The mt-DNA mutator mouse

mt-DNA突变小鼠

• 批准号: 7733847
• 负责人: Barry J Hoffer
• 金额: $ 64.58万
• 依托单位: NATIONAL INSTITUTE ON DRUG ABUSE
• 依托单位国家: 美国
• 资助国家: 美国
• 起止时间: 至
• 项目状态: 未结题
• 来源: https://reporter.nih.gov/project-details/7733847
• 关键词: Affect; Alleles; Animals; Brain; Cognitive; Cytochrome-c Oxidase Deficiency; DNA-Directed DNA Polymerase; Data; Functional disorder; Ischemic Brain Injury; Knock-in Mouse; Mitochondria; Mitochondrial DNA; Motor; Mus; Mutant Strains Mice; Mutation; Pattern; Pharmaceutical Preparations; Phenotype; Premature aging syndrome; Production; Reading; Respiratory Chain; Structure; Thick; age related; mitochondrial DNA mutation

We are characterizing the CNS phenotypes caused by elevated mtDNA mutation levels and relating these findings to age-related functional changes. Furthermore, we will investigate the affects of ischemic brain injury in these same mice. We have already documented change in cortical thickness and lamination patterns. There are also changes in oxidative energy production and mitochondrial function. These changes parallel cognitive and motor deficiencies in the mtDNA mutators. Drugs that upregulate mitochondrial function are being evaluated.

我们正在描述由mtDNA突变水平升高引起的CNS表型，并将这些发现与年龄相关的功能变化联系起来。 此外，我们将研究缺血性脑损伤对这些小鼠的影响。我们已经记录了皮质厚度和分层模式的变化。氧化能产生和线粒体功能也发生变化。这些变化与mtDNA突变子中的认知和运动缺陷平行。正在评估上调线粒体功能的药物。