Gnanapavan S, Ho P, Heywood W, Jackson S, Grant D, Rantell K, Keir G, Mills K, Steinman L, Giovannoni G.Progression in multiple sclerosis is associated with low endogenous NCAM. J Neurochem. 2013 Mar 15. doi: 10.1111/jnc.12236. [Epub ahead of print]
Multiple sclerosis (MS) is a central nervous system (CNS) disorder characterised 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 studies in 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.
This study shows that following demyelination in a test tube in animals and progressive MS there is a loss of neural cell adhesion molecule in culture, the CNS tissues or CSF in MS. There is noticeable a loss of this molecule when RRMSers develop SPMS. This molecule is associated with nerve outgrowth as nerves are lost the levels of NCAM drop. Is this causal to the disease process or part of the consequence of the disease process but the less NCAM there is in the CSF the more likely the MSer is to have more disability. We will have to wait until further studies are reported.
CoI: This is work from Team G and was part of the Promise2010 initative