Version history

{
  "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.\n\nGap type: unexplained_observation\nSource paper: Galectin-3 aggravates microglial activation and tau transmission in tauopathy. (2024, The Journal of clinical investigation, PMID:37988169)",
  "domain": "neurodegeneration",
  "status": "open",
  "priority_score": 0.86,
  "importance_score": 0.88,
  "tractability_score": 0.82,
  "source": "pubmed: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\"]",
  "market_price": 0.5
}