I've often wondered if Alzheimer's is actually novel instances of prion disease.
For instance, Kuru was developed within I think a handful of generations in a population of ~20,000 with limited opportunities for transmission (only transmitted when someone dies and their family eats their brain).
If the base incidence rate for a novel prion is that high, can you explain Alzheimer's as just that? It would be sad news for pharmaceutical companies - it would render Alzheimer's as a disease in the same class as cancer. Total systems breakdowns that are low-probability but inevitable on a long enough timescale.
it’s almost certainly not, or you would see epidemiological evidence for chains of transmission. prion diseases require contact transmission which is all but absent from the alzheimer’s story.
> it’s almost certainly not, or you would see epidemiological evidence for chains of transmission. prion diseases require contact transmission which is all but absent from the alzheimer’s story.
I think what the parent comment is saying is, what if it isn't transmitted, what if a prion is just occurring in the brains of the people who develop alzheimers?
That seems unlikely to me, but on the other hand, the article seems to be suggesting that transferring brain proteins from people with alzheimers to people who are younger will cause them to develop alzheimers which would be roughly consistent with that.
I don't know whether that would be possible, but, for example, what if there was somehow a specific protein in the brain that could easily be misfolded to become a prion, and the eventually if people live long enough they tend to produce that prion at least once, so it occurs essentially as a result of old age, but it can theoretically also be transmitted in the manner described in the article?
consumption of neural tissue isn’t the only transmission vector though. (See TFA for an example, in fact.) If it were a prion disease, just the law of averages dictates that we’d see some transmission from things like organ transplants from pre-symptomatic carriers. There’s no evidence of that at all that i’m aware of. (disclaimer: I work at a startup in cognitive testing, so while i’m certainly not a researcher in the field, i do see quite a bit of research on dementia-adjacent diseases)
But don't you also have a windowing effect there? How many >50 y/o people are donating their organs?
You could also explain the age skewness by allowing for the fact that it takes time for the prions to replicate to the point that you notice symptoms.
Other I think this would predict: lifetime exposure to mutagens is a predictor for Alzheimer's. Alzheimer's is more heritable from the mother than the father.
For instance, Kuru was developed within I think a handful of generations in a population of ~20,000 with limited opportunities for transmission (only transmitted when someone dies and their family eats their brain).
If the base incidence rate for a novel prion is that high, can you explain Alzheimer's as just that? It would be sad news for pharmaceutical companies - it would render Alzheimer's as a disease in the same class as cancer. Total systems breakdowns that are low-probability but inevitable on a long enough timescale.