The study analyzed astrocyte- and microglia-enriched transcriptomes from aged Atxn2-CAG100 mice to investigate mechanisms underlying neurodegeneration. Transcriptomic profiling revealed dysregulation of ribosomal RNA processing, RNA metabolism, translation pathways, and stress granule/U-body-associated factors. Astrocytes showed stronger alterations than microglia, supporting a major glial contribution to ATXN2-associated neurodegeneration.
Aged Atxn2-CAG100 mice exhibited strong glial transcriptomic dysregulation involving ribosome biology, RNA handling pathways, stress response factors, and U-body-associated transcripts. Astrocytes displayed more pronounced molecular alterations than microglia.
Atxn2-CAG100 Knockin mouse — genOway-developed polyglutamine expansion model of spinocerebellar ataxia type 2
Spinocerebellar ataxia type 2, neurodegeneration, RNA metabolism, glial dysfunction, polyglutamine disease, ribosome pathology
Knockin insertion of expanded CAG100 repeat into Atxn2 locus, astrocyte and microglia transcriptome isolation, RNA sequencing, pathway enrichment analysis, aging neurodegeneration model, glial subtype comparison
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