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Int Rev Cell Mol Biol. 2017;328:49-103. doi: 10.1016/bs.ircmb.2016.08.003. Epub 2016 Sep 28.

Mitochondria in Multiple Sclerosis: Molecular Mechanisms of Pathogenesis.

Author information

1
Department of Morphology, Surgery and Experimental Medicine, Section of Pathology, Oncology and Experimental Biology, Laboratory for Technologies of Advanced Therapies (LTTA), University of Ferrara, Ferrara, Italy.
2
The New York Stem Cell Foundation Research Institute, New York, NY, United States.
3
Department of Biochemistry, Nencki Institute of Experimental Biology, Warsaw, Poland.
4
Department of Morphology, Surgery and Experimental Medicine, Section of Pathology, Oncology and Experimental Biology, Laboratory for Technologies of Advanced Therapies (LTTA), University of Ferrara, Ferrara, Italy. Electronic address: paolo.pinton@unife.it.

Abstract

Mitochondria, the organelles that function as the powerhouse of the cell, have been increasingly linked to the pathogenesis of many neurological disorders, including multiple sclerosis (MS). MS is a chronic inflammatory demyelinating disease of the central nervous system (CNS) and a leading cause of neurological disability in young adults in the western world. Its etiology remains unknown, and while the inflammatory component of MS has been heavily investigated and targeted for therapeutic intervention, the failure of remyelination and the process of axonal degeneration are still poorly understood. Recent studies suggest a role of mitochondrial dysfunction in the neurodegenerative aspects of MS. This review is focused on mitochondrial functions under physiological conditions and the consequences of mitochondrial alterations in various CNS disorders. Moreover, we summarize recent findings linking mitochondrial dysfunction to MS and discuss novel therapeutic strategies targeting mitochondria-related pathways as well as emerging experimental approaches for modeling mitochondrial disease.

KEYWORDS:

mitochondria; multiple sclerosis; oligodendrocytes; therapy

PMID:
28069137
DOI:
10.1016/bs.ircmb.2016.08.003
[Indexed for MEDLINE]

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