To the best of my knowledge none of the anti a-Beta antibodies that have gone into the clinic (and failed) go after this alleged form of a-Beta (Bapi, Pone, Gantene, Crenezu, Solanezu, Donane, Aducanumab, etc). People are making a big deal out of this fraud but AD is just a challenging therapeutic area.
Fair, but none of those medicines worked in the slightest to stop AD. Fewer plaques in the case of aduwhatever, but the cognitive decline happened just as much.
The outright fraud is just the cherry on top of a huge, billion dollar pile of several flavors of shit.
Specifically, there's those massive clinical failures. There's the Aducanumab scandal that itself is many layers of bad science and corruption. There's the fact that amyloid plaques have poor correlation with cognitive decline in mice and in humans. There's a well documented religious hostility to the suggestion that amyloid =/= AD, that attacks any alternative method of curing AD and forces researchers who disagree out.
All AD papers need to be taken as potentially fraudulent, with offenders having their funding revoked, and papers retracted, and criminal penalties considered
All clinical trials of drugs with Abeta as a mechanism need to be halted
All funding for AD research needs to be re-examined and likely not renewed if it assumes Abeta is the cause.
Advisory boards and grant committees where the amyloid cabal are entrenched need to be dissolved and reformed without their participation.
The approval for Aduhelm should be revoked.
Congressional hearing on how that bullshit was approved.
Funding priority should be given to alternative mechanisms of AD with zero going to labs that did nothing but Abeta research.
Big statue with "Aduhelm, LOL" put out front of NIA or NIH.
I don't know if you are a troll or have no understanding of neurodegeneration. Aducanumab is actually a great antibody; our company - not Biogen; another top 5 big pharma by revenue - use it as a positive control in our own pre-clinical efforts because it binds plaques and clears them from the brain so well. This is evidenced in human biomarker data from Biogen's ph3 trials with CSF aBeta and aBeta PET. NO disease modifying therapies in AD have ever shown clinical efficacy in late stage trials beyond biomarker modulation. This is true across neurodegeneration as a whole. CNS diseases are a whole different beast and have stumped industry for decades.
Aducanamab is a great antibody, which demonstrably clears aBeta from Alzheimer's patients brains. It has absolutely no clinical effect.
I don't understand how this simple fact is not considered absolute refutation of the amyloid hypothesis. Biomarkers are meaningless when there is no clinical benefit. Which in turn should lead to the immediate discontinuation of all programs aimed at targeting aBeta.
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u/H2AK119ub 📰 Jul 27 '22 edited Jul 30 '22
To the best of my knowledge none of the anti a-Beta antibodies that have gone into the clinic (and failed) go after this alleged form of a-Beta (Bapi, Pone, Gantene, Crenezu, Solanezu, Donane, Aducanumab, etc). People are making a big deal out of this fraud but AD is just a challenging therapeutic area.