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Subject: Aducanumab: A cure for Alzheimer's? rss

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Shawn Fox
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http://www.nature.com/news/alzheimer-s-treatment-appears-to-...

The first human trials have just past the 12 month mark and Aducanumab has been shown to reverse the buildup of the amyloid-β plaques which are associated with Alzheimer's. Whether this is a cure remains to be seen. The trail did show that a reduction in the plaques was associated with a slowing of the mental decline associated with Alzheimer's, but the sample size of the initial trial (165 people, varying dosages, placebos, etc) is too small to confirm the results for certain. Larger phase III trails are already underway.

Nothing scares me more than slowly losing my ability to think, so I really hope this new drug is finally the breakthrough everyone has been looking for in Alzheimer's treatment. My grandmother went out that way and it is truly an awful thing to watch happen to someone.
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Born To Lose, Live To Win
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Re: Aducanumab: A cure of Alzheimer's?
Yeah, I read this earlier, hopefully the plaques are not just a treatable symptom for something else that actually does the real damage.
 
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Andy Leighton
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Well it isn't a cure as such and no one is saying it is.

Even the people behind the trials are saying that it is very likely going to be of no help to someone with the advanced disease, it has just been tested on people with very early stage Alzheimers and the next phase will also be on people with very early stage Alzheimers.

But even if it just results in a delay to, or slowdown of, the onset of major symptoms it will be welcomed. Those extra years without major impairment would be a real boon to many families.
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Shawn Fox
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It also may be just overblown hype. Certainly the stock market didn't move much on the news, but that is apparently because it isn't really new information. There was already a similar study on the drug published last year, I'm not sure what hte difference is this year vs. last, maybe a different dosage or a slight modification to the drug to reduce side effects?

http://www.fiercebiotech.com/r-d/updated-a-setback-biogen-s-...

It seems the real test is the phase III trails, using the drug over a long time period, to see what the long term effects are. Of course, in the drug industry, requiring the drug to be taking once a month for the rest of your life is good news, assuming it works.
 
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Born To Lose, Live To Win
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sfox wrote:
It seems the real test is the phase III trails, using the drug over a long time period, to see what the long term effects are. Of course, in the drug industry, requiring the drug to be taking once a month for the rest of your life is good news, assuming it works.
This concerns me at times with our current system, if you can get a maintenance drug on the market, the incentive to pursue a cure is less. There is less demand pressure since the severity seems less. I don't want researchers to take their foot off the gas, but I don't want people to suffer to keep the hammer down. The dark side of profit motive.
 
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M M
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http://www.nature.com/neuro/journal/v18/n6/full/nn.4017.html

"Nearly 20 years ago, with the combination of observations from biochemistry, neuropathology and genetics, a compelling hypothesis known as the amyloid cascade hypothesis was formulated. The core of this hypothesis is that it is pathological accumulations of amyloid-β, a peptide fragment of a membrane protein called amyloid precursor protein, that act as the root cause of AD and initiate its pathogenesis. Yet, with the passage of time, growing amounts of data have accumulated that are inconsistent with the basically linear structure of this hypothesis. And while there is fear in the field over the consequences of rejecting it outright, clinging to an inaccurate disease model is the option we should fear most."


"The amyloid cascade hypothesis, like all good hypotheses, makes clear, testable predictions. As it is currently stated, there are two basic types of experiments that should be done to test its validity. The first type would involve taking healthy people and adding amyloid to their brains. According to the hypothesis, they should get AD. The second test would be to take people who already have AD and remove the amyloid from their brains. According to the hypothesis, they should get better; or at least they should not get any worse."

"The first test has been done in humans and in mice. Although the full interpretation of the findings in human brain is still being discussed29, there is evidence from autopsy studies and from live imaging using PET ligands such as PiB (the 11C-labeled Pittsburgh compound B)30 or its 18F-labeled cousins, florbetapir, flutemetamol, florbetaben and others31. These studies are all in substantial agree- ment with one another: individuals can present with few if any clinical symptoms of dementia and yet carry substantial amyloid burdens in their brains32,33. That is basically an experiment of nature that fulfills the first test—adding amyloid to healthy people’s brains. They should have Alzheimer’s dementia, but they do not. Such individuals are not rare; rather, they account for a quarter to a third of all older individuals with normal or near-normal cognitive function. Having a detectable amyloid burden by PET scanning increases the risk that a healthy individual or a person with mild cognitive impairment will progress to AD by about fourfold34. But data are still accumulating on the question of how long amyloid deposits can persist without major cognitive illness. It is already clear, however, that the time will be measured in years, not in weeks35.
The existence of this group of individuals (healthy, but amyloid pos- itive) is a substantial challenge to the amyloid cascade hypothesis. It is clearly possible to have amyloid deposits without dementia; therefore amyloid is not sufficient to cause disease. And since the deposits are the macroscopic result of a process that starts with smaller oligomeric aggregates, we may speculate that these plaque-positive individuals have been oligomer-positive for even longer periods of time; they should thus be well along the disease pathway. Yet the absence of any overt signs of dementia in 25% to 30% of such individuals suggests that they are not.
-Osmium
 
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