CLINICAL TRIAL: -K

临床试验：-K

• 批准号: 7717968
• 负责人: JOHN M RINGMAN
• 金额: $ 0.04万
• 依托单位: UNIVERSITY OF CALIFORNIA LOS ANGELES
• 依托单位国家: 美国
• 财政年份: 2007
• 资助国家: 美国
• 起止时间: 2007-12-01 至 2008-11-30
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/7717968
• 关键词: Affect; Amyloid; Biological Markers; Blood - brain barrier anatomy; Brain; Cholesterol; Clinical Trials; Cognitive; Computer Retrieval of Information on Scientific Projects Database; Data; Deposition; Diet; Dietary Cholesterol; Funding; Grant; Institution; Intervention; Lead; Link; Mus; Process; Production; Research; Research Personnel; Resources; Risk Factors; Safety; Senile Plaques; Source; United States National Institutes of Health; cognitive function; neuropathology

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. Amyloid plaque in the brain is evident in the neuropathology of AD. The manipulation of the making and accumulating of this amyloid is one of the most proposed mechanisms in the intervention of AD. There are studies that have shown the link between cholesterol and AD and that the decreasing of the cholesterol levels may then change the processing of the amyloid which in turn would decrease the levels of A beta production decreasing plaque formation. There have been studies to show the association between dietary cholesterol and biological markers for AD where high cholesterol diets in mice increase A beta production. The studies support the notion that circulating cholesterol may be a risk factor for increasing A beta production. There is also some data show that differences in cholesterol levels also affect cognitive function. The studies indicate that elevated cholesterol levels may be related to amyloid deposits and cognitive function and that lowering the cholesterol may lead to cognitive benefit. Simvistatin was chosen due to its ability to cross blood brain barrier, has a good safety profile and it is the second most commonly used agent.

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。 大脑中的淀粉样蛋白斑块在 AD 的神经病理学中很明显。 控制这种淀粉样蛋白的产生和积累是AD干预中最被提出的机制之一。 有研究表明胆固醇和 AD 之间存在联系，并且胆固醇水平的降低可能会改变淀粉样蛋白的加工，从而降低 Aβ 的产生水平，从而减少斑块的形成。 有研究表明膳食胆固醇与 AD 生物标志物之间存在关联，其中小鼠的高胆固醇饮食会增加 Aβ 的产生。 这些研究支持这样的观点，即循环胆固醇可能是增加 Aβ 产生的危险因素。 还有一些数据表明，胆固醇水平的差异也会影响认知功能。 研究表明，胆固醇水平升高可能与淀粉样蛋白沉积和认知功能有关，而降低胆固醇可能会带来认知益处。 选择辛维他汀是因为它能够穿过血脑屏障，具有良好的安全性，并且是第二常用的药物。