NON-INVASIVE QUANTITATION OF CELLU & BIOCHEM CHANGES IN SPINOCEREBELLAR ATAXIAS

细胞的非侵入式定量

• 批准号: 8362814
• 负责人: Gulin Oz
• 金额: $ 2.27万
• 依托单位: UNIVERSITY OF MINNESOTA
• 依托单位国家: 美国
• 财政年份: 2011
• 资助国家: 美国
• 起止时间: 2011-06-01 至 2012-05-31
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/8362814
• 关键词: Age; Ataxia; Biochemical; Cessation of life; Chicago; Collaborations; Event; Friedreich Ataxia; Funding; Gliosis; Goals; Grant; LY6E gene; Magnetic Resonance Imaging; Multiple System Atrophy; NMR Spectroscopy; National Center for Research Resources; Nerve Degeneration; Neurology; Neurons; Oxidative Stress; Patients; Philanthropic Fund; Principal Investigator; Research; Research Infrastructure; Resources; Scanning; Source; Spinocerebellar Ataxias; United States National Institutes of Health; Universities; cost; neurochemistry; oculomotor

This subproject is one of many research subprojects utilizing the resources provided by a Center grant funded by NIH/NCRR. Primary support for the subproject and the subproject's principal investigator may have been provided by other sources, including other NIH sources. The Total Cost listed for the subproject likely represents the estimated amount of Center infrastructure utilized by the subproject, not direct funding provided by the NCRR grant to the subproject or subproject staff. (in collaboration with Dr.s Khalaf Bushara, Neurology and Christopher Gomez, University of Chicago, Neurology, supported by R21 NS056172, philanthropic funds and Bob Allison Ataxia Research Center, PI Oz): In this project we study the neurochemical alterations that are associated with neurodegeneration in spinocerebellar ataxias (SCAs). The goal is to establish and validate markers of multiple cellular and biochemical events associated with neurodegeneration, such as neuronal death, gliosis and oxidative stress. We have so far scanned patients with SCA1, SCA2, SCA6, Friedreich's ataxia, cerebellar multiple system atrophy and ataxia with oculomotor apraxia type 2, as well as age-matched healthy controls. We have detected alterations in the neurochemical profile in ataxias by high field nuclear magnetic resonance spectroscopy (MRS) and found that these are specific for different ataxia subtypes.

该子项目是利用资源的众多研究子项目之一 由 NIH/NCRR 资助的中心拨款提供。子项目的主要支持 并且子项目的主要研究者可能是由其他来源提供的， 包括其他 NIH 来源。 子项目可能列出的总成本 代表子项目使用的中心基础设施的估计数量， NCRR 赠款不直接向子项目或子项目工作人员提供资金。 （与神经病学的 Khalaf Bushara 博士和芝加哥大学神经病学的 Christopher Gomez 博士合作，由 R21 NS056172、慈善基金和 PI Oz 的 Bob Allison 共济失调研究中心支持）：在这个项目中，我们研究与脊髓小脑共济失调 (SCA) 神经变性相关的神经化学改变。目标是建立并验证与神经变性相关的多种细胞和生化事件的标记，例如神经元死亡、神经胶质增生和氧化应激。到目前为止，我们已经扫描了 SCA1、SCA2、SCA6、弗里德赖希共济失调、小脑多系统萎缩和共济失调伴动眼神经失用症 2 型的患者，以及年龄匹配的健康对照。我们通过高场核磁共振波谱（MRS）检测到共济失调神经化学谱的改变，并发现这些改变对于不同的共济失调亚型是特异性的。