ALS Lou Gehrig and Inflammation

Dr. Weeks’ Comment: Like all chronic degenerative illnesses – especially those which manifest in the neurological system – lowering inflammation is the goal.

“…Patients with sporadic amyotrophic lateral sclerosis (sALS) show inflammation in the spinal cord and peripheral blood…”

In ALS (Lou Gehrig’s disease), we see that the treatment is always one sort of anti-inflammatory agent or another. The problem is that all the anti-inflammatory drugs used by neurologists offer benefits but also deliver toxic side-effects. Prednisone (suppresses the immune system), tylenol (liver toxocity), NSAIDS (heart attack risk and renal failure) Aspirin (bleeding out from GI ulcers) all are used and in this study, a new anti-inflammatory agent Tocilizamab is so dangerous that 100’s of people are said to have died from it

Actemra (known generically as tocilizumab), a rheumatoid arthritis (RA) medication, may be associated with life-threatening side effects and may have caused hundreds of deaths, according to a new investigation published in STAT that has called Actemra’s safety into question.”

So if you or someone you love suffers from ALS, choose the safest and most powerful anti-inflammatory remedy – a 3-seed drink made from the worlds most anti-inflammatory organic and non-GMO seeds: black cumin, raspberry and Chardonnay grape.

Am J Neurodegener Dis. 2013; 2(2): 129–139. Published online 2013 Jun 21. PMCID: PMC3703125PMID: 23844337

Tocilizumab infusion therapy normalizes inflammation in sporadic ALS patients

Milan Fiala,1Mathew T Mizwicki,1Rachel Weitzman,1Larry Magpantay,2 and  Norihiro Nishimoto3Author informationArticle notesCopyright and License informationDisclaimer

Patients with sporadic amyotrophic lateral sclerosis (sALS) show inflammation in the spinal cord and peripheral blood. The inflammation is driven by stimulation of macrophages by aggregated superoxide dismutase 1 (SOD1) through caspase1, interleukin 1 (IL1), IL6 and chemokine signaling. Inflammatory gene activation is inhibited in vitro by tocilizumab, a humanized antibody to IL6 receptor (IL6R). Tocilizumab inhibits global interleukin-6 (IL6) signaling, a key mechanism in chronic rheumatoid disorders. Here we studied in vivo baseline inflammatory gene transcription in peripheral blood mononuclear cells (PBMCs) of 10 sALS patients, and the effects of tocilizumab (ActemraR) infusions. At baseline, one half of ALS subjects had strong inflammatory activation (Group 1) (8 genes up regulated >4-fold, P<0.05 vs. controls) and the other half (Group 2) had weak activation. All patients showed greater than four-fold up regulation of MMP1, CCL7, CCL13 and CCL24. Tocilizumab infusions in the Group 1 patients resulted in down regulation of inflammatory genes (in particular IL1β), whereas in the Group 2 patients in up regulation of inflammatory genes. Post-infusion serum and CSF concentrations of tocilizumab inhibited caspase1 activation in vitro. Three of 5 patients receiving tocilizumab infusions showed time-limited attenuation of clinical progression. In conclusion, inflammation of sALS patients at baseline is up- or down-regulated in comparison to controls, but is partially normalized by tocilizumab infusions.

This article has been cited by other articles in PMC.

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