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Drug slows Alzheimer's but can it make a real difference?

17 Comments
By LAURAN NEERGAARD

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Doctors are divided over how much difference that may make for patients and families

Unfortunately this is something expected for something that has been so difficult to develop, a miracle drug that had clear curative properties is what everybody is aiming for, but if it has been impossible to find it until now something like Iecanemab, a drug with risks and limited benefits.

Still, this is advancement in something that was stuck almost at zero for decades, more research and investment (hopefully from governments so the motivation becomes public health more than profit) and we may have better options working on similar mechanisms in the near future.

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Japanese drugmaker Eisai

Wow! I used to teach English there in their Myogadani branch over 10 years ago! Natsukashii!

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I just use snus, much cheaper

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1670208/

https://www.science.org/content/article/nicotine-and-alzheimers

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I just use snus, much cheaper

It also have much less clinical data that shows a benefit on Alzheimer patients. The double blind cohort study that could indicate if nicotine have any actual clinical relevance still have not reported their results.

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Unfortunately this is something expected for something that has been so difficult to develop,

No, because if this is what the experts had expected, then they wouldn't engage in a study to try and find out if it is effective or not.

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Extremely skeptical, especially because just a few months ago there was a bombshell article from Science magazine ( https://www.science.org/content/article/potential-fabrication-research-images-threatens-key-theory-alzheimers-disease ) that exposed what seems to be fabrication and falsification by researches on what had become the main theory behind what causes alzheimer's disease (The amyloid theory), which this drug is trying to attack as many other drugs did since this theory was published, and drug after drug that tried to tackle this main problem didn't actually solved alzheimer's disease or even slowed it.

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No, because if this is what the experts had expected, then they wouldn't engage in a study to try and find out if it is effective or not.

Of course they do, expecting something and corroborating/proving that something with objective data is a perfectly valid motivation to do a study. There is always the possibility the expectations turn out to be false or the results different in some way.

You have repeatedly argued that you have no expertise on scientific or medical topics, this can explain this belief, but it could have been easily dispelled by searching for any source where scientists say there is no point in doing a study if they were already expecting a result (since you would find only information that contradicts you)

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that exposed what seems to be fabrication and falsification by researches on what had become the main theory behind what causes alzheimer's disease 

Your sources clearly contradict this conclusion.

Selkoe adds that the broader amyloid hypothesis remains viable. “I hope that people will not become faint hearted as a result of what really looks like a very egregious example of malfeasance that’s squarely in the Aβ oligomer field,” 

The article is about fabrication and falsification on the role of one variety of deposits, not on the general theory itself, and since phase 3 clinical trials of therapeutics including Iecanemab have reported positive results (something that would be impossible if the whole theory was false) this remains a valid target for therapies.

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I believe the only direct evidence that the amyloid fibrils actually cause (i.e., are not just associated with) Alzheimer's disease is that study that turned out to be falsified.

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I believe the only direct evidence that the amyloid fibrils actually cause (i.e., are not just associated with) Alzheimer's disease is that study that turned out to be falsified.

That would be completely wrong, the reference already provided clearly says that other preclinical studies have concluded the deposits are a cause uf the same kind of problems that Alzheimer causes. The one disproved is again only about  Aβ, not amyloid deposits in general.

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Raw BeerToday  01:41 pm JST

I believe the only direct evidence that the amyloid fibrils actually cause (i.e., are not just associated with) Alzheimer's disease is that study that turned out to be falsified.

This is absolutely true because no study has ever concluded and been supported by medical consensus that amyloid fibrils actually cause Alzheimer's disease.

It is not enough to say any deposits that cause the same problems that Alzheimer's causes are therefore the cause of Alzheimer's and in fact, no medical professional would make such claim.

Amyloid fibrils are self-assembled fibrous protein aggregates that are associated with a number of presently incurable diseases such as Alzheimer's but associated does not mean the cause of such disease.

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Amazing how many experts at Google-Fu we have here

Amyloid fibrils are self-assembled fibrous protein aggregates that are associated with a number of presently incurable diseases such as Alzheimer's but associated does not mean the cause of such disease.

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4286994/

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StrangerlandToday  03:01 pm JST

Amazing how many experts at Google-Fu we have here

Amyloid fibrils are self-assembled fibrous protein aggregates that are associated with a number of presently incurable diseases such as Alzheimer's but associated does not mean the cause of such disease.

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4286994/

You showed you're one of them--besides, there are no Alzheimer experts here so where do you think people get their information from?

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You showed you're one of them

Yes, I'm good with Google. I don't pretend to know anything about Alzheimer's though.

besides, there are no Alzheimer experts here

Yet so many people commenting as if they know what they're talking about...

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Amyloid fibrils are self-assembled fibrous protein aggregates that are associated with a number of presently incurable diseases such as Alzheimer's but associated does not mean the cause of such disease.

Yep, that sums it up nicely...

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This is absolutely true because no study has ever concluded and been supported by medical consensus that amyloid fibrils actually cause Alzheimer's disease.

It is not enough to say any deposits that cause the same problems that Alzheimer's causes are therefore the cause of Alzheimer's and in fact, no medical professional would make such claim.

That would be false, as the reference already provided proves. Making an appeal to a consensus that can be so easily contradicted means this is just a personal opinion, and one that can be proved mistaken.

Schrag says oligomers might still a play role in Alzheimer’s. Following the Nature paper, other investigators connected combinations of oligomers to cognitive impairment in animals. 

The same happens with professional communications from many other sources

https://www.nia.nih.gov/health/what-happens-brain-alzheimers-disease

Emerging evidence suggests that Alzheimer’s-related brain changes may result from a complex interplay among abnormal tau and beta-amyloid proteins and several other factors. It appears that abnormal tau accumulates in specific brain regions involved in memory. Beta-amyloid clumps into plaques between neurons. As the level of beta-amyloid reaches a tipping point, there is a rapid spread of tau throughout the brain.

So it was terribly easy to prove your claim that professionals would never make say this was false. Obviously the NIH National Institute of Aging is a real authority and should be a better reference than your own appeal to be one (since you have not provided any reference but your own opinion).

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You showed you're one of them--besides, there are no Alzheimer experts here so where do you think people get their information from?

What evidence do you have about what other people commenting here are or do for a living? How can you claim there are no Alzheimer experts here?

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