Tumor necrosis factor alpha antagonism improves neurological recovery in murine intracerebral hemorrhage

August 20, 2013:

A new basic science study from a research group at Duke provides new evidence supporting the rationale of TNF Inhibition following certain forms of stroke. The scientific rationale was discussed more than a decade earlier by Edward Tobinick in U.S. patent 6,419,934, filed September 5, 2000. On August 20, 2013, in the Journal of Neuroinflammation, the study authors  wrote: “Antagonism of pro-inflammatory cytokines by specific antibodies represents a compelling therapeutic strategy to improve neurological outcome in patients after ICH“. (Lei, B., et al., Tumor necrosis factor alpha antagonism improves neurological recovery in murine intracerebral hemorrhage. J Neuroinflammation, 2013. 10(1): p. 103). The background and conclusions of the abstract follow: Background: Intracerebral hemorrhage (ICH) is a devastating stroke subtype characterized by a prominent neuroinflammatory response. Antagonism of pro-inflammatory cytokines by specific antibodies represents a compelling therapeutic strategy to improve neurological outcome in patients after ICH. To test this hypothesis, the tumor necrosis factor alpha (TNF-alpha) antibody CNTO5048 was administered to mice after ICH induction, and histological and functional endpoints were assessed. Conclusions: Post-injury treatment with the TNF-alpha antibody CNTO5048 results in less neuroinflammation and improved functional outcomes in a murine model of ICH. See also: (Tobinick, E., Rapid improvement of chronic stroke deficits after perispinal etanercept: three consecutive cases. CNS Drugs, 2011. 25(2): p. 145-55; and Tobinick, E., et al., Selective TNF Inhibition for Chronic Stroke and Traumatic Brain Injury : An Observational Study Involving 629 Consecutive Patients Treated with Perispinal Etanercept. CNS Drugs, 2012. 26(12): p. 1051-70. Results can vary. Please see the Terms of Use.