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J Neuroimmunol. 2014 Dec 15;277(1-2):176-85. doi: 10.1016/j.jneuroim.2014.10.010. Epub 2014 Oct 30.

A role for Apolipoprotein A-I in the pathogenesis of multiple sclerosis.

Author information

1
Research Service VAMC, Memphis, TN 38104, United States.
2
Research Service VAMC, Memphis, TN 38104, United States; Department of Neurology, University of Tennessee Health Science Center, Memphis, TN 38163, United States.
3
Research Service VAMC, Memphis, TN 38104, United States; Department of Neurology, University of Tennessee Health Science Center, Memphis, TN 38163, United States. Electronic address: lgardne5@uthsc.edu.

Abstract

Apolipoprotein A1 (Apo A-I), the most abundant component of high-density lipoprotein (HDL), is an anti-inflammatory molecule, yet its potential role in the pathogenesis of multiple sclerosis (MS) has not been fully investigated. In this study, Western blot analyses of human plasma showed differential Apo A-I expression in healthy controls compared to MS patients. Further, primary progressive MS patients had less plasma Apo A-I than other forms of MS. Using experimental allergic encephalomyelitis (EAE) as a model for MS, Apo A-I deficient mice exhibited worse clinical disease and more neurodegeneration concurrent with increased levels of pro-inflammatory cytokines compared to wild-type animals. These data suggest that Apo A-I plays a role in the pathogenesis of EAE, a model for MS, creating the possibility for agents that increase Apo A-I levels as potential therapies for MS.

KEYWORDS:

Apolipoprotein A-I; EAE; Multiple sclerosis; Neurological disease

PMID:
25468275
DOI:
10.1016/j.jneuroim.2014.10.010
[Indexed for MEDLINE]

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