Novel mechanism of action as therapeutic strategy for optic neuritis
作为视神经炎治疗策略的新作用机制
基本信息
- 批准号:8511676
- 负责人:
- 金额:$ 35.63万
- 依托单位:
- 依托单位国家:美国
- 项目类别:
- 财政年份:2012
- 资助国家:美国
- 起止时间:2012-08-01 至 2015-06-30
- 项目状态:已结题
- 来源:
- 关键词:AcuteAddressAffectAftercareAnimal ModelAutoimmune ProcessAutoimmunityAxonBehavioralBiologicalBiological PreservationBiological ProductsBlindnessBrainCNS autoimmune diseaseCNS autoimmunityCNS degenerationCell physiologyCellsCharacteristicsClinicalClinical TrialsCombined Modality TherapyComplementComplexComplicationConfocal MicroscopyCytophotometryDataDegenerative DisorderDetectionDevelopmentDiagnosisDiagnosticDifferential DiagnosisDiseaseDisease ProgressionDisease modelDoseDrug CombinationsEventExperimental ModelsEyeGeneric DrugsGenomicsGoalsHealthcareHeat shock proteinsHumanHuman PathologyImmunoblot AnalysisIn VitroInflammationInflammatoryInterdisciplinary StudyInterventionKnowledgeMeasuresMediatingMethodsMinorityModelingMultiple SclerosisMyelinMyelin ProteinsNatural regenerationNerveNerve DegenerationNeuronsOptic NerveOptic NeuritisPathologicPathologyPathway interactionsPatientsPatternPerformancePharmaceutical PreparationsPhasePhenotypePopulationPreclinical TestingPreventionProcessProductivityQuality of lifeRattusRegimenResearchResearch Project GrantsResveratrolRetinaRodent ModelSequential TreatmentSignal TransductionStagingStructureTestingTherapeuticTherapeutic InterventionToxic effectTreatment EfficacyTreatment ProtocolsUnited StatesVisionVisual AcuityVisual impairmentautoimmune optic neuritisaxon regenerationaxonal degenerationbasecare burdenclinical phenotypeclinically relevantdisease phenotypedrug developmentfunctional disabilityfunctional outcomesgeranylgeranylacetonehealth care deliveryhuman diseaseimmunoreactivityimprovedin vivoinhibitor/antagonistinnovationneuron lossneuroprotectionnovelnovel therapeuticsoptic nerve regenerationphysical conditioningprenylationpreventregenerativeremyelinationrepairedresearch studysmall moleculetherapy designtherapy developmenttrans-resveratroltreatment strategy
项目摘要
DESCRIPTION (provided by applicant): Degeneration or damage of the optic nerve and the retina due to optic neuritis is a leading cause of visual loss and blindness in the United States and worldwide associated with multiple sclerosis and autoimmune damage to the CNS. The proposed multidisciplinary research project will focus on the development and characterization of a novel pharmacological intervention strategy that combines drugs to control structural and functional degeneration in autoimmune optic neuritis. Suppression of CNS inflammation, prevention of loss and damage of myelinated axons, and stimulation of regeneration and remyelination of damaged axons are the primary goals of the study. To this end, preclinical testing of the new therapeutic strategy will be performed in established models of human autoimmune optic neuritis. These experiments will determine efficacy of treatment in terminating and/or preventing autoimmune optic neuritis associated neuronal loss and preservation of visual function, and to generate data to support feasibility for and move positive findings to phase 1 or 2 clinical trials. Specifically, we will test the hypothesis that the proposed treatment strategy cn target and remedy specific phenotypes that include combinations of separate pathologies encountered during distinct stages of optic neuritis and multiple sclerosis, leading to improvement of visual impairment and functional deficits associated with the disease. The determination of neuronal viability and the acquired knowledge on associated therapeutic parameters will indicate the potential of the method to remedy autoimmune optic neuritis as the overall goal of the project. This therapy approach for autoimmune optic neuritis focuses on suppression of CNS autoimmunoreactivity, neuroprotection, axon regeneration and remyelination via different mechanisms. It has the potential to be both preventative and therapeutic and to complement existing treatment designs and rationales addressing other aspects of autoimmune optic neuritis treatment.
描述(由申请人提供):视神经炎引起的视神经和视网膜变性或损伤是美国和世界范围内视力丧失和失明的主要原因,与多发性硬化症和CNS自身免疫损伤相关。拟议的多学科研究项目将侧重于开发和表征一种新的药理学干预策略,结合药物来控制自身免疫性视神经炎的结构和功能变性。抑制CNS炎症、预防有髓鞘轴突的损失和损伤以及刺激受损轴突的再生和髓鞘再生是本研究的主要目标。为此,将在已建立的人类自身免疫性视神经炎模型中进行新治疗策略的临床前测试。这些实验将确定治疗在终止和/或预防自身免疫性视神经炎相关神经元损失和视觉功能保留方面的功效,并生成数据以支持可行性并将阳性结果转移到1期或2期临床试验。具体来说,我们将测试的假设,提出的治疗策略cn目标和补救特定的表型,包括在不同阶段的视神经炎和多发性硬化症,导致改善视力障碍和功能缺陷与疾病的不同阶段遇到的单独的病理组合。神经元活力的测定和获得的相关治疗参数的知识将表明该方法治疗自身免疫性视神经炎的潜力,作为该项目的总体目标。这种治疗方法的自身免疫性视神经炎的重点是抑制中枢神经系统自身免疫反应,神经保护,轴突再生和髓鞘通过不同的机制。它具有预防和治疗的潜力,并补充现有的治疗设计和原理,解决自身免疫性视神经炎治疗的其他方面。
项目成果
期刊论文数量(0)
专著数量(0)
科研奖励数量(0)
会议论文数量(0)
专利数量(0)
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Peter Koulen其他文献
Peter Koulen的其他文献
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{{ truncateString('Peter Koulen', 18)}}的其他基金
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10288383 - 财政年份:2020
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$ 35.63万 - 项目类别:
Novel mechanism controlling calcium signaling to treat and prevent neurodegeneration in early stage glaucoma
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9916194 - 财政年份:2020
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$ 35.63万 - 项目类别:
Novel mechanism controlling calcium signaling to treat and prevent neurodegeneration in early stage glaucoma
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- 批准号:
10333217 - 财政年份:2020
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$ 35.63万 - 项目类别:
Novel mechanism controlling calcium signaling to treat and prevent neurodegeneration in early stage glaucoma
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- 批准号:
10190022 - 财政年份:2020
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$ 35.63万 - 项目类别:
Novel mechanism controlling calcium signaling to treat and prevent neurodegeneration in early stage glaucoma
控制钙信号传导以治疗和预防早期青光眼神经变性的新机制
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Novel mechanism of action as therapeutic strategy for optic neuritis
作为视神经炎治疗策略的新作用机制
- 批准号:
8675259 - 财政年份:2012
- 资助金额:
$ 35.63万 - 项目类别:
Novel mechanism of action as therapeutic strategy for optic neuritis
作为视神经炎治疗策略的新作用机制
- 批准号:
8366675 - 财政年份:2012
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