ABSTRACT
Multiple sclerosis (MS) is the leading cause of neurologic disability
in young adults. The clinical signs and symptoms of MS are caused
by an autoimmune attack on the myelin sheath surrounding the
central nervous system (CNS) neurons, leading to demyelination and
axonal loss. Recent data suggest that permanent disability is due
to oxidative damage to neurons resulting in apoptosis of the cells.
The approved therapeutic agents for MS are costly and only partially
effective because they primarily target the autoimmune aspect of the
disease pathogenesis. Experimental autoimmune encephalomyelitis
(EAE) is the primary animal model of MS. Low-level laser (light)
therapy (LLLT) has shown therapeutic potential in the resolution
of chronic inflammation and protection against neurodegeneration,
both key components in the pathology of MS. Published data in
the EAE model demonstrated the therapeutic potential of 670 nm
light-mediated photobiomodulation, in association with the down-
regulation of pro-inflammatory mediators and the upregulation of
anti-inflammatory proteins. These recent observations indicate that
photobiomodulation is a promising therapeutic approach for the
treatment of MS.
