Plasma neurofilament light chain levels in patients with MS switching from injectable therapies to fingolimod
Fredrik Piehl, Ingrid Kockum, Mohsen Khademi, Kaj Blennow, Jan Lycke, Henrik Zetterberg, Tomas Olsson
Multiple Sclerosis Journal, First Published 19 Jun 2017.doi: 10.1177/1352458517715132
Neurofilament light chain (NFL) is a cerebrospinal fluid (CSF) marker of neuroaxonal damage in multiple sclerosis (MS).
To determine the correlation of NFL in CSF and serum/plasma, and in plasma after switching from injectable MS therapies to fingolimod.
A first cohort consisted of MS patients (n = 39) and neurological disease controls (n = 27) where CSF and plasma/serum had been collected for diagnostic purposes. A second cohort (n = 243) consisted of patients from a post-marketing study of fingolimod. NFL was determined with Single Molecule Array (Simoa™) technology (detection threshold 1.95 pg/mL).
Mean NFL pg/mL (standard deviation (SD)) was 341 (267) and 1475 (2358) in CSF and 8.2 (3.58) and 17.0 (16.94) in serum from controls and MS, respectively. CSF/serum and plasma/serum levels were highly correlated (n = 66, rho = 0.672, p < 0.0001 and n = 16, rho = 0.684, p = 0.009, respectively). In patients starting fingolimod (n = 243), mean NFL pg/mL (SD) in plasma was reduced between baseline (20.4 (10.7)) and at 12 months (13.5 (7.3), p < 3 × 10−6), and levels remained stable at 24 months (13.2 (6.2)).
NFL in serum and CSF are highly correlated and plasma NFL levels decrease after switching to highly effective MS therapy. Blood NFL measurement can be considered as a biomarker for MS therapy response.
Yesterday, I spoke at the European Academy of Neurology (EAN) Congress 2017 in Amsterdam about the utility of neurofilament analysis in neurological disorders. My point was to get across to the audience that neurofilaments as a biomarker was here to stay, but also to make it known that as far as MS management is concerned the goal post is shifting. We are looking to a future in which long-term remission (tantamount to a cure) is achievable, and not simply a woefully inadequate hype that recedes at the end of a conference. So how do the current biological fare in slowing down nerve loss?
There are a lot of archived samples sitting in freezers around the world from clinical trials, now may be the time to start analysing them…I say London is open!