Description
The study reveals that pTau enhances EV release in a Gal3-dependent manner, suggesting Gal3 controls EV biogenesis, but the underlying cellular machinery and signaling pathways are not characterized. This gap limits understanding of how tau pathology spreads between cells.
Gap type: unexplained_observation Source paper: Galectin-3 aggravates microglial activation and tau transmission in tauopathy. (2024, The Journal of clinical investigation, PMID:37988169)
Resolution criteria
[“CRISPR knockout of Gal3 in BV2 cells abolishes pTau-induced EV release increase (NTA and CD63+ flow cytometry)”, “siRNA knockdown of ESCRT machinery (HGS, TSG101) blocks Gal3-dependent EV biogenesis pathway”, “Gal3 proximity labeling (BioID) identifies 5+ candidate intracellular partners regulating EV cargo selection”, “pTau-stimulated EVs from Gal3-KO vs WT mice show different miRNA cargo profiles by small RNA-seq”]