Trial in Remyelination is safe in humans

You want to hear about remyelination trials and here is one. The idea that there are naturally occurring antibodies that promote remyelination was suggested by the group of Moses Rodriguez at the Mayo clinic many, many years ago. 
They then generated an oligodendrocyte/myelin-specific recombinant human monoclonal IgM, rHIgM22. Apparently the antibody is well-endowed with strong anti-apoptotic and pro-proliferative effects on oligodendrocytes.

So this study says it is safe in humans
However, I must admit that I find the whole approach very weird. 
We know that to promote remyelination that the treatment has to enter the brain and bind the oligodendrocytes.
In the Lingo-1 studies they injected massive amounts of antibody such as up to 100mg/kg, which was was about 99.9% excluded from the target. But that tiny percent apparently did something. 
In this current study they used 50 to 100th less antibody and amazing 99.997%  was excluded although this increased to about 99.95 at 1mg/kg and 99.5 at 2mg/kg so again most of what injected went no where useful.
Surely the starting point needs to develop agents that get into the brain.  Maybe I'm just being thick again.

However, I guess other people think differently

Eisen A, Greenberg BM, Bowen JD, Arnold DL, Caggiano AO. A double-blind, placebo-controlled, single ascending-dose study of remyelinating antibody rHIgM22 in people with multiple sclerosis. Mult Scler J Exp Transl Clin. 2017 Nov 21;3(4):2055217317743097.

OBJECTIVE:The objective of this paper is to assess, in individuals with clinically stable multiple sclerosis (MS), the safety, tolerability, pharmacokinetics (PK) and exploratory pharmacodynamics of the monoclonal recombinant human antibody IgM22 (rHIgM22).
METHODS:Seventy-two adults with stable MS were enrolled in a double-blind, randomized, placebo-controlled, single ascending-dose, Phase 1 trial examining rHIgM22 from 0.025 to 2.0 mg/kg. Assessments included MRI, MR spectroscopy, plasma PK, and changes in clinical status, laboratory values and adverse events for three months. The final cohort had additional clinical, ophthalmologic, CSF collection and exploratory biomarker evaluations. Participants were monitored for six months.
RESULTS: rHIgM22 was well tolerated with no clinically significant safety signals. Non-compartmental PK modeling demonstrated linear dose-proportionality both of Cmax and AUC0-Last. The steady-state apparent volume of distribution of approximately 58 ml/kg suggested primarily vascular compartmentalization. CSF:plasma rHIgM22 concentration increased from 0.003% on Day 2 for both 1.0 and 2.0 mg/kg to 0.056% and 0.586% for 1.0 and 2.0 mg/kg, respectively, on Day 29. No statistically significant treatment-related changes were observed in exploratory pharmacodynamic outcome measures included for the 21 participants of the extension cohort.
CONCLUSIONS: Single doses of rHIgM22 were well tolerated and exhibited linear PK, and antibody was detected in the CSF.