IMAGING DECREASED BRAIN DOCOSAHEXAENOIC ACID METABOLISM AND SIGNALING

大脑二十二碳六烯酸代谢和信号传导下降的成像

• 批准号: 8361447
• 负责人: Stanley I. Rapoport
• 金额: $ 0.81万
• 依托单位: WASHINGTON UNIVERSITY
• 依托单位国家: 美国
• 财政年份: 2011
• 资助国家: 美国
• 起止时间: 2011-01-01 至 2011-12-31
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/8361447
• 关键词: Brain; Docosahexaenoic Acids; Dystonia; Enzymes; Funding; Grant; Image; In Vitro; Iron; Mass Spectrum Analysis; Metabolism; Mus; Mutation; National Center for Research Resources; Nerve Degeneration; Neurologic Dysfunctions; PLA2G6 gene; Parkinsonian Disorders; Patients; Phospholipases A; Phospholipids; Principal Investigator; Research; Research Infrastructure; Resources; Signal Transduction; Source; United States National Institutes of Health; biomedical resource; cost; neuropathology

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. Ca(2+)-independent phospholipase A(2)¿ (iPLA(2)¿) selectively hydrolyzes docosahexaenoic acid (DHA, 22:6n-3) in vitro from phospholipid. Mutations in the PLA2G6 gene encoding this enzyme occur in patients with idiopathic neurodegeneration plus brain iron accumulation and dystonia-parkinsonism without iron accumulation, whereas mice lacking PLA2G6 show neurological dysfunction and neuropathology after 13 months. We hypothesized that brain DHA metabolism and signaling would be reduced in 4-month-old iPLA(2)¿-deficient mice without overt neuropathology.

该副本是利用资源的众多研究子项目之一 由NIH/NCRR资助的中心赠款提供。对该子弹的主要支持 而且，副投影的主要研究员可能是其他来源提供的 包括其他NIH来源。列出的总费用可能 代表subproject使用的中心基础架构的估计量， NCRR赠款不直接向子弹或副本人员提供的直接资金。 Ca（2+） - 独立的磷脂酶A（2）€（IPLA（2）€）在体外从磷脂中选择性水解二十六烯酸（DHA，22：6n-3）。编码这种酶的PLA2G6基因的突变发生在特发神经退行性的患者以及脑铁的积累和肌铁的积累和肌张力障碍 - 甲状腺抑制无铁积累的情况下，而缺乏PLA2G6的小鼠在13个月后显示神经系统功能障碍和神经病理学。我们假设在没有明显的神经病理学的4个月大的IPLA（2）�-缺陷的小鼠中，脑DHA代谢和信号传导将降低。