Filtered By:
Cancer: Brain Cancers
Drug: Enbrel

This page shows you your search results in order of date.

Order by Relevance | Date

Total 12 results found since Jan 2013.

Rapid improvement in severe long COVID following perispinal etanercept
CONCLUSION: Perispinal etanercept is a promising treatment for the chronic neurologic dysfunction that may persist after resolution of acute COVID-19, including chronic cognitive dysfunction, fatigue, and depression. These results suggest that long COVID brain neuroinflammation is a potentially reversible pathology and viable treatment target. In view of the increasing unmet medical need, clinical trials of perispinal etanercept for long COVID are urgently necessary. The robust results of the present case suggest that perispinal etanercept clinical trials studying long COVID populations with severe fatigue, depression and ...
Source: Current Medical Research and Opinion - July 6, 2022 Category: Research Authors: Edward Tobinick Robert N Spengler Tracey A Ignatowski Manar Wassel Samantha Laborde Source Type: research

Effect of Inflammation on the Process of Stroke Rehabilitation and Poststroke Depression
Conclusions Stroke comprises ischemic stroke and ICH. The immuno-inflammatory process is involved in neural plasticity following events such as a hemorrhage or ischemic stroke. After ischemia, astrocytes, microglia, and MDMs play important roles during rehabilitation with the modulation of cytokines or chemokines, such as TNF-α and IL-1. Moreover, MiRNAs are also important posttranscriptional regulators in these glial mitochondrial responses to cerebral ischemia. ICH involves processes similar and different to those seen in ischemia, including neuronal injury, astrocytic and microglial/macrophage activation, and n...
Source: Frontiers in Psychiatry - April 10, 2019 Category: Psychiatry Source Type: research

Therapeutically Targeting Tumor Necrosis Factor-{alpha}/Sphingosine-1-Phosphate Signaling Corrects Myogenic Reactivity in Subarachnoid Hemorrhage Basic Sciences
Conclusions— Vascular smooth muscle cell TNFα and sphingosine-1-phosphate signaling significantly enhance cerebral artery tone in SAH; anti-TNFα and anti–sphingosine-1-phosphate treatment may significantly improve clinical outcome.
Source: Stroke - July 27, 2015 Category: Neurology Authors: Yagi, K., Lidington, D., Wan, H., Fares, J. C., Meissner, A., Sumiyoshi, M., Ai, J., Foltz, W. D., Nedospasov, S. A., Offermanns, S., Nagahiro, S., Macdonald, R. L., Bolz, S.-S. Tags: Animal models of human disease, Acute Cerebral Hemorrhage, Brain Circulation and Metabolism, Other Stroke Treatment - Medical, Other Vascular biology Basic Sciences Source Type: research

Chronic Elevation of Tumor Necrosis Factor-{alpha} Mediates the Impairment of Leptomeningeal Arteriogenesis in db/db Mice Basic Sciences
Conclusions— These results indicate that leptomeningeal arteriogenesis is impaired in db/db mice and that suppression of the tumor necrosis factor-α response to hypoperfusion is the major contributing factor.
Source: Stroke - May 22, 2015 Category: Neurology Authors: Yukami, T., Yagita, Y., Sugiyama, Y., Oyama, N., Watanabe, A., Sasaki, T., Sakaguchi, M., Mochizuki, H., Kitagawa, K. Tags: Cerebrovascular disease/stroke, Type 2 diabetes, Other Vascular biology Basic Sciences Source Type: research

Systemically administered anti-TNF therapy ameliorates functional outcomes after focal cerebral ischemia
Conclusions: Our data suggest that XPro1595 and etanercept improve functional outcome after focal cerebral ischemia by altering the peripheral immune response, changing blood and spleen cell populations and decreasing granulocyte infiltration into the brain. Blocking solTNF, using XPro1595, was just as efficient as blocking both solTNF and tmTNF using etanercept. Our findings may have implications for future treatments with anti-TNF drugs in TNF-dependent diseases.
Source: Journal of Neuroinflammation - December 12, 2014 Category: Neurology Authors: Bettina ClausenMatilda DegnNellie MartinYvonne CouchLeena KarimiMaria OrmhøjMaria-Louise MortensenHanne GredalChris GardinerIan SargentDavid SzymkowskiGéraldine PetitTomas DeierborgBente FinsenDaniel AnthonyKate Lambertsen Source Type: research

Tumor necrosis factor-{alpha} inhibition attenuates middle cerebral artery remodeling but increases cerebral ischemic damage in hypertensive rats
Hypertension causes vascular inflammation evidenced by an increase in perivascular macrophages and proinflammatory cytokines in the arterial wall. Perivascular macrophage depletion reduced tumor necrosis factor (TNF)-α expression in cerebral arteries of hypertensive rats and attenuated inward remodeling, suggesting that TNF-α might play a role in the remodeling process. We hypothesized that TNF-α inhibition would improve middle cerebral artery (MCA) structure and reduce damage after cerebral ischemia in hypertensive rats. Six-week-old male stroke-prone spontaneously hypertensive rats (SHRSP) were treated ...
Source: AJP: Heart and Circulatory Physiology - September 1, 2014 Category: Cardiology Authors: Pires, P. W., Girgla, S. S., Moreno, G., McClain, J. L., Dorrance, A. M. Tags: VASCULAR BIOLOGY AND MICROCIRCULATION Source Type: research

Tumor necrosis factor-alpha inhibition attenuates middle cerebral artery remodeling but increases cerebral ischemic damage in hypertensive rats.
Abstract Hypertension causes vascular inflammation evidenced by an increase in perivascular macrophages and proinflammatory cytokines in the arterial wall. Perivascular macrophages depletion reduced tumor necrosis factor (TNF)-α expression in cerebral arteries of hypertensive rats and attenuated inward remodeling, suggesting that TNF-α might play a role in the remodeling process. We hypothesized that TNF-α inhibition would improve middle cerebral artery (MCA) structure and reduce damage after cerebral ischemia in hypertensive rats. Six-week-old male stroke-prone spontaneously hypertensive rats (SHRSP) were trea...
Source: American Journal of Physiology. Heart and Circulatory Physiology - July 11, 2014 Category: Physiology Authors: Pires PW, Girgla SS, Moreno G, McClain JL, Dorrance AM Tags: Am J Physiol Heart Circ Physiol Source Type: research