The TRAILBLAZER-ALZ 2 LTE data showed that Kisunla’s benefit continued to grow over three years, with delayed-start patients still experiencing benefit but to a lesser degree. How clinically significant is this finding in reinforcing the value of early initiation of amyloid-lowering therapies?

Early Kisunla treatment reduced the risk of disease progression by 27% compared to delayed initiation. How should clinicians interpret this magnitude of risk reduction in real-world decision-making for early AD patients?

Over 75% of Kisunla-treated patients reached amyloid clearance within 76 weeks, with only slow plaque reaccumulation afterwards. Does this support the concept of limited-duration treatment with durable effects, and how might this contrast with chronic therapy approaches?

ARIA continues to be a concern with amyloid-targeting antibodies. Kisunla’s LTE data reported no new safety signals. How does the field view ARIA risk today, and could new titration strategies or genetic screening (e.g., ApoE4 carriers) improve safety management?

Eisai and Biogen presented data showing weekly subcutaneous maintenance dosing of Leqembi maintained efficacy and biomarkers with fewer infusion reactions (<1% vs 26% with IV). How important is this shift toward SC delivery for patient adherence and healthcare system capacity?

With Kisunla pursuing a finite-duration dosing strategy and Leqembi developing a chronic SC maintenance option, how might these different approaches appeal to distinct patient populations or healthcare systems?

Given their different mechanisms—Kisunla primarily plaque clearance and Leqembi also targeting protofibrils—do you foresee combination or sequential use of these therapies, or will the market likely consolidate around one dominant approach?

Looking ahead, what are the most critical unanswered questions for amyloid-targeting therapies—durability of cognitive benefit, functional outcomes, or integration with tau-targeted or other emerging treatments?