Yes, I think that the trial results are much better explained with the controlling genetics taken into account.
You get a nice, immediate, classical curve result from the mabs. That's because they are all attacking the plaques, and the plaques are all the same. The APOE4 carriers probably have worse plaques, and therefore more inflammation, but the nature of the battlefield is the same for every patient.
Blarcamesine operates in four different environments, depending on the genetic status of the two identified genes. If you can segregate them one from another through genotyping, you should get four subgroups, each with a classical response curve. The problem arises when you try to combine these unlike events and still expect to find a classic distribution curve.
Blarcamesine is also acts far upstream from the symptomatic plaques. This creates a delayed effect on plaque reduction, since the Anavex drug is attacking much closer to the source of the disease and reduces plaques, indirectly, over a longer time frame.
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