Dysregulated cholinergic transmission contributes to aging of the lower motor system
胆碱能传输失调导致下运动系统老化
基本信息
- 批准号:9565885
- 负责人:
- 金额:$ 39.4万
- 依托单位:
- 依托单位国家:美国
- 项目类别:
- 财政年份:2017
- 资助国家:美国
- 起止时间:2017-09-30 至 2019-08-31
- 项目状态:已结题
- 来源:
- 关键词:AcetylcholineAddressAdultAffectAgeAgingAmyotrophic Lateral SclerosisAxonBiological MarkersCachexiaDataDendritesDiseaseFunctional disorderGene ExpressionGenesGoalsGrantHealthIncidenceKnowledgeLightLongevityMitochondriaMolecularMotorMotor NeuronsMusMuscleMuscle FibersMuscular AtrophyMuscular DystrophiesNatural regenerationNeuromuscular JunctionOutcomePathway interactionsPharmacologyRenshaw CellResearchSchwann CellsSiteSkeletal MuscleSourceSpinal CordSynapsesSynaptic CleftSynaptic VesiclesSystemTestingTherapeuticTransgenic MiceWild Type Mouseage relatedagedbasecholinergiccholinergic synapseexperimental studyfallsinsightmotor deficitmotor neuron degenerationmotor neuron functionmouse modelmutantneuromuscular functionneuromuscular systemneuronal cell bodynormal agingnovelnovel markerpreventrepairedskeletal muscle wastingsynaptic functiontooltransmission processvesamicolyoung adult
项目摘要
Project Summary/ Abstract
The loss of motor function that occurs with aging is closely associated with adverse health
outcomes. To date, the contribution of different components of the motor system to age-related
motor deficits remains unknown and despite extensive efforts. In addition, there are no
therapeutics that can prevent the cellular and molecular changes that underlie loss of motor
function with aging. The purpose of this proposal is to identify the contribution of the
neuromuscular system to loss of motor function. We also seek to identify and test factors that
function to maintain healthy skeletal muscles and motor neurons in the spinal cord, and thus
preserve motor function. Specifically, we will determine whether maintaining normal levels of
acetylcholine, genetically and pharmacologically, is sufficient to slow aging of skeletal muscle
and motor neurons.
项目摘要/摘要
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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Gregorio Valdez其他文献
Gregorio Valdez的其他文献
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{{ truncateString('Gregorio Valdez', 18)}}的其他基金
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Targeting the fibroblast growth factor binding protein-1 to slow degeneration of neuromuscular junctions
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- 批准号:
9290385 - 财政年份:2017
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$ 39.4万 - 项目类别:
Targeting the fibroblast growth factor binding protein-1 to slow degeneration of neuromuscular junctions
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- 批准号:
9903183 - 财政年份:2017
- 资助金额:
$ 39.4万 - 项目类别:
Synaptic FGFs are required and sufficient to maintain and repair aged NMJs
突触 FGF 是维持和修复老化 NMJ 所必需的且足够的
- 批准号:
9143829 - 财政年份:2015
- 资助金额:
$ 39.4万 - 项目类别:
Role of Target-derived FGFs in Maintaining and Repairing Synapses
靶标衍生的 FGF 在维持和修复突触中的作用
- 批准号:
8618387 - 财政年份:2013
- 资助金额:
$ 39.4万 - 项目类别:
Role of Target-derived FGFs in Maintaining and Repairing Synapses
靶标衍生的 FGF 在维持和修复突触中的作用
- 批准号:
8738734 - 财政年份:2013
- 资助金额:
$ 39.4万 - 项目类别:
Role of Target-derived FGFs in Maintaining and Repairing Synapses
靶标衍生的 FGF 在维持和修复突触中的作用
- 批准号:
8896083 - 财政年份:2013
- 资助金额:
$ 39.4万 - 项目类别:
Molecular basis of age-related synaptic alterations
年龄相关突触改变的分子基础
- 批准号:
7539575 - 财政年份:2008
- 资助金额:
$ 39.4万 - 项目类别:
Molecular basis of age-related synaptic alterations
年龄相关突触改变的分子基础
- 批准号:
7683976 - 财政年份:2008
- 资助金额:
$ 39.4万 - 项目类别:
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