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glaugh | 1 year ago

> …small amounts of clumping tau protein in the brain and cerebrospinal fluid, which lead to Alzheimer's disease.

I don’t think this should be stated as a proven fact anymore, given the doubt now cast over the amyloid hypothesis

This is a nice summary of the case: https://podcasts.apple.com/us/podcast/plain-english-with-der...

discuss

order

pedalpete|1 year ago

The problem with the amyloid hypothesis is most likely not that it is wrong, but that it is incomplete, and I would say that is the problem with this test as well.

I work in neurotech/sleeptech, and AD researchers are using (or want to use) slow-wave enhancement to prevent and possibly manage AD.

However, the test for AD is still a psychological tests along with neuroimaging to look for tau tangles and amyloid plaque build up.

It has been discussed that we may be looking at multiple different diseases which have similar symptoms and without completely understanding the disease itself, we are categorizing them as AD, though they may have different pathways.

Though we can't ignore the challenges to the amyloid hypothesis, we also shouldn't completely throw it out. Most of the experts I've spoken with still believe it is the best hypothesis we have, but that we also should not ignore other possibilities.

tim333|1 year ago

It surprises me that some obvious clues to treatment are passed over as I guess they don't fit the politics? Like

>A team of researchers in Jerusalem, he says, decided to look at patients who survived bladder cancer and compare dementia prevalence among patients treated with BCG and those who weren’t. “Do they differ in the rate at which they get Alzheimer’s disease?” The answer is yes – the BCG group appeared to get 75% protection against Alzheimer’s. A number of studies have now found varying levels of protection from BCG, with an average, according to one meta‑analysis, of 45%.

There's a lot of evidence a lot of it is set off by infectious microbes which can be treated in the usual way. (From https://www.theguardian.com/lifeandstyle/2024/dec/01/the-bra...)

The 'politics' puzzles me. Maybe the head of department got fame for hypothesis A and feels his power or money is threatened by hypothesis B? It's not what science should be about.

(There was an entertaining angry Sabine Hossenfelder youtube a few minutes ago on the corruption of science just wasting money, but really letting people die of Alzheimer's is worse. https://youtu.be/shFUDPqVmTg)

giantg2|1 year ago

"The problem with the amyloid hypothesis is most likely not that it is wrong, but that it is incomplete,"

If the hypothesis is that amalyoid causes AD, then I think we've disproved that (even with your statement that it's incomplete). If I remember correctly, there are individuals who have amalyoid without developing AD, or who have had their amalyoid levels reduced without improvement. At this point, it seems that amalyoid is more of a symptom than a cause. But you are correct that the data is dirty - many studies have not tested for amalyoid itself, instead relying on clinical diagnosis, and subsequent studies are finding at 25% of mild to moderate AD may be other forms of neural degeneration. So many of the AD studies out there focusing on amalyoid reduction are garbage because many of them happened before being able to use imaging to test amalyoid levels.

alfiedotwtf|1 year ago

Damn! I know nothing about AD and while reading these comments you mentioned sleep tech. I didn’t understand the connection or what amyloid hypothesis even was, so looked it up.

As someone who’s on < 4 hours of sleep a day with at least one day for 36 hours straight awake a week, umm… should I be worried?

robwwilliams|1 year ago

Agree strongly with you. This statement make Alzheimer’s into a wonderfully “simple” monogenic disease like Huntington’s but all age-related disease have many complex interwoven weaker and stronger causes—-even Huntington’s disease in which the same mutation type (numbers of CAG mutations in neurons) can cause symptoms over a 20 year range.

Too bad that headlines are inherently short and sometimes misleading. Simple sells.

swores|1 year ago

Is it not still the case that they do correlate, and therefore the article talking about them as biomarkers is not making the mistake you think it is (as if it was talking about them as the thing to get rid of to prevent Alzheimer's)? Because "lead to" is not the same as "causes".

Or has latest research shown that even a non-causal link should be dismissed?

dimal|1 year ago

Ok “lead to” might not be exactly equivalent to “causes”, but it’s not even accurate because tau doesn’t ALWAYS lead to Alzheimer’s. The correlation is not strong. People have tau and no Alzheimer’s and other people have Alzheimer’s symptoms and no tau. So what good does it do you to test for tau? It’s a higher probability of Alzheimer’s, but not nearly definitive. I suspect that if this test is productized, this nuance will be lost on many doctors.

Seems like a good test to give someone so you can scare them into taking a drug that also has very little evidence of effectiveness.

kadoban|1 year ago

"Lead to" is a synonym for "causes".

im3w1l|1 year ago

I've seen this point brought up many times over the years and yet research in this direction seems to continue, so I think there must be more to it. I asked chatgpt about it, and it claims that the controversial paper was influential but it was more about a certain sub-hypothesis that got called into question after that rather than the entire thing.

Now I know that bringing up chatgpt is frowned upon here but I thought I should make an exception for this case as its not so easy for me to answer otherwise.