Identification of shared molecular signatures between multiple sclerosis and Parkinson's disease using systems biology approach

Neurodegenerative diseases (NDs) collectively afflict more than 40 million people worldwide. NDs are relatively common disorders in the central nervous system with progressive neurological symptoms, including various degrees of physical disability. Multiple Sclerosis (MS) and Parkinson's Disease (PD) are the leading cause of disability and dysregulation of immune system effector cells. The clinical and epidemiological analyses indicate the co-morbidity of MS and PD that drive the progression and severity of the central nervous system. This study aimed to revive researchers' enthusiasm in studying the potential role of common genes between MS and PD as novel biomarkers for MS/PD diseases. Hence, two data series of expression profiling by array were used; the expression profiling by array study identified the contributing genes. Then, these genes were filtered with cell gene ontology, PPI network, functional annotation, and enrichment analysis. By calculating the similarity between PD and MS, several common genes were found between MS and PD. We have provided a list of the genes such as BACE2, CD69, CLC, CPA3, DEFA1, and DEFA4. The role of these hub genes could be further explored and discussed. The results of this study would be practical to develop new diagnostic strategies and find new drugs and novel drug targets.

Automated summary

Neurodegenerative diseases (NDs) are common disorders affecting over 40 million people worldwide. Multiple Sclerosis (MS) and Parkinson's Disease (PD) are two leading causes of disability and immune system dysregulation. This study aimed to investigate the potential role of common genes between MS and PD as biomarkers for these diseases. By analyzing gene expression data, several common genes between MS and PD were identified. These findings have practical implications for the development of diagnostic strategies and the search for new drugs and drug targets.