I agree that reduction in brain atrophy is a much more significant measure of a drug's efficacy in regards to Alzheimer's disease than inhibiting the build up or removing amyloid (especially the plaques). The question is how much reduction in hippocampal atrophy is needed to significantly slow down cognitive loss in Alzheimer's disease. To reverse the disease, you need to see an increase in hippocampal neurons. Pbt2 seems to occupy that netherworld between success and failure. I still think a hybrid is the key to the drug's survival, but perhaps further analysis will turn up a silver lining.
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