Transcriptomic profiling of symptomatic and end-stage SOD1-G93A transgenic mice reveals extracellular matrix components as key players in ALS pathogenesis

ALS is a neurodegenerative disease marked by the loss of motor neurons. Damaged neurons are not regenerated but attract immune cells, fibroblasts, and astrocytes. Research suggests fibrosis and inflammation contribute to ALS progression. This study profiled spinal cord tissues from SOD1-G93A male mice at different disease stages using RNA sequencing. We identified differentially expressed genes and pathways linked to disease progression. We highlighted notable changes in ECM-related genes: Fmod, S100a4, S100a6 and Col1a1. These findings provide insights into ALS pathology and potential therapeutic targets.