Hi
I got some questions from the Authors and would appreciate their answer:
1-Mechanistic Gaps in Glioblastoma Results:
The data shows that BMAA enhances glioblastoma cell proliferation without involving ROS or Wnt signaling. What mechanisms do you propose for this observation, and why weren’t these explored further?
2-Dose Selection:
What is the rationale behind the specific BMAA concentrations used in the study? Do these doses reflect environmentally or clinically relevant exposure levels, or were they chosen for experimental convenience?
3-Therapeutic Claims:
How do you justify suggesting that Wnt inhibitors could reverse BMAA’s effects when the data is based solely on neuroblastoma cells in vitro? Shouldn’t preclinical data or additional validation be required before proposing therapeutic strategies?
4-Generalization Across Cell Types:
The study uses two specific cell lines (IMR-32 and U118-MG) yet makes broader claims about neuronal and glial responses to BMAA. How can these findings be generalized without testing primary cells or more physiologically relevant models?