Tysabri treatment blocks nerve loss and atrophy.

#MSResearch #MSblog Proof that relapses are not good for you so we need to stop them.

Epub: Kuhle et al. Neurofilament light and heavy subunits compared as therapeutic biomarkers in multiple sclerosis.Acta Neurol Scand. 2013 Jun 13. 

BACKGROUND: Neurofilaments are promising biomarkers in multiple sclerosis (MS) and increased levels in cerebrospinal fluid (CSF) indicate axonal damage or degeneration. In a previous study, neurofilament light chain (NfL) levels in CSF of relapsing remitting (RR) patients with MS were normalized by natalizumab treatment.


AIMS OF THE STUDY: We compared the coherence between NfL and neurofilament heavy chain (NfHSMI 35 ) levels in longitudinal CSF samples in a subset of these patients.

METHODS: In 30 patients with RRMS, CSF was obtained prior to and following 12 months of natalizumab treatment. 


RESULTS: NfHSMI 35 decreased in 73.3% and NfL in 90% of the MSers following natalizumab treatment (32.4 vs 27.4 pg/ml, P = 0.002 and 820 vs 375 pg/ml, P < 0.0001). MSers experiencing a relapse showed higher NfHSMI 35 levels compared with MSers in remission (47.7 vs 27.6 pg/ml, n = 8, P = 0.001). This difference was less obvious for NfL (1055 vs 725 pg/ml, P = 0.256). In patients in remission, NfL levels were lower following natalizumab treatment (830 vs 365 pg/ml, n = 20, P = 0.0002), whereas the same comparison failed significance for NfHSMI 35 (28.3 vs 26.9 pg/ml, P = 0.086).
 
CONCLUSIONS: We confirm previous findings, indicating reduced axonal damage under natalizumab treatment by measuring NfHSMI 35 , using an assay with independent methodology. In comparison with NfHSMI 35 , NfL changes were more pronounced and the treatment effect also included patients in remission. Our results suggest that NfL is superior over NfHSMI 35 as therapeutic biomarker and is a promising candidate to measure neuroaxonal damage in MS treatment trials.



Neurofilament are not just promising biomarkers, they ARE biomarkers. I can't wait for the lamotrigine trial data to come out....It didn't work I hear you say....there is more in the story to come, but that's for another day.

As we and Prof G have been saying for sometime now, inflammatory responses in your brains are not a good thing. 


Treating early and aggressively with highly active DMT will be beneficial. This is yet further clear evidence for this concept and only an ostrich should not be able to see this. On balance allowing an immune response into the brain, which is what Tysabri stops, is not beneficial. Having relapses are damaging just as was told from EAE studies.

When nerves are damaged they release their content and this can be measured by looking for nerve structural proteins (Neurofilaments) in the brain fluid and sometimes in the blood. High levels in brain fluid imply that there is brain damage going on. This study repeats earlier studies published in Aanals of Neurology that clearly show that Tysabri treatment slows nerve loss. Therefore the blocking lesion formation and relapse is clearly a good thing and to deny this is simply ignoring the data. 

There are different forms of neurofilament (SMI35 is the name of the antibody which detects heavy chain, SMI32 detects a phosphorylation variant which is found in unhealth nerves) which are structural proteins. The smaller one (Neurofilament Light) is better as a predictory of nerve damage. We know this already, but yet more evidence that use of measuring neurofilament levels in trials is a good thing.

So when some of you, in denial, say DMT are a waste of time...think again! We need to get people on highly active DMT and "Say no to brain shred".

CoI: Team G were involved in this study.

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