ALZHEIMER'S DISEASE: MODELING PATHOLOGIC STRAIN-LIKE VARIANTS OF MULTIMERIC A?

阿尔茨海默病：模拟多聚体 A 的病理菌株样变体？

• 批准号: 7958265
• 负责人: LARY C WALKER
• 金额: $ 2.75万
• 依托单位: EMORY UNIVERSITY
• 依托单位国家: 美国
• 财政年份: 2009
• 资助国家: 美国
• 起止时间: 2009-05-01 至 2010-04-30
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/7958265
• 关键词: Alzheimer' s Disease; Base of the Brain; Benign; Binding; Brain; Computer Retrieval of Information on Scientific Projects Database; Crystallization; Disease; Disease model; Funding; Grant; Image; Institution; Life; Pathologic; Primates; Process; Proteins; Research; Research Personnel; Resources; Shapes; Source; United States National Institutes of Health; Variant

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. There is now strong evidence that Alzheimer's disease is caused by proteins that mistakenly bind to one another to form toxic aggregates in the brain. The protein that drives this process is known as A¿. Little is known about the strains of disease-causing proteins in the living brain. We have developed a new way of causing proteins to aggregate in the brain based on the simple principle that a particular protein molecule with a particular abnormal shape can cause normal versions of the same molecule to become abnormal by a process analagous to seeded crystallization. Recently we have found that molecules that have been developed to image A¿ in Alzheimer's disease may actually distinguish between toxic and benign aggregates of A¿. A¿-binding agents thus have the potential to distinguish among stuctural variants of A¿ that may be differentially toxic to the brain.

该副本是使用众多研究子项目之一 由NIH/NCRR资助的中心赠款提供的资源。子弹和 调查员（PI）可能已经从其他NIH来源获得了主要资金， 因此可以在其他清晰的条目中代表。列出的机构是 对于中心，这是调查员的机构。 现在有强有力的证据表明，阿尔茨海默氏病是由蛋白质误认为彼此结合以形成大脑中有毒骨料的蛋白质引起的。驱动这一过程的蛋白质对活大脑中引起疾病​​的蛋白质的菌株知之甚少。我们已经开发了一种新的方法，该方法是基于简单的原理，即具有特定异常形状的特定蛋白质分子会导致同一分子的正常版本通过相似的物质结晶而变得异常。 最近，我们发现已经开发出来在阿尔茨海默氏病中成像A的分子实际上可能区分了a。的毒性和良性聚集体。因此，结合剂有可能区分A字的构型变体，这些变体可能对大脑有所不同。