BEHAVIORAL AND NEUROCHEMICAL CORRELATES OF PRESENILIN-1 MUTATION STATUS

PRESENILIN-1 突变状态的行为和神经化学相关性

• 批准号: 8167076
• 负责人: JOHN M RINGMAN
• 金额: $ 2.11万
• 依托单位: UNIVERSITY OF CALIFORNIA LOS ANGELES
• 依托单位国家: 美国
• 财政年份: 2009
• 资助国家: 美国
• 起止时间: 2009-12-01 至 2010-11-30
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/8167076
• 关键词: Age; Behavioral; Biological Markers; Computer Retrieval of Information on Scientific Projects Database; Episodic memory; Funding; Genetic Status; Grant; High Prevalence; Institution; Measures; Mental Depression; Mutation; Neuropsychological Tests; Onset of illness; Pathogenesis; Research; Research Personnel; Resources; Source; United States National Institutes of Health; depressive symptoms; executive function; mutation carrier; neurochemistry; pre-clinical; presenilin-1

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. Specific Aims: 1. To determine if pre-clinical PS1 mutation carriers will perform significantly worse than their non-mutation carrying kin on neuropsychological tests measuring episodic memory and executive function as they approach the age of disease onset. 2. To determine if pre-clinical PS1 mutation carriers will have a higher prevalence of depression and higher levels of depressive symptoms than their non-mutation carrying kin despite being unaware of their genetic status. 3. To determine if biomarkers of AD pathogenesis such as CSF Ab oligomers will be found to be elevated in pre-clinical PS1 mutation carriers.

该子项目是利用该技术的众多研究子项目之一 资源由 NIH/NCRR 资助的中心拨款提供。子项目及 研究者 (PI) 可能已从 NIH 的另一个来源获得主要资金， 因此可以在其他 CRISP 条目中表示。列出的机构是 对于中心来说，它不一定是研究者的机构。 具体目标： 1. 确定临床前 PS1 突变携带者在接近疾病发病年龄时，在测量情景记忆和执行功能的神经心理学测试中的表现是否会明显差于其非突变携带者。 2. 确定临床前 PS1 突变携带者是否比其非突变携带者具有更高的抑郁症患病率和更高水平的抑郁症状，尽管不知道他们的遗传状态。 3. 确定临床前 PS1 突变携带者中是否会发现 AD 发病机制的生物标志物（例如 CSF Ab 寡聚体）升高。