Alois, I am objective I think. There is a big difference between...

Alois, I am objective I think. There is a big difference between a post hoc analysis of a complete trial and data mining a sub group, as your first two candidates did. There is no comparison with Prana's trial. In the words of Rudy Tanzi,"the trial doctor made a mistake" It was corrected and published.
Interesting you acknowledge the trial correction but post the original flawed results. Makes you look like a short and anything but objective.

In Bapi's case they backed it with a now ongoing trial which has already been extended to collect biomarkers. This ongoing Bapi trial is aiming to show stat sig in APOE negative patients. If it does it will be the first Bapi trial to show stat sig effect.

By appearaing to work, I mean reverse the disease. That is neuron repair. That is higher scores at the end of the trial than at the start. That is getting better. That is solid lab work that can demonstrate just how it was done. That is Prana only as far as I can see. If you know any others that fit that bill please let me know. Until then lets not put it to bed.

The best of your drugs there is Imunoglobulin which has slowed the disease in a real trial, with real trial stat sig results. Imunoglobulin so far is the best of that lot you mentioned. It slows progress of Alzheimers.
You have to know I have posted lots of information about the trial results of both imunoglobulin(gammagard) & Bapi in this forum, and Roch's trial. I am objective.

You on the other hand have appeared just when the shorts have a big day tomorrow. If they can destroy confidence in PBT2 and drive the price under $2 on the Nasdaq it would be very good for them and hurt PRANs ability to raise cash. You dont fool me for a second. Pran looks very cheap for what they have. I dont think the shorts can do it. Read the BioHealth Investor report. They have it flagged as a 10 bagger.
It makes real sense to go for prodormal AD if your drug does not work against the later stages. What doesnt make sense is going into a large phase3 without a clear signal in a phase2, and without actually knowing exactly how your MOA is going to stop Alzheimers. There has been a lot of research since those monoclonal antibodies(MAB) were developed to attack amyloid, some that indicates their target is part of the brains repair mechanism. Roch has a MAB as does JNJ,PFE/ELN.

As for the weaker PBT1. These results can be found on the prana site in the SC ananysis. [The outperformance of PBT1 continued well beyond one year. An open label extension study beyond the original 36 week trial period studied patients out to week 84, with results announced by PBT in October 2004. By this stage the notional ADAS-cog gap between treated and untreated had widened to 10 points, so that while the treated patients were still declining cognitively, PBT1 appeared to have cut the expected rate of disease progression in half.]