Monday, 14 March 2016

Natalizumab reduces damage

Wiebenga OT, Schoonheim MM, Hulst HE, Nagtegaal GJ, Strijbis EM, Steenwijk MD, Polman CH, Pouwels PJ, Barkhof F, Geurts JJ. White Matter Diffusion Changes during the First Year of Natalizumab Treatment in Relapsing-Remitting Multiple Sclerosis. AJNR Am J Neuroradiol. 2016 Mar 10. [Epub ahead of print]

BACKGROUND AND PURPOSE:Natalizumab treatment strongly affects relapsing-remitting multiple sclerosis, possibly by restraining white matter damage. This study investigated changes in white matter diffusivity in patients with relapsing-remitting multiple sclerosis during their first year of natalizumab treatment by using diffusion tensor imaging.
MATERIALS AND METHODS:The study included patients with relapsing-remitting multiple sclerosis initiating natalizumab at baseline (n = 22), patients with relapsing-remitting multiple sclerosis continuing interferon-β or glatiramer acetate (n = 17), and healthy controls (n = 12). Diffusion tensor imaging parameters were analyzed at baseline and month 12. We measured the extent and severity of white matter damage with diffusion tensor imaging parameters such as fractional anisotropy, comparing the patient groups with healthy controls at both time points.
RESULTS:The extent and severity of white matter damage were reduced significantly in the natalizumab group with time (fractional anisotropy-based extent, 56.8% to 47.2%; severity, z = -0.67 to -0.59; P = .02); this reduction was not observed in the interferon-β/glatiramer acetate group (extent, 41.4% to 39.1%, and severity, z = -0.64 to -0.67; P = .94). Cognitive performance did not change with time in the patient groups but did correlate with the severity of damage (r = 0.53, P = < .001).
CONCLUSIONS: In patients with relapsing-remitting multiple sclerosis starting natalizumab treatment, the extent and severity of white matter damage were reduced significantly in the first year of treatment. These findings may aid in explaining the large observed clinical effect of natalizumab in relapsing-remitting multiple sclerosis.


These findings may aid in explaining the large observed clinical effect of natalizumab in relapsing-remitting multiple sclerosis. Yep you are saying Duh (NSS) at the moment. 

We have been told that Natalizumab is a highly effective agent and the CRAB drugs are not. Don't believe it?. 

Look in a scanner and you can see changes and they are more reduced with Tysabri. 

Cognitive performance correlated (r=0.5 = in my humble opinion is a pants correlation as it does not allow you to predict anything for the individual) with severity of damage.

2 comments:

  1. I posted today a comment /question placed under the blog post published 26th febr 2016:

    http://multiple-sclerosis-research.blogspot.com/2016/02/researchspeak-reply-to-email-from.html

    But since I am not sure if this comment will be published or addresssed, since post is a couple of weeks old, I publish it here on todays blog post, in relation to subject Brain Atrophy and neuroprotection:


    So then, I have a question about Brain Atrophy and atrophy in NABT (Normal appearing Brain Tissue):


    BACKGROUND:
    I read the following article about laquinimod and neurodegeneration:

    "Placebo-controlled trial of oral laquinimod in multiple sclerosis: MRI evidence of an effect on brain tissue damage."


    Source:
    http://www.ncbi.nlm.nih.gov/pubmed/24029546

    I also read som other articles on the subject connected to this agent laquinimod, which also support laquinimods ability to prevent neurodegeneration.

    QUESTION to MD or PROFESSOR Gavin, as a follow up on your nice post about laquinimod above.

    So, I was obvioulsy positively triggered by the above post about laquinimod and reflections from Professor Gavin about this agents prospects in Brain Atrophy / neuroprotection.

    So given that, I tried to learn a little bit more about published results about laquinimod in neuroprotection and its ability to prevent brain atrophy and neurodegeneration

    Now, according to the article that I refer to above, this experimental agent laquinimod was able to significantly inhibit the number of permanent black holes (PBH= irreversible neuro damage)compare to placebo. That is very good.

    BUT ... there is one thing which I need a´better insight to - i.e. I don´t fully understand the meaning or purpose about one specific MRI measure, which puzzels me.

    It is about that laquinimods prevents neurodegeneration in NABT (normal-appearing Brain Tissue) from baseline to month 24 (p-value 0.015). In fact the NABT tissue seem to significantly increase in laquinimod patients, as oposed to placebo, where the NABT tissue in fact decreased.

    SO HERE IS MY QUESTION:
    But NABT is tissue without lesions, in essence the tissue is not damaged. I interpret NABT as healthy tissues. And here I am lost.

    What is the use / purpose (sorry if I don´t understand) that laquinimod seem to increase the NABT tissue, while at the the same time drecreased in placebo Group, since this tissue is healthy and not damaged by lesions ?

    ReplyDelete
  2. Whilst reading this this morning - I discovered a relationship between amount of breakfast cereal consumed and fullness.

    ReplyDelete

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