IMAGING DECREASED BRAIN DOCOSAHEXAENOIC ACID METABOLISM AND SIGNALING

这个子项目是许多利用资源的研究子项目之一 由NIH/NCRR资助的中心拨款提供。子项目的主要支持 而子项目的主要调查员可能是由其他来源提供的， 包括其它NIH来源。 列出的子项目总成本可能 代表子项目使用的中心基础设施的估计数量， 而不是由NCRR赠款提供给子项目或子项目工作人员的直接资金。 钙非依赖性磷脂酶A（2）<$（iPLA（2）<$）在体外选择性地从磷脂中水解二十二碳六烯酸（DHA，22：6 n-3）。编码这种酶的PLA 2G 6基因突变发生在患有特发性神经变性加脑铁蓄积和肌张力障碍-帕金森综合征而无铁蓄积的患者中，而缺乏PLA 2G 6的小鼠在13个月后显示神经功能障碍和神经病理学。我们假设，在4个月大的iPLA（2）<$-缺陷小鼠中，大脑DHA代谢和信号传导将减少，而没有明显的神经病理学。

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.