Impaired remyelination due to degeneration of both postmitotic oligodendrocytes 
and oligodendrocyte progenitors (OPs) is the major hallmark of inflammatory 
demyelination in multiple sclerosis (MS) lesions and experimental autoimmune 
encephalomyelitis (EAE). Here, we have demonstrated the potential of lovastatin, 
a HMG-CoA reductase inhibitor, for the restoration of impaired remyelination 
mediated through enhanced survival and differentiation of OPs in the spinal cord 
of treated EAE animals. Lovastatin treatment significantly increased the level 
of myelin lipids in the spinal cord of treated EAE animals, coinciding with the 
attenuation of disease severity and inflammatory demyelination as compared with 
untreated EAE animals. The increased expression of myelin proteins and 
transcription factors associated with differentiating oligodendrocytes along 
with the increase in number of NG2+/BrdU- and NG2+/BrdU+ cells, and the 
expression of proliferating OP-specific proteins, demonstrated the restoration 
of remyelination in the spinal cord of lovastatin-treated EAE animals. 
Corresponding to this, in vitro studies further corroborated the increased 
survival and differentiation of OPs in lovastatin-treated activated mixed glial 
cells suggesting that lovastatin protects against the degeneration of OPs and 
enhances their differentiation through induction of a pro-remyelinating 
environment in the spinal cord of treated EAE animals. Together, these data 
demonstrate that lovastatin has the potential to augment remyelination in MS 
lesions and other neuroinflammatory diseases.