Hacker News Reader

Comment by amp108 | Hacker News Reader

> It looks like it was "too hard" so standards are being lowered.

Not at all. It turns out one of the standards was not relevant to the target population. As you quoted: "This is because in early cases of Alzheimer’s, patients may have the biological indicators of the disease without actually showing symptoms."

There's no point in trying to alleviate symptoms where there are no symptoms. If I develop a drug that removes tumors that eventually caused headaches, is it somehow lowering standards if it removes tumors before a headache appears?

View on HN

>"This is because in early cases of Alzheimer’s, patients may have the biological indicators of the disease without actually showing symptoms."

This is called a "degenerating research programme". The theory always lags the facts, this is just another ad hoc adjustment to keep it going for some reason. Why? I really cant understand. Whats the last interesting prediction that has come out of the amyloid hypothesis?

Here is an interesting prediction: Amyloid accumulation will be found to be associated with every single disease state where it is investigated. Every single one. This is because amyloid formation is very thermodynamically favorable for polypeptide chains and a cell must be healthy to prevent it.

That's interesting. I've got a kidney infection at the moment, are you suggesting that I have amyloid plaques in my brain?

Well pretty much everyone does have some amyloid plaques in their brain but I mean that there is a higher level of amyloid in your kidney now than before you had the infection.

Wikipedia has a bit on it:

>"Amyloidosis is a group of diseases in which abnormal protein, known as amyloid fibrils, builds up in tissue. [...] The presentation of amyloidosis is broad and depends on the site of amyloid accumulation. The kidney and heart are the most common organs involved. [...] AA is suspected on clinical grounds in individuals with longstanding infections or inflammatory diseases." https://en.wikipedia.org/wiki/Amyloidosis

but arent the biological markers of Alzheimer's still theoretical? i thought that is part of why a cure is so hard to come by -- we don't know if it's the plaques or something else. so if you measure a drug that reduces plaques but you don't measure its affects on cognition how do you know you are making progress?

They've defined it circularly so that the same symptoms without extensive plaques is a different disease.

Reply on news.ycombinator.com