Mediation of Lipocalin-2 Suggests Therapeutic Target in Progressive MS

Combined results of these studies also confirmed that intrathecal LCN2 production was increased in MS patients, and to a greater degree in patients with SPMS and PPMS compared with RRMS (P < 0.005), although the difference between groups was not statistically significant. Levels of LCN2 in brain microdialysates were as many as 13 to 853 times higher than in the CSF, indicating the addition of local LCN2 production contributing to progressive forms of MS.

These findings, combined with evidence from earlier mouse models of induced experimental autoimmune encephalomyelitis (EAE), suggested that LCN2 is a potential therapeutic target in MS. Increased LCN2 in plasma and CSF in mice correlated with increased disease severity through potential mechanisms of enhancing T cell production and demyelination.

“There is an urgent need to identify biomarkers of pathophysiology that can increase our knowledge and possibly lead to the identification of new therapeutic targets,” the authors wrote. They suggested that while LCN2 levels many not offer a suitable biomarker for clinical diagnosis and prognosis, the correlation between LCN2 increase and NFL in SPMS and PPMS indicates a functional role in progressive forms of MS.

Reference

Al Nimer, F, Elliott C, Bergman J, et al. Lipocalin-2 is increased in progressive multiple sclerosis and inhibits remyelination. Neurol Neuroimmunol Neuroinflamm. 2016;3:e191.