脱髓鞘疾病神经元损伤的分子机制-猫眼课题宝

脱髓鞘疾病神经元损伤的分子机制

批准号：

8470259

负责人：

Patrizia Casaccia

金额：

$35.79万

依托单位：

ICAHN SCHOOL OF MEDICINE AT MOUNT SINAI

依托单位国家：

美国

项目类别：

财政年份：

2011

资助国家：

美国

项目状态：

已结题

起止时间：

2011-04-01 至 2015-03-31

来源：

https://reporter.nih.gov/project-details/8470259

关键词：

Acetylation Acute Address Amino Acids Area Axon Axonal Transport Binding Brain Calcium Cells Clinical Collaborations Cuprizone Cytosol Deacetylation Demyelinating Diseases Demyelinations Detection Disease Early Diagnosis Enzymes Event Family member Fiber Glutamates Grant HDAC1 gene Hippocampus (Brain)Histone Deacetylase Histones Impairment In Vitro Knock-in Mouse Knowledge Laboratories Lead Mitochondria Modification Molecular Movement Multiple Sclerosis Mus Mutation Nerve Degeneration Neurites Neurodegenerative Disorders Neurons Nuclear Nuclear Export Nuclear Receptors Oxidative Stress Pathway interactions Patients Phosphorylation Point Mutation Post-Translational Protein Processing Property Protein Isoforms Proteins Recycling Reporting Role Signal Transduction Slice Specificity Spectrometry, Mass, Matrix-Assisted Laser Desorption-Ionization Stimulus Swelling Synaptic Vesicles TNF gene Testing Therapeutic Toxic effect Transgenic Model Transport Vesicles Ubiquitination axonopathy base cell type disability immunoreactivity in vivo in vivo Model inhibitor/antagonist mutant nervous system disorder new therapeutic target novel prevent protective effect public health relevance repaired research study response young adult

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中文摘要

翻译

描述(由申请人提供)：轴突损伤是包括多发性硬化症(MS)在内的一系列神经系统疾病的主要临床残疾原因。虽然轴突损伤早期征象的检测已经取得了相当大的进展，但对潜在的致病因素和相关的信号事件仍知之甚少。因此，目前还没有旨在预防或修复受损轴突的治疗方法。我们的实验室最近报道了细胞质HDAC1参与了线粒体运输的损害和轴突肿胀的发生。这项实验计划建议表征这种新的细胞内信号机制，并使用体外和体内模型来表征特定亚型的组蛋白脱乙酰酶在脱髓鞘疾病轴突损伤中的作用。

英文摘要

DESCRIPTION (provided by applicant): Axonal damage is cause of major clinical disability in a wide range of neurological disorders, including multiple sclerosis (MS). Although considerable progress has been made in the detection of the early signs of axonal damage, still very little is known about the potential causative factors and the related signaling events. Thus, therapeutic approaches aimed at preventing or repairing damaged axons are not yet available. Our laboratory has recently reported the involvement of cytoplasmic HDAC1 in the impairment of mitochondrial transport and the onset of axonal swellings. This experimental plan proposes to characterize this novel intracellular signaling mechanism and use in vitro and in vivo models to characterize the role of specific isoforms of histone deacetylases in axonal damage in demyelinating disorders.

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