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REVIEW: Involvement of Mitochondria in Neurodegeneration in Multiple Sclerosis

M. S. Kozin1,2,a*, O. G. Kulakova1,2,b, and O. O. Favorova1,2

1Pirogov Russian National Research Medical University, 117997 Moscow, Russia

2National Medical Research Center of Cardiology, 121552 Moscow, Russia

* To whom correspondence should be addressed.

Received December 25, 2017; Revision received March 6, 2018
Functional disruption and neuronal loss followed by progressive dysfunction of the nervous system underlies the pathogenesis of numerous disorders defined as “neurodegenerative diseases”. Multiple sclerosis, a chronic inflammatory demyelinating disease of the central nervous system resulting in serious neurological dysfunctions and disability, is one of the most common neurodegenerative diseases. Recent studies suggest that disturbances in mitochondrial functioning are key factors leading to neurodegeneration. In this review, we consider data on mitochondrial dysfunctions in multiple sclerosis, which were obtained both with patients and with animal models. The contemporary data indicate that the axonal degeneration in multiple sclerosis largely results from the activation of Ca2+-dependent proteases and from misbalance of ion homeostasis caused by energy deficiency. The genetic studies analyzing association of mitochondrial DNA polymorphic variants in multiple sclerosis suggest the participation of mitochondrial genome variability in the development of this disease, although questions of the involvement of individual genomic variants are far from being resolved.
KEY WORDS: neurodegenerative diseases, neurodegeneration, mitochondria, multiple sclerosis, haplogroup, single nucleotide polymorphism

DOI: 10.1134/S0006297918070052