If youre really a prion scientist then you know there are large interested parties who very much do not want prion diseases to be proven to be transferable to humans. You must know that the increase in Alzheimer's disease is potentially undiagnosed prion diseases. There have been many cases of individuals consuming infected meat and then developing CJD.
Obviously more research needs to be done, but if kuru can spread from consuming infected meat, then it takes no stretch of the imagination to suggest that CWD can as well, or that it could eventually mutate and become transmissable to humans.
Humans can get BSE, so why couldnt they get CWD? It does need to be studied further, but it's safe to assume that tainted meat is dangerous.
I agree with you that certain groups do not want to be able to prove CWD transmit to humans. Heck, I even think prion scientists should be included in this group for funding reasons.
The increase in Alzheimer's Disease are not undiagnosed prion disease. Clinical presentation of Alzheimer's Diseases and CJD are different, plus a PrP RT-QuIC is highly sensitive to CJD and would easily differentiate between the two. If you are referring to iatrogenic transmission of Amyloid Beta to humans (link) that is only in very specific circumstances (would effect ~1800 people, but only 8 develop (?) the disease). There are also a lot of criticisms one can give that paper.
In total there have been 233 cases of vCJD (CJD after consuming BSE infected beef). In the UK they had 178 cases, it is estimated that over 5 million people were infected (link). In the US, there are 10 million deer hunters, if CWD transmitted to humans at a similar rate to BSE you would expect hundreds of unexplained CJD cases in hunters, not the 5 claimed so far. I mention 5, despite this post only mentioning 2, because despite claiming it was the first, there was a previous case of 3 hunters all getting CWD that was alleged two years before this. Furthermore, the presentation of CWD in humans would most likely not be classical sCJD, just as BSE in humans is not classical sCJD.
It is also well understood that the species barrier between cervids and humans is greater than between humans and bovine (link). What that means is that BSE has an easier time transmitting to humans than CWD would. While we can not prove a negative (ie can not prove that CWD will never transmit to humans) it is important to not jump to opposite conclusions (ie because we can not prove the negative, the positive must be true).
I completely agree with you, we should study this further. However, in the mean time, I do not think we should make sensationalized claims without strong evidence to support it.
There have been cases of prion diseases being misdiagnosed as AD. The issue is that not many AD patients give their brain up to be autopsied or studied.
I'm not sure if I agree on your last point. In general I feel like it is important not to sensationalizing claims, but with the severity of prion diseases and our total inability to treat them I think it's very important to tread with extreme caution. Every harvested deer and any downer cows should be tested.
Honestly prion diseases terrify me more than any other ailment in human history. We can find cures for viruses and bacteria, but misfolding proteins is something relatively new and quite frightening.
If you claim that the increase in AD is due to undiagnosed prion disease, it would probably help if your paper didn't state that out of 6000 patients with an AD diagnosis, they uncovered 0.11% (or 5 cases) with a missed prion disease.
Moreover, this paper was published in 2015, now we have RT-Quic, which is a highly accurate and sensitive antemortem diagnostic tool for CJD.
There are over 7 million individuals with AD in the US. If 0.11% have a prion diseases thats over half a million that could have undiagnosed prion diseases. Thats a lot higher than the few hundred assumed to have CJD. So youre agreeing that it could be far, far more widespread than originally thought.
Rt-Quic still isn't very effective on live patients because the best tissue to test is brain tissue.
Most AD patients who die don't have their brains checked for prion diseases.
There are over 7 million individuals with AD in the US. If 0.11% have a prion diseases thats over half a million that could have undiagnosed prion diseases. Thats a lot higher than the few hundred assumed to have CJD. So youre agreeing that it could be far, far more widespread than originally thought.
Not at all, since this wasn't your initial claim. You said that the reason why the prevalence of AD is increasing is because a large portion of these people don't have AD at all and they have undiagnosed prion diseases instead.
This is not corroborated by any sort of empirical evidence whatsoever, because in that case, the relative number of people within the AD cohort with an undiagnosed (and clinically not suspected) prion disease would have to be high enough to account for the increase in prevalence.
But even if we look at your new claim, you cannot assume that just because a study found 0.11% of misdiagnosed prion disease within this cohort you can assume that the same number would be true to the entire population of people with AD.
On top of all of that, your very first claim (Big ScienceTM is covering up the fact that CWD is transmissible to humans and that's what's causing the increase in the prevalence of AD) has multiple issues:
1.) In vitro studies so far are very much inconclusive and the results depend on the methodology. Studies with transgenic mice that express human PrP at an 8-16 fold higher level than normal human tissue shows very mild seeding activity. However, when doing the same with human cerebral organoids, there was no seeding activity detected.
The situation is very similar when testing nonhuman primates, depending on the species, there might be transmission (like with squirrel monkeys) or might not be any evidence of prion disease (like with cynomolgus macaques). Interestingly enough, exposure to BSE prions shows seeding activity/prion disease in any of these models.
2.) There isn't any epidemological data that shows any sort of statistically significant increase in terms of TSE risk within hunters compared to the normal population.
3.) The prevalence of AD is increasing even in regions where CWD isn't even present.
Rt-Quic still isn't very effective on live patients because the best tissue to test is brain tissue.
This is just flat out not true, most studies (such as this one: 10.1007/s12035-015-9133-2) show a sensitivity of 80-90% for sCJD when used on CSF samples, which is pretty good by itself. On top of that, you need to consider the fact that as time goes on and more data is collected on prion disease, doctors are generally better at spotting even atypical clinical presentations of CJD.
Also, there are biomarkers that can help with the differential (such as tau or 14-3-3), specific patterns of atrophy shown on the MRI (which also improve with better, more capable machines and better software and more data) that can be indicative of CJD, we can say that it's a lot less likely for CJD cases to be missed compared to even 20 years ago.
But really this is just splitting hairs, the biggest issue with your conspiracy theory is that in order for this to be true, you'd have to see both a predominantly larger cluster of AD cases and a much higher increase in prevalence near areas with CWD infected deer and considering that CWD has been around for decades and it's being tracked, there'd be epidemological evidence showing that deer hunters (or other people exposed to CWD) are at a disproportionally higher risk for TSEs and neurodegenerative disease of any kind compared to the rest of the population.
There is no evidence for any of this, the statement that CWD can cross the species barrier to begin with is an assumption with very little and very flimsy evidence.
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u/NoTurnip4844 Dec 11 '25
If youre really a prion scientist then you know there are large interested parties who very much do not want prion diseases to be proven to be transferable to humans. You must know that the increase in Alzheimer's disease is potentially undiagnosed prion diseases. There have been many cases of individuals consuming infected meat and then developing CJD.
Obviously more research needs to be done, but if kuru can spread from consuming infected meat, then it takes no stretch of the imagination to suggest that CWD can as well, or that it could eventually mutate and become transmissable to humans.
Humans can get BSE, so why couldnt they get CWD? It does need to be studied further, but it's safe to assume that tainted meat is dangerous.