4.4 Article Proceedings Paper

Mechanisms of neuronal damage in multiple sclerosis and its animal models: role of calcium pumps and exchangers

期刊

BIOCHEMICAL SOCIETY TRANSACTIONS
卷 35, 期 -, 页码 923-926

出版社

PORTLAND PRESS LTD
DOI: 10.1042/BST0350923

关键词

calcium dyshomoeostasis; experimental autoimmune encephalomyelitis; multiple sclerosis; neurodegeneration; plasma-membrane Ca2+-ATPase (PMCA)

资金

  1. NINDS NIH HHS [R01 NS046363, F31 NS054336] Funding Source: Medline

向作者/读者索取更多资源

Multiple sclerosis is an inflammatory, demyelinating and neurodegenerative disorder of the central nervous system. Increasing evidence indicates that neuronal pathology and axonal injury are early hallmarks of multiple sclerosis and are major contributors to progressive and permanent disability. Yet, the mechanisms underlying neuronal dysfunction and damage are not well defined. Elucidation of such mechanisms is of critical importance for the development of therapeutic strategies that will prevent neurodegeneration and confer neuroprotection. PMCA2 (plasma-membrane Ca2+-ATPase 2) and the NCX (Na+/Ca2+ exchanger) have been implicated in impairment of axonal and neuronal function in multiple sclerosis and its animal models. As PMCA2 and NCX play critical roles in calcium extrusion in cells, alterations in their expression or activity may affect calcium homoeostasis and thereby induce intracellular injury mechanisms. Interventions that restore normal PMCA2 and NCX activity may prevent or slow disease progression by averting neurodegeneration.

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