Multiple sclerosis (MS) is a chronic inflammatory demyelinating disease of
the central nervous system (CNS) frequently starting in young adulthood. However, the
pathogenesis of the progressive disease phase is still not well-understood, and the
inflammation as well as the mechanisms of demyelination and tissue damage is
currently being discussed. The available drugs approved in the treatment of different
clinical forms of MS prevent the relapses, alleviate the symptoms only partially and
slow progression of the disease; however, none of these treatments is capable in
stopping the MS clinical course. Moreover, approved MS treatments lead to
unpredictable adverse effects associated with a range from mild (such as flu-like
symptoms, fatigue, liver transaminase elevation, stomach pain or irritation at an
injection site) to serious (such as bradycardia or progressive multifocal
leukoencephalopathy). It is time to revise the MS drug development strategy by relying
on our endogenous defense mechanisms. Endogenous fatty acid amides (FAAs) are a
family of structurally different molecules found in mammalian systems. These
compounds include anandamide, oleoylethanolamide and palmitoylethanolamide;
research preclinical and clinical reported anti-inflammatory and neuroprotective
activity of FAAs making them an alternative therapeutic approach in neurological
disorders. In consideration that an endogenous compound able in the control of
endogenous defense mechanisms can assume extraordinary importance, this chapter
includes a discussion on current approved drugs in MS, and on pharmacological
properties of FAAs that may play a promising role in complementing of medication
approved for use in MS.
Keywords: Autoimmune disease, Anandamide, Cortical lesions, Endogenous
mechanisms, Experimental autoimmune encephalomyelitis, Grey matter, Immune
regulatory molecules oleoylethanolamide, Multiple sclerosis, Neuroinflammation,
Pain, Palmitoylethanolamide, Preclinical studies, White matter.
