Progression in multiple sclerosis is associated with low endogenous NCAM

被引:14
作者
Gnanapavan, Sharmilee [1 ,2 ]
Ho, Peggy [3 ]
Heywood, Wendy [4 ]
Jackson, Sam [2 ]
Grant, Donna [1 ]
Rantell, Khadija [5 ]
Keir, Geoff [1 ]
Mills, Kevin [4 ]
Steinman, Lawrence [3 ]
Giovannoni, Gavin [2 ]
机构
[1] Inst Neurol, Dept Neuroimmunol, London WC1N 3NG, England
[2] Queen Mary Univ London, Barts & London Sch Med & Dent, Blizard Inst Cell & Mol Sci, London, England
[3] Stanford Univ, Sch Med, Dept Neurol & Neurol Sci, Stanford, CA 94305 USA
[4] Inst Child Hlth, Clin & Mol Genet Unit, Biochem Grp, London, England
[5] Inst Neurol, London WC1N 3NG, England
关键词
EAE; mass spectrometry; multiple sclerosis; NCAM; neuroplasticity; CELL-ADHESION MOLECULE; CENTRAL-NERVOUS-SYSTEM; N-CAM; SYNAPTIC PLASTICITY; CEREBROSPINAL-FLUID; MICE; REMYELINATION; BRAIN; DEFICIENT; DEFECTS;
D O I
10.1111/jnc.12236
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Multiple sclerosis (MS) is a CNS disorder characterized by demyelination and neurodegeneration. Although hallmarks of recovery (remyelination and repair) have been documented in early MS, the regenerative capacity of the adult CNS per se remains uncertain with the wide held belief that it is either limited or non-existent. The neural cell adhesion molecule (NCAM) is a cell adhesion molecule that has been widely implicated in axonal outgrowth, guidance and fasciculation. Here, we used in vitro and in vivo of MS to investigate the role of NCAM in disease progression. We show that in health NCAM levels decrease over time, but this occurs acutely after demyelination and remains reduced in chronic disease. Our findings suggest that depletion of NCAM is one of the factors associated with or possibly responsible for disease progression in MS.
引用
收藏
页码:766 / 773
页数:8
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