Hello, Gabrielly, congrats! 👏  I’ve been studying ncRNAs (microRNAs) for 3 years, and there is no doubt about the power of these molecules in biomedical sciences, especially their use as biomarkers. Are you planning to compare the expression between lncRNAs and sncRNAs? Comparing lncRNAs and sncRNAs can give you a broader view of how gene expression regulation occurs in Parkinson’s disease.  Thanks for your attention ☺️ 

Were the microRNAs chosen based on their abundance in the serum, but they showed different expression levels (low or high), this could interfere with the results?

Congrats on your work and I hope things keep working out for the rest of your PhD. 

Congrats for you presentation! This is not my area of expertise, but I found your explanation very clear and engaging, and your project is very well designed and developed. Have you considered performing additional functional assays to confirm the pluripotency of your iPSC lines beyond OCT3/4 and NANOG expression, such as embryoid body formation or teratoma assays?

Thanks for your amazing talk and results! I have some questions, as follows: 1) Since HOTTIP and FIRRE are overexpressed across all phenotypes, do you hypothesize they act as general PD-related neuroinflammatory regulators, and have you explored whether their upregulation correlates with circulating cytokine levels or immune cell activation markers? 2) From a translational perspective, do you foresee lncRNA-based blood signatures serving as reliable liquid biopsy biomarkers for PD diagnosis and subtyping in clinical practice, considering challenges of specificity (neurodegeneration vs systemic inflammation) and stability of circulating lncRNAs? Thanks and congrats again!

Thanks for your amazing talk and results! I have some questions, as follows: 1) You propose that mtIDH compensates for LDH loss under hypoxia by providing an alternative NAD⁺ regeneration pathway, so I wonder whether you have quantified intracellular NAD⁺/NADH and NADP⁺/NADPH ratios in mtIDH-expressing vs LDH-deficient glioma cells, and how do these values compare to in vivo glioma samples from TCGA or patient-derived xenografts? 2) How do you comprehend the observed inverse correlation between mtIDH and LDH expression with the well-established “Warburg effect” in gliomas? Could mtIDH tumors represent a distinct metabolic subtype that preferentially uses glutamine or alternative substrates under hypoxia, and have isotope-tracing experiments been performed to map carbon flux? 3) In your hypoxia survival assays, have you examined whether mtIDH expression impacts HIF1α stabilization or transcriptional activity, given that α-KG and 2-HG differentially regulate prolyl hydroxylases?   Thanks and congrats again!