1. Is an issue, but not due to your explanation. Simply because there was no dose arm separation as most patient landed on about the same 30mg dose due to tolerability / titration issues. Hence pooled dose arms and not ITT TLD dose/response data.
2. You are again incorrectly on about a non-standard distribution.
3. Tau and microtubules sit at the heart of the neuronal injury in Alzheimer’s. Tau based biomarkers in CSF, blood and imaging are not tied to the monoclonal antibody class. They are part of the core biological definition, staging, and prognosis of the disease, and regulators already recognise CSF tau together with amyloid measures as qualified biomarkers for trial enrichment. For any putative disease modifying therapy that acts downstream of amyloid, or in parallel to it, movement in tau and related neurodegeneration markers will remain highly relevant as supportive evidence, even though at present regulators still insist on clinical benefit rather than tau alone as the primary basis for approval.