Agreed. The trial wasn’t run cleanly — biomarker N collapses, variance is high, and missingness is large — so even the MRI “N” data (while promising) sits on a weak overall biomarker foundation. Outside of a small Aß42/40 effect, there’s essentially no robust A/T/N evidence that Blarca works through amyloid or tau pathways, which is exactly why CHMP is struggling with the MoA story.
Doc — how do you think CHMP interprets this? Do they see the weak A/T/N dataset as mainly a statistical-power issue, a methodological flaw, or as evidence that the MoA simply isn’t acting through amyloid/tau at all? Is there anything AVXL realistically could bring into re-exam — correlations, responder analyses, longer-term OLE biomarker trends — that might change CHMP’s view, or is the MoA gap simply too large to bridge at this point?
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