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Here is the abstract:
I do not think it illustrates how much remains to be lerned about degenerative brain diseases. It's target was totally very different than to measure knowledge. It produced only one small piece of it. But it is a a paper among thousands of other papers and the value of it will be very big or very small, who knows. Every month there are already hundreds of papers about neurodegeneration and this is one of them.
It does not illustrate anything about PBT2 but it illustrates that misfolding of a protein (what is already known) is one step in neurodegeneration and also something more about cell death. Even from the works of Susan Lindquist (December 2011) we already know that PBT2 prevents this misfolding to happen. Different MPACs in Prana's portfolio have similar effects in these deurodegenerative disease, preventing misfolding, demonstrated by Linquist. A couple of days ago I posted a study demonstrating how the metals on atomistic level cause misfolding.
This paper does not give any "dual approach" possibility about MPAC and something else to prevent cell death. It is already known that PBT2 prevents cell death ( many papers, an example the mouse study over 1 y ago), but PBT2 treatment also demonstrated regrowth of the neural structures. It is much more than just explaining cell death as was done in this study. But best of all PBT2 did not only prevent the death of neurons in the brain but improved cognition. That means that the neurons started to work as they had been doing before the degenerative process. It would be wonderful if one day there would be a new compound which would improve the effect of PBT2 but I do not think this article has nothing to with improving the cognition improving effect of PBT2.
However it is an interesting paper and published in a top journal. It may one day be much more than what I can value it today from the point of Prana investor. This is only my opinion.
>> I do not think it illustrates how much remains to be lerned about degenerative brain diseases. <<
Really? Do you think we already fully understand neurodegenerative diseases? Do you think that the finding of the "switch" that controls brain-cell death is not a significant piece of new knowledge?
>> It does not illustrate anything about PBT2 <<
I agree. But it does illustrate that other approaches besides MPAC may have therapeutic benefit. We Prana shareholders are often tempted to assume that PBT2 is the be-all and end-all of Alzheimer's drugs, and that no competing approaches to treating the disease will ever become viable. The fact that someone has discovered a completely different way to precent cell death serves as an illustration that we must not remain so narrow-minded.
>> This paper does not give any "dual approach" possibility about MPAC and something else to prevent cell death. It is already known that PBT2 prevents cell death... <<
But do we know that PBT2 will be 100% effective at preventing cell death in humans? No, we don't. Again, I think it's important to keep an open mind about these things rather than to assume that PBT2 will be some sort of magic bullet that will, by itself, end Alzheimer's once and for all.
[But do we know that PBT2 will be 100% effective at preventing cell death in humans? No, we don't. Again, I think it's important to keep an open mind about these things rather than to assume that PBT2 will be some sort of magic bullet that will, by itself, end Alzheimer's once and for all.]
Do we know the mouse work cited in the article will work in humans? No we dont.
What we do know from human tests is that PBT2 can halt the disease in just 12 weeks, maybe reverse it.
The Planck Institute in Germany did some testing of their own and it looks like they agree.
Sure a lot of the investigation of the PBT2 MOA to explain the trial results was done in mice, but the big difference is that it was to evaluate a stat sig effect seen in a human trial. As Pivalde said, there are lots of mice papers out here, but papers talking about reversing the progression in humans are a bit rare.
The above link is very good and I recommend anybody who does not know too much about Prana to read the whole page. This paper may well prove to be very valuable, but with PBT2 already in trials to stop the disease, and with prodormal patients in the trial, we will soon know. Goutah, if they can reverse the decline in prodormal patients, Alzheimers is over for some, providing reliable testing for prodormal condition is available.
Another thing worth remembering, the response is very dose dependent. It may be possible to jack the dose. I know there is a trial in Canada against some cancers with clioquinol using doses over twice Prana's maximum.
Scroll down that page on the link above. There is a lot of relevant info on PBT2. Those Germans seem to know a lot about Prana.
Note: here are different types of Alzheimers with different causes, one being vascular, which maybe will not see the same advantage from PBT2. Of course there will be multiple treatments used.
Goutah, this study does not illustrate the need of information on degenerative brain diseases because it is just a very small piece of information about a single nerve cell. Many new pieces of information are produced every day and when the methods improve, the more we will understand about neurodegeneration. But this article is not the one illustrating the lack of info and I would say that there is lot of work for the next 100 years to fully or almost fully understand neurodegenerative diseases.
You know also very well that PBT2 is not based on a single scientific work but on more than 15 years of talented scientists' work produced hundreds of scientific papers. PBT2 is a product of huge effort to help AD patients, not a single study report.
It is clear that there will be new AD drugs after PBT2, in fact many of them, working on a similar and/or on a different mechanism as PBT2. Some of them likely also developed by Prana scientists.
Goutah, you know very well the human studies made by clioquinols PBT1 and PBT2 on humans. The study that will prove that every human brain cell will survive if you take PBT2 has not been done, yet. It may be never even needed because this kind of demand is IMO just stupid. But it is much more important that the brain cells what MBI persons have work together better and produce better coginition to these human beings when they are taking PBT2 than not taking it. I know that you do not trust this latter statement based on the Ph2a study.
Now Prana is trying to get further evidence on that as you well know to convince many as you on this issue.
At the moment PBT2 can be regarded as a "magic bullet" because not an other drug has improved human cognition (Immunoglobulin has). But for sure there will be new ways to target AD and other degenerative brain diseases.