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DavidSJ

HN member
Joined
Sat, Feb 24, 2007, 12:46 AM UTC
HN karma
7,237
Public activity
1,324 items

About DavidSJ

XMPP OTR (username: davidsj) 404.city: C2D1BE4A 2DDD0681 644DC72D 4EBE9AD9 B8802186 chatme.im: 7C68B740 C563D961 BA93FF1B 85B543D4 17C60C76 gmail.com: 22798DAA 74B98F68 B8A89920 9668AA03 9959D789

GPG pub 4096R/0x4C01388C6C449B9A 2016-01-19 [expires: 2021-01-17] Key fingerprint = A1A7 D57A 9CF9 E7C7 CB59 C086 4C01 388C 6C44 9B9A uid David Schneider-Joseph sub 4096R/0x6FFE45B4F22981D3 2016-01-19 [expires: 2021-01-17]

[ my public key: https://keybase.io/dsj; my proof: https://keybase.io/dsj/sigs/tTLcos1JjcAqM39zfQU6J5PhjMoA_iLZHpFCLyTyGYI ]

Recent public activity

  1. comment
    Comment #49065307

    > Worse than 0.01% of humans means that there are 8,000,000 people better than it. I know that's being pedantic I understand what you're saying. Since we're being pedantic, it mean…

  2. comment
    Comment #48578306

    I've been a regular reader of Alzforum, and cite multiple of their articles in the blog post that was linked up above. https://www.astralcodexten.com/p/in-defense-of-the-amyloid-h.…

  3. comment
    Comment #48564407

    Perhaps I am just not well-informed but 30% slowdown in progression translates to sufferers have some mild improvement in cognitive tests and live a few months longer. A few years …

  4. comment
    Comment #48563512

    Note that not all AD-causing mutations in APP also cause amyloid accumulation, for example APP-Osaka (loss of APP residue E693) results in familial AD without any accumulation of a…

  5. comment
    Comment #48562737

    Yes, there is a clear sequence of how AD pathology develops, starting with amyloidopathy and progressing to tauopathy, but 1) there is as yet no established molecular connection be…

  6. comment
    Comment #48561623

    Thanks, great challenges. One may then ask, what is being remedied in the many, many, studies that claim to successfully target amyloid toxicity in mice? And is this relevant to th…

  7. comment
    Comment #48560767

    This is a reasonable challenge. I won't and shouldn't be able to convince you that my process was satisfactory, but I'll describe it anyways. I agree that I don't have the qualific…

  8. comment
    Comment #48559838

    I did. I started out very skeptical, then got convinced by the quality of the evidence.

  9. comment
    Comment #48559578

    That's fair. I responded to hostility with hostility. Perhaps I should have ignored the comment or just responded kindly despite the hostility.

  10. comment
    Comment #48559503

    The drug was discontinued later. You're thinking of aducanumab. Lecanemab and donanemab have been in widespread use for several years now, and open-label extensions vs. external co…

  11. comment
    Comment #48559478

    Those are amyloid-only mice. It's an amyloid+tau disease, with tau the proximate cause of neurodegeneration. Normal mice don't get tau pathology, whereas even healthy human beings …

  12. comment
    Comment #48555226

    Thanks for these comments! The multiple pathways into a common entrypoint is definitely a challenge to communicate.

  13. comment
    Comment #48551334

    You read the article in which I discuss the matter you say I was unfamiliar with?

  14. comment
    Comment #48550560

    Not reverse; the neurons have died. Cease, yes, if the cause is removed early enough. But if you intervene too late (once symptoms are detectable), then the downstream tau patholog…

  15. comment
    Comment #48549417

    The hypothesis that amyloid is simply a downstream effect, not a cause, is of course worth considering, and where my mind was at when I first approached the literature skeptically.…

  16. comment
    Comment #48547369

    Now if we consider amyloid beta therapies: we have treatments that target amyloid beta with varying degrees of success but at least some show definite reductions in amyloid beta pl…

  17. comment
    Comment #48547341

    As noted elsewhere in this thread, which you seem not to have read, I discuss that matter in the article, which you also seem not to have read.

  18. comment
    Comment #48546080

    What started as an argument to ignore arguments and evidence and instead rely on authority, seems now to have morphed into an argument that we should ignore the authority of the es…

  19. comment
    Comment #48545689

    You said the camp promoting the amyloid hypothesis has struggled greatly to come up with evidence to support its position. What did you mean by that if not a read of the quality of…

  20. comment
    Comment #48545401

    Is your view that amyloid is actually a minority view among researchers? That seems completely wrong based on basically every conference proceeding I've viewed and the volume of pa…

  21. comment
    Comment #48545149

    1. I don't say Derek Lowe is wrong because he's in the minority. Minorities are sometimes right. But since the parent comment was arguing on authority and my lack thereof, I point …

  22. comment
    Comment #48544819

    This frequently comes up as a critique of my article, but I don't claim to be disrupting the field as a smart outsider. Rather, I looked at the field and concluded that the experts…

  23. comment
    Comment #48418756

    My oh shit moment was probably deep Q learning in 2013 (I guess that's not gen AI), but GPT-3 was pretty remarkable too.

  24. comment
    Comment #48348514

    Yes, I can't find a 30%-slowdown number either. I'll add to this: the referenced trial occurred over 8 weeks, so even if we stipulate that the improvements in cognition (which are …

  25. comment
    Comment #48044993

    Little changed in 18 years: https://web.archive.org/web/20080511133831/https://www.vatic...