期刊
MITOCHONDRION
卷 12, 期 2, 页码 173-179出版社
ELSEVIER SCI LTD
DOI: 10.1016/j.mito.2011.03.007
关键词
Mitochondria; Multiple sclerosis; Demyelination; Axonal degeneration
资金
- Wellcome Trust
- Multiple Sclerosis Society (UK)
- Newcastle Healthcare Charity and Newcastle upon Tyne Hospitals NHS Charity
The loss of myelin sheath (demyelination) renders axons vulnerable to a variety of insults. Axonal degeneration is well recognised in inflammatory demyelinating disorders of the central nervous system (CNS) such as multiple sclerosis (MS) and also certain neurodegenerative diseases. Energy required for nerve impulse conduction and maintenance of structural integrity of axons is met by mitochondria. Based on the distribution of ion channels and the Na+/K+ ATPase, the energy requirements of demyelinated and dysmyelinated axons are likely to differ from myelinated axons. In this review we discuss the changes in mitochondrial presence within axons in relation to presence or absence of healthy myelin sheaths and propose the increase in mitochondrial presence following demyelination as an adaptive process. An energy deficit within demyelinated axons is likely to be more detrimental compared to myelinated axons, judging by the neuropathological findings in primary mitochondrial disorders due to mitochondrial and nuclear DNA mutations and the mitochondrial changes that follow demyelination. Agents that enhance and protect mitochondria, as potential therapy, need to be considered and investigated in earnest for demyelinating disorders of the CNS such as MS. (C) 2011 Elsevier B.V. and Mitochondria Research Society. All rights reserved.
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