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Although hallmarks of recovery (remyelination and repair) have been documented in early <jats:styled-content style=\"fixed-case\">MS<\/jats:styled-content>, the regenerative capacity of the adult <jats:styled-content style=\"fixed-case\">CNS<\/jats:styled-content> per se remains uncertain with the wide held belief that it is either limited or non\u2010existent. The neural cell adhesion molecule (<jats:styled-content style=\"fixed-case\">NCAM<\/jats:styled-content>) is a cell adhesion molecule that has been widely implicated in axonal outgrowth, guidance and fasciculation. Here, we used <jats:italic>in vitro<\/jats:italic> and <jats:italic>in vivo<\/jats:italic> of <jats:styled-content style=\"fixed-case\">MS<\/jats:styled-content> to investigate the role of <jats:styled-content style=\"fixed-case\">NCAM<\/jats:styled-content> in disease progression. We show that in health <jats:styled-content style=\"fixed-case\">NCAM<\/jats:styled-content> levels decrease over time, but this occurs acutely after demyelination and remains reduced in chronic disease. Our findings suggest that depletion of <jats:styled-content style=\"fixed-case\">NCAM<\/jats:styled-content> is one of the factors associated with or possibly responsible for disease progression in <jats:styled-content style=\"fixed-case\">MS<\/jats:styled-content>.<\/jats:p>","DOI":"10.1111\/jnc.12236","type":"journal-article","created":{"date-parts":[[2013,3,16]],"date-time":"2013-03-16T03:56:22Z","timestamp":1363406182000},"page":"766-773","source":"Crossref","is-referenced-by-count":16,"title":["Progression in multiple sclerosis is associated with low endogenous <scp>NCAM<\/scp>"],"prefix":"10.1111","volume":"125","author":[{"given":"Sharmilee","family":"Gnanapavan","sequence":"first","affiliation":[{"name":"Department of Neuroimmunology Institute of Neurology London UK"},{"name":"Blizard Institute of Cell and Molecular Science Barts and The London School of Medicine and Dentistry Queen Mary University of London London 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