarian bloggers, and neuroscience public intellectuals, who point out problems like:
Some of the research establishing amyloid's role turned out to be fraudulent.
The level of amyloid in the brain doesn’t correlate very well with the level of cognitive impairment across Alzheimer’s patients.