Next generation systems analysis of pathogenetic mechanisms underlying CNS autoimmunity
中枢神经系统自身免疫发病机制的下一代系统分析
基本信息
- 批准号:9768066
- 负责人:
- 金额:$ 27.3万
- 依托单位:
- 依托单位国家:美国
- 项目类别:
- 财政年份:2019
- 资助国家:美国
- 起止时间:2019-06-25 至 2021-05-31
- 项目状态:已结题
- 来源:
- 关键词:AddressAllelesAnimal ModelArchitectureAutoimmune DiseasesAutoimmune ProcessAxonCNS autoimmunityCandidate Disease GeneCellsCentral Nervous System DiseasesChromosomesChronicChronic DiseaseClinicalComplexComputational algorithmCongenic StrainConsomic StrainDataData SetDemyelinationsDeteriorationDiseaseDisease ProgressionEtiologyExhibitsExperimental Autoimmune EncephalomyelitisExperimental GeneticsFemaleGenesGeneticGenetic ModelsGenetic RecombinationGenetic RiskGenetic StructuresGenetic VariationGenomeGliosisHeritabilityHeterogeneityHumanImmuneIncidenceIndividualInfiltrationInflammatoryMediatingModelingMolecularMultiple SclerosisMusNetwork-basedNeuraxisNeurologicNeurologic DysfunctionsPathogenesisPathologyPhenotypePopulationPredispositionPrimary Progressive Multiple SclerosisPublishingRelapseRelapsing-Remitting Multiple SclerosisResolutionRiskRoleSJL/J MouseSeveritiesSex DifferencesSusceptibility GeneSystemSystems AnalysisTechnologyTimeTissuesWomanWorkanalytical toolaxon injurycausal variantchronic autoimmune diseasecohortconsomicdesigndisabilitydisorder riskexperimental studyforward geneticsgenetic analysisgenetic approachgenetic architecturegenetic associationgenetic resourcegenetic variantgenome wide association studygenome-widegenomic datainsightknockout genemalemenmouse modelnext generationnoveloutcome forecastreverse geneticssuccesstoolyoung adult
项目摘要
Project Abstract/Summary
Multiple sclerosis (MS) is a chronic disease that is the leading cause of non-traumatic neurological disability in
young adults. The disease is caused by an aberrant immune-mediated attack on the central nervous system,
which causes tissue destruction and subsequent neurologic disability. Disease course varies greatly from
individual to individual, from relapsing-remitting MS, to primary progressive MS. MS is three times more
common in women, but tends to be more severe in men. MS has a significant heritable component, with up to
30% of the disease risk being genetically determined. While recent studies have identified candidate genes
that are associated with MS risk, it remains unclear how these genes work and whether these are truly
causative. Additionally, it is unclear why some individuals get different forms of this disease, and why there are
differences between men and women. These types of questions are very difficult, if not impossible, to address
in studies in humans. In this application, we propose to use a mouse model of MS to address this question.
Mouse models offer powerful genetic tools, and allow for cause/effect mechanistic studies. We will use a novel
mouse genetic model that is designed to better represent the complex genetic structure of human populations,
which will allow us to dissect the complex genetic architecture underlying MS pathogenesis, and to identify
specific genes responsible for various poorly understood aspects of this disease.
项目摘要/总结
项目成果
期刊论文数量(0)
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会议论文数量(0)
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Dimitry N Krementsov其他文献
Dimitry N Krementsov的其他文献
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{{ truncateString('Dimitry N Krementsov', 18)}}的其他基金
Novel mouse models to dissect the role of genetics, sex, and environment in heterogeneous outcomes in CNS autoimmune disease
新型小鼠模型可剖析遗传、性别和环境在中枢神经系统自身免疫性疾病异质性结果中的作用
- 批准号:
10680560 - 财政年份:2022
- 资助金额:
$ 27.3万 - 项目类别:
Novel mouse models to dissect the role of genetics, sex, and environment in heterogeneous outcomes in CNS autoimmune disease
新型小鼠模型可剖析遗传、性别和环境在中枢神经系统自身免疫性疾病异质性结果中的作用
- 批准号:
10538863 - 财政年份:2022
- 资助金额:
$ 27.3万 - 项目类别:
Regulation of myeloid cell function by a novel putative lncRNA
一种新型推定lncRNA调节骨髓细胞功能
- 批准号:
10530689 - 财政年份:2021
- 资助金额:
$ 27.3万 - 项目类别:
Regulation of myeloid cell function by a novel putative lncRNA
一种新型推定lncRNA调节骨髓细胞功能
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10372592 - 财政年份:2021
- 资助金额:
$ 27.3万 - 项目类别:
Interactions Between Host Genetics and the Gut Microbiome in CNS Autoimmunity
中枢神经系统自身免疫中宿主遗传学与肠道微生物组之间的相互作用
- 批准号:
10093145 - 财政年份:2017
- 资助金额:
$ 27.3万 - 项目类别:
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