Multiple sclerosis (MS) is a disease which manifests demyelination of neuronal 
cells in the brain. Despite extensive research on the mechanisms of disease 
development and progression, the exact mechanism is not elucidated yet, which 
has hampered drug development and subsequent treatment of the disease. We have 
recently shown that the serum levels of arsenic and malondialdehyde, a lipid 
peroxidation marker, are high in MS patients. In this article, we would like to 
formulate the hypothesis that arsenic may cause MS by induction of inflammation, 
degeneration, and apoptosis in neuronal cells. The induction of ROS generation 
in cells upon exposure to arsenic as a heavy metal may be involved in the 
pathogenesis of MS. Tau protein, a member of the family of 
microtubule-associated proteins, is mainly expressed in neurons and contribute 
to the assembly of neuronal microtubules network. Arsenic may affect the 
hyperphosphorylation and aggregation of tau proteins and may be involved in the 
cascade leading to deregulation of tau function associated with 
neurodegeneration. For validation of this hypothesis, studies might be conducted 
to evaluate the association of arsenic levels and tau protein levels in MS 
patients. Further studies might also focus on the trafficking along microtubules 
in neurons of MS patient with regard to hyperphosphorylation of tau protein. 
This hypothesis may add a new dimension to the understanding of MS etiology and 
help to design novel therapeutic agents against potential targets that might be 
discovered. If this hypothesis proves to be true, tau phosphorylation inhibitors 
can be potential candidates for MS drug development.