is supposedly treating using his proprietary method of injecting etanercept. Dr. Tobinick could have solved this TNF question years ago if he had only actually run clinical tests on etanercept.
Abstract
Tumor
necrosis factor-α (TNF-α) is one of the key players in stroke
progression and can interfere with brain functioning. We previously
documented an impairment of experience-dependent plasticity in the
cortex neighboring the stroke-induced lesion, which was accompanied with
an upregulation of Tnf-α level in the brain of ischemic mice 1 week
after the stroke. Because TNF receptor 1 (TnfR1) signaling is believed
to be a major mediator of the cytotoxicity of Tnf-α through activation
of caspases, we used an anti-inflammatory intervention aimed at Tnf-α R1
pathway, in order to try to attenuate the detrimental effect of
post-stroke inflammation, and investigated if this will be effective in
protecting plasticity in the infarct proximity. Aged mice (12–14 months)
were subjected to the photothrombotic stroke localized near
somatosensory cortex, and immediately after ischemia sensory deprivation
was introduced to induce plasticity. Soluble TNF-α R1 (sTNF-α R1),
which competed for TNF-α with receptors localized in the brain, was
delivered chronically directly into the brain tissue for the whole
period of deprivation using ALZET Micro-Osmotic pumps. We have shown
that such approach undertaken simultaneously with the stroke reduced the
level of TNF-α in the peri-ischemic tissue and was successful in
preserving the post-stroke deprivation-induced brain plasticity.
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