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.

这个子项目是利用这些资源的众多研究子项目之一