LAUSR

The protein abnormality participates in the development of ALS that meets with the widespread approval from major researchers. However, these currently found abnormal proteins aren't far enough to explain all pathogenesis of ALS. Therefore, the search of novel abnormal proteins participated in the pathogenesis of ALS is very necessary. In this study, we screened, compared and analyzed the differentially expressed proteins in the spinal cord of the SOD1 G93A transgenic and wild-type (WT) mice applying the isobaric tags for relative and absolute quantitation (iTRAQ) and the bioinformatics methods. The results revealed the details of significantly differentially expressed proteins between the SOD1 G93A transgenic and WT mice, and the damaged and/or regulated cellular components, molecular functions and biological processes and the significant enrichment pathways of these proteins. Our study comprehensively described the details of the possible abnormal proteins participated in the pathogenesis of SOD1 G93A transgenic mice, extensively explored their possible molecular mechanisms how to play the role in the development in this animal model, and provided some evidences and clues for further and deeply studying the relationship between the abnormal proteins and the pathogenesis of ALS in the other animal models and ALS patients.