The identification of peptides of albumin and serotransferrin stands out in the tables of the differentially abundant peptides and proteins. While the identifications are essentially correct it must be noted that only 2.4% of the identified albumin peptides and 4.8% of the identified serotransferrin peptides had p-values below 0.01, which means that the values for the peptides of these two particular proteins are most likely due to other reasons than large abundance differences in these two proteins. In comparison, most of the other differentially abundant proteins that we identified were found by a small number of peptides with a low p-value or a single peptide with a low p-value. For these proteins we did not observe any other peptides with non-significant p-values, with the exception of bromodomain adjacent to zinc finger domain protein 1A and Rho GTPase-activating protein 18-like. For both of these proteins another peptide was identified with high p-value, indicating these proteins were likely not differentially abundant. The peptides with low p-values of these proteins were also characterized by a low fold increase, making them less interesting for independent immunoassay follow-up. Because of the healthy state of the CSF control group, no intrathecal inflammatory response was to be expected in this group. Therefore the very clear difference in immunoglobulin abundance in the comparison with the both MScl disease types can be explained. In the two comparisons of both MScl types with the control group, several proteins are present in both comparisons, for example Ig gamma-1 chain C region and apolipoprotein D. Apolipoproteins have been previously implicated in MScl. Proteomics studies have shown apolipoprotein E abundances to be elevated in CSF of MScl patients compared to controls [9, 12] . In the central nervous system apolipoprotein D is a lipocalin that is mainly expressed in glia, but also in neurons. This protein has been repeatedly implicated in MScl, and it has been shown that it has a neuroprotective effect in a number of neurodegenerative diseases by controlling the level of peroxidated lipids, which coincides with glial activation in mouse models of encephalitis [39] . A previous proteomics study showed increased levels of apolipoprotein D in patients with a clinically isolated syndrome of demyelination, indicating that abundance levels of this protein are highest in MScl patients at the time of their first exacerbation [10, 17] . Another potentially interesting protein found to be differentially elevated in the comparisons of both MScl types with the controls is ryanodine receptor 1. This receptor is involved in the maintenance of the calcium-equilibrium in brain tissue. The release of toxic levels of positively charged calcium ions may, due to the deleterious effects of excitotoxicity, represent a key mechanism of axonal degeneration in disorders such as MScl [40] .