ASSESSING NEURAL MECHANISMS OF INJURY IN INBORN ERRORS OF UREA METABOLISM

评估尿素代谢先天性缺陷损伤的神经机制

• 批准号: 7719061
• 负责人: Andrea Lynne Gropman
• 金额: $ 13.77万
• 依托单位: GEORGETOWN UNIVERSITY
• 依托单位国家: 美国
• 财政年份: 2008
• 资助国家: 美国
• 起止时间: 2008-04-01 至 2009-03-31
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/7719061
• 关键词: Affect; Base of the Brain; Cognitive; Computer Retrieval of Information on Scientific Projects Database; Funding; Genes; Goals; Grant; Inborn Genetic Diseases; Individual; Injury; Institution; Learning; Magnetic Resonance Imaging; Metabolism; Motor; Ornithine carbamoyltransferase deficiency; Procedures; Research; Research Personnel; Research Project Grants; Resources; Source; United States National Institutes of Health; Urea; Work; base; behavior test; cognitive function; experience; neuromechanism

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. This research project will study the brain basis of motor and cognitive functions and any difficulties in learning experienced by individuals who are affected by or carriers of inborn errors of urea metabolism. The goal of the study is to use behavioral testing and MRI procedures in typically developed people and compare this with a group of people with inborn erors of urea metabolism which may affect cognitive and motor function. This study is based upon a previous work demonstrating learning problems in some individuals who are carriers of the Ornithine transcarbamylase deficiency gene.

这个子项目是许多利用 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 研究中心，而研究中心不一定是研究者所在的机构。 该研究项目将研究运动和认知功能的大脑基础，以及受先天性尿素代谢缺陷影响或携带者在学习中遇到的任何困难。这项研究的目的是在典型的发达人群中使用行为测试和MRI程序，并将其与一组可能影响认知和运动功能的先天性尿素代谢异常的人群进行比较。这项研究是基于以前的工作，证明学习问题，在一些人谁是携带者的鸟氨酸转氨甲酰酶缺乏症基因。