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• W2029997013 endingPage "PD4.001" @default.
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• W2029997013 abstract "Objective: Parkinson9s disease (PD) is the second most common neurodegenerative disorder. No effective therapy is available to stop its onset or halt its progression. The present study evaluates the ability of RNS60, produced by Revalesio9s novel technology platform, to prevent nigrostriatal degeneration in the 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) mouse model of PD and establish a therapeutic role for RNS60 in human parkinsonism. Background Chronic inflammation is a hallmark of many human diseases including neurodegenerative disorders. Glial inflammation is a critical component of PD pathogenesis. Since transcription of many pro-inflammatory molecules depends on the activation of NF-κB, a multifunctional transcription factor, NF-κB is a critical therapeutic target for inflammatory diseases. Here we report a novel approach to attenuate NF-κB activation and inflammation in the MPTP model of PD. Design/Methods: RNS60 was generated by subjecting normal saline to Taylor-Couette-Poiseuille (TCP) flow and cavitation forces under high oxygen pressure. Six- to eight-week old C57BL/6 mice were intoxicated with four intraperitoneal (i.p.) injections of MPTP-HCl in saline at 2-h intervals. Mice were then treated with RNS60 (300 μL/mouse/d) via i.p. injections from 2 d prior to MPTP intoxication until the end of experiment on day 7. Various disease parameters including locomotor function, MPTP induced neuro-degeneration, and expression of multiple pro and anti-inflammatory markers such as inducible nitric oxide synthase (iNOS), NF-κB, and IκBα were assessed. Results: Intraperitoneal injections with RNS60 increased the level of IκBα, inhibited the activation of NF-κB, and attenuated the expression iNOS in vivo in the substantia nigra pars compacta (SNpc). These findings paralleled dopaminergic neuronal protection, normalization of striatal neurotransmitters, and improvement of motor functions in MPTP-intoxicated mice. Conclusions: These results delineate a novel anti-inflammatory property of RNS60 and suggest TCP-modified solutions as a potential class of novel therapeutics for the treatment of inflammatory and neurodegenerative disorders. Supported by: Revalesio Corporation, Tacoma, WA, has supported this study. Disclosure: Dr. Khasnavis has nothing to disclose. Dr. Jana has nothing to disclose. Dr. Roy has nothing to disclose. Dr. Wood has received personal compensation for activities with Revalesio Corporation as a full time employee. Dr. Ghosh has received personal compensation for activities with Revalesio Corporation as an employee. Dr. Watson has received personal compensation for activities with Revalesio Corporation as an employee. Dr. Pahan has received research support from Revalesio Corporation." @default.
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• W2029997013 date "2012-04-22" @default.
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• W2029997013 title "Suppression of NF- B Activation and Inflammation in Glial Cells by RNS60, a Novel Therapeutic: Implications for Neurodegenerative Disorders (PD4.001)" @default.
• W2029997013 doi "https://doi.org/10.1212/wnl.78.1_meetingabstracts.pd4.001" @default.
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