Mobp, short for myelin-associated oligodendrocyte basic protein, is a relatively abundant CNS-specific myelin protein. It plays a crucial role in stabilizing the myelin sheath in the central nervous system (CNS), and its synthesis is regulated by Fyn kinase, which also affects the morphological differentiation of oligodendrocytes [3,5]. Myelination is essential for rapid saltatory conduction of action potentials within the CNS and maintaining neuronal health, and Mobp is thus important for normal CNS function.

In multiple system atrophy (MSA), decreased MOBP mRNA levels are significantly correlated with increased DNA methylation. MOBP is also mislocalized into the glial cytoplasmic inclusions (GCIs) in MSA, where it interacts with α-synuclein, emphasizing its relevance to the pathogenesis of MSA [2]. In multiple sclerosis (MS), T-cell autoimmunity against MOBP can be detected, and MOBP-reactive T-cells can be pathogenic in some mouse strains, suggesting it is a relevant primary target autoantigen in MS [3]. A study on sporadic frontotemporal dementia (sFTD) found a candidate locus on chromosome 3 in the intergenic region between RPSA and MOBP, contributing to increased risk for sFTD through effects on expression and/or splicing in brain cortex [1]. However, a case-control study in a Greek population found no association between MOBP rs616147 polymorphism and amyotrophic lateral sclerosis (ALS) [4].

In conclusion, Mobp is vital for myelin sheath stability and oligodendrocyte morphological differentiation in the CNS. Its role has been revealed in diseases such as MSA, MS, and potentially sFTD through various research models. Although no link was found between a specific polymorphism and ALS in one study, further research could potentially clarify its role in other neurodegenerative diseases and complex genetic disorders.