Comparison Log
2026-03-15 08:20:19.653171
mwtab Python Library Version: 2.0.0
Source:      https://www.metabolomicsworkbench.org/rest/study/analysis_id/AN007906/mwtab/...
Study ID:    ST004681
Analysis ID: AN007906
Status:      Inconsistent

Sections "STUDY" contain missmatched items: {'STUDY_SUMMARY': ["We have identified a population of lipofuscin-laden microglia in the Grn KO mouse brain that colocalizes with GPNMB, a key marker of Grn KO-specific transcriptomic signatures. In this study, we investigated the lipidomic and metabolomic signatures of this population through FACS-based isolation of lipofuscin 'high' and 'low' microglia (CD11b+/CD45+) from dissociated brain tissue of aged (20-mo) WT and Grn KO mice (n = 5-6/group). This analysis identified an increase of glucosylceramide (GlcCer) and ganglioside GM3 species in lipofuscin-high microglia, which was further elevated in Grn KO background, indicative in part of GCase defects. Lysosomal phospholipid BMP was elevated in lipofuscin-high WT microglia, suggestive of lysosomal dysfunction. However, this increase was significantly attenuated in Grn KO cells, consistent wth a failure to elicit a compensatory response. Myelin lipid sulfatide was enriched in Grn KO microglia, in agreement with previous reports of myelin debris accumulation in this genotype. Finally, metabolomic profiling showed a broad reduction of analytes that was specific to lipofuscin-high microglia in Grn KO background, indicating bioenergetic defects in this population.", "We have identified a population of lipofuscin-laden microglia in the Grn KO mouse brain that colocalizes with GPNMB, a key marker of Grn KO-specific transcriptomic signatures. In this study, we investigated the lipidomic and metabolomic signatures of this population through FACS-based isolation of lipofuscin ''high'' and ''low'' microglia (CD11b+/CD45+) from dissociated brain tissue of aged (20-mo) WT and Grn KO mice (n = 5-6/group). This analysis identified an increase of glucosylceramide (GlcCer) and ganglioside GM3 species in lipofuscin-high microglia, which was further elevated in Grn KO background, indicative in part of GCase defects. Lysosomal phospholipid BMP was elevated in lipofuscin-high WT microglia, suggestive of lysosomal dysfunction. However, this increase was significantly attenuated in Grn KO cells, consistent wth a failure to elicit a compensatory response. Myelin lipid sulfatide was enriched in Grn KO microglia, in agreement with previous reports of myelin debris accumulation in this genotype. Finally, metabolomic profiling showed a broad reduction of analytes that was specific to lipofuscin-high microglia in Grn KO background, indicating bioenergetic defects in this population."]}
'Metabolites' section of 'MS_METABOLITE_DATA' block do not match.
'Data' section of 'MS_METABOLITE_DATA' block do not match.