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My understanding was the beta-amyloid hypothesis itself is under some amount of scrutiny and may not truly explain Alzheimer's. Wonder if this finding adds more evidence for the amyloid hypothesis.


This finding definitely supports a brain protein hypothesis, but it could just as easily point to tau protein as amyloid.

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3399531/


The short version as I understand it: amyloid plaques are a symptom but not a cause.

There was a theory floating around that they're a neurological immune response to viral infection but I don't think there's enough evidence to prove that yet.


I thought CJD was caused by a prion. Was it in the growth hormone prep from the cadavers?


From the article:

> In the interim, scientists had discovered that that type of hormone treatment they got could unwittingly transfer bits of protein into recipients’ brains. In some cases, it had induced a fatal brain disease called Creutzfeldt-Jakob disease, or CJD — a finding that led to the banning of the procedure 40 years ago.


Yeah that's correct. The article mentions a few cases of people who died from transmitted CJD that may have also received some beta amyloid or tau proteins that could have catalyzed development into Alzheimer's if only they didn't die from CJD, which seems to develop more quickly through that route. If Alzheimer's is truly is some kind of prion-related disease, which the research is suggesting.


there's transmissible CJD, but most cases are a genetic version where you get the prions from your own cells and then it cascades, if I recall


Not sure why scientists has to pin point a single cause where as you have different vectors that can cause the same disease is also plausible


Or that we've been lumping multiple different types of cognitive decline as a single disease.


Can’t you make a definitive diagnosis from an autopsy. Could be that multiple diseases lead to the same findings in the autopsy.

While someone is alive a diagnosis of Alzheimers is more of a diagnosis of elimination. There are several drugs that can be used to slow the progression and I assume that those have a role to play in solidifying the diagnosis.


You can check for amyloid plaques in an autopsy, but apparently plenty of old people that show no significant cognitive decline also have amyloid plaques.

So, while we would definitively call it Alzheimer's if you have significant cognitive decline + amyloid plaques, it's not 100% clear that this is a single diagnostic.


That ventures wildly into whether the realm of physicalism explains malaises that happen in the "consciousness" realm. spooky


Scientists are a bit more savvy than you are giving them credit. Anything neurological is unlikely to have a silver bullet treatment. So researchers are going after what looks most promising with respect to understanding the disease as well as a path towards treatment. Which is currently AB (or Tau), but there is plenty of skepticism that we are chasing the only measurement we have.

Yet many other correlations are even hazier than AB.


They don't, but my surface understanding is that the medicines that effectively nuke beta amyloid have no effect overall. Which would mean it's not even one of many causes, it seems to not be a cause at all.


I think the medicines likely reduce beta amyloid rather than get rid of all of it which if it has a prion like mechanism wouldn't really fix things.


I don't think scientists are necessarily assuming a single cause so much as that it's a moot point since we still haven't identified any causes for sure.

If some cases are caused by amyloid plaques and some aren't, for example, and we develop a treatment that cures the amyloid plaque cases but not the others, it will probably become extremely obvious that there are different causes at that point.




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