Comparison Log
2025-12-15 03:05:08.929941
mwtab Python Library Version: 2.0.0
Source:      https://www.metabolomicsworkbench.org/rest/study/analysis_id/AN006539/mwtab/...
Study ID:    ST003972
Analysis ID: AN006539
Status:      Inconsistent

Sections "STUDY" contain missmatched items: {'STUDY_SUMMARY': ["Objective: This study aimed to characterize the lipidomic profiles of brain-derived extracellular vesicles (BDEVs) isolated from human APOE3/3 and APOE4/4 Alzheimer's disease (AD) brains, and to evaluate how APOE4-associated lipid alterations contribute to tau pathology and neuroinflammation. Methods: Using a multidimensional mass spectrometry-based shotgun lipidomics approach, we profiled BDEVs from 40 postmortem AD brain samples (20 APOE3/3, 20 APOE4/4). Statistical and bioinformatic analyses were applied to identify significant genotype-specific lipidomic changes and their associations with key pathological and biological outcomes. Results: BDEVs from APOE4/4 brains exhibited a distinct lipidomic signature characterized by altered levels of free fatty acids, sphingolipids, cholesterol esters, and phospholipids. These changes were notably associated with increased tau accumulation and heightened neuroinflammatory markers. Among these alterations, specific lipid species demonstrated strong correlations with tau pathology and glial activation, suggesting a mechanistic link between APOE4-driven lipid remodeling and AD progression. Conclusion: Our findings uncover a novel APOE4-specific mechanism in which lipid alterations within BDEVs may drive tau propagation and neuroinflammatory responses. These results provide new insights into lipid-mediated pathways of neurodegeneration and highlight the potential for targeting lipid metabolism and extracellular vesicle pathways in APOE4-related AD.", "Objective: This study aimed to characterize the lipidomic profiles of brain-derived extracellular vesicles (BDEVs) isolated from human APOE3/3 and APOE4/4 Alzheimer''s disease (AD) brains, and to evaluate how APOE4-associated lipid alterations contribute to tau pathology and neuroinflammation. Methods: Using a multidimensional mass spectrometry-based shotgun lipidomics approach, we profiled BDEVs from 40 postmortem AD brain samples (20 APOE3/3, 20 APOE4/4). Statistical and bioinformatic analyses were applied to identify significant genotype-specific lipidomic changes and their associations with key pathological and biological outcomes. Results: BDEVs from APOE4/4 brains exhibited a distinct lipidomic signature characterized by altered levels of free fatty acids, sphingolipids, cholesterol esters, and phospholipids. These changes were notably associated with increased tau accumulation and heightened neuroinflammatory markers. Among these alterations, specific lipid species demonstrated strong correlations with tau pathology and glial activation, suggesting a mechanistic link between APOE4-driven lipid remodeling and AD progression. Conclusion: Our findings uncover a novel APOE4-specific mechanism in which lipid alterations within BDEVs may drive tau propagation and neuroinflammatory responses. These results provide new insights into lipid-mediated pathways of neurodegeneration and highlight the potential for targeting lipid metabolism and extracellular vesicle pathways in APOE4-related AD."]}