Amyotrophic lateral sclerosis (ALS) is one of the most common adult-onset 
neurodegenerative diseases, with progressive paralysis and muscle atrophy. The 
exact pathogenic mechanism remains unknown, but recent evidence suggests that 
differential gene expression and gene splicing may play a significant role. We 
used Affymetrix GeneChip Mouse Exon 1.0 ST Array to investigate the expression 
profiling of lumbar spinal cord samples from SOD1-G93A transgenic mice, the 
widely used animal model of ALS. The de-regulated genes analyzed either from the 
expression level or from the alternative splicing level both showed overlapping 
GO categories and pathway mapping. Our findings indicate that cell adhesion, 
immune-inflammation response and lipid metabolism all play important roles in 
the onset of ALS. Detailed analysis by RT-PCR of key genes confirmed the 
experimental results of microarrays. These results suggest a multi-factor 
mechanism in ALS development.