NETWORK-BASED IMAGING BIOMARKERS IN SPORADIC DYSTONIA

散发性肌张力障碍中基于网络的成像生物标志物

• 批准号: 8167287
• 负责人: Marc Niethammer
• 金额: $ 0.08万
• 依托单位: FEINSTEIN INSTITUTE FOR MEDICAL RESEARCH
• 依托单位国家: 美国
• 财政年份: 2010
• 资助国家: 美国
• 起止时间: 2010-04-01 至 2011-03-31
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/8167287
• 关键词: Adolescence; Adult; Biological Markers; Childhood; Chronic; Computer Retrieval of Information on Scientific Projects Database; Disease; Dystonia Musculorum Deformans; Funding; Genetic; Grant; Image; Inherited; Institution; Involuntary Movements; Metabolic; Movement Disorders; Muscle Contraction; Network-based; Patients; Pattern; Posture; Research; Research Personnel; Resources; Source; Sporadic Dystonias; Structure; United States National Institutes of Health; white matter

This subproject is one of many research subprojects utilizing the resources provided by a Center grant funded by NIH/NCRR. The subproject and investigator (PI) may have received primary funding from another NIH source, and thus could be represented in other CRISP entries. The institution listed is for the Center, which is not necessarily the institution for the investigator. Primary torsion dystonia (PTD) is a chronic movement disorder manifesting clinically as focal or generalized sustained muscle contractions, postures, and/or involuntary movements. Genetic forms of PTD (e.g., DYT1 and DYT6) typically begin in childhood or adolescence and are often generalized. By contrast, sporadic PTD is more common, begins in adulthood, and is often focal or segmental in distribution. In previous studies, we have identified a consistent pattern of abnormal metabolic activity in PTD. We have also described microstructural white matter abnormalities in patients with inherited forms of PTD. In the proposed study, we will determine if similar structure/function abnormalities underlie the more common sporadic forms of PTD and whether these changes constitute useful biomarkers of the disorder.

这个子项目是许多研究子项目中的一个 由NIH/NCRR资助的中心赠款提供的资源。子项目和 研究者（PI）可能从另一个NIH来源获得了主要资金， 因此可以在其他CRISP条目中表示。所列机构为 中心，但不一定是研究者所在的机构。 原发性扭转肌张力障碍（PTD）是一种慢性运动障碍，临床表现为局灶性或全身性持续肌肉收缩、姿势和/或不自主运动。PTD的遗传形式（例如，DYT 1和DYT 6）通常开始于儿童或青春期，并且通常是全身性的。相比之下，散发性PTD更常见，开始于成年期，并且通常是局灶性或节段性分布。在以前的研究中，我们已经确定了PTD异常代谢活动的一致模式。 我们还描述了遗传性PTD患者的微结构白色物质异常。在拟议的研究中，我们将确定类似的结构/功能异常是否是更常见的散发性PTD形式的基础，以及这些变化是否构成该疾病的有用生物标志物。