CARDIOVASCULAR HEALTH STUDY (CHS)

这个子项目是利用资源的许多研究子项目之一。 由NIH/NCRR资助的中心拨款提供。对子项目的主要支持 子项目的首席调查员可能是由其他来源提供的， 包括美国国立卫生研究院的其他来源。为子项目列出的总成本可能 表示该子项目使用的中心基础设施的估计数量， 不是由NCRR赠款提供给次级项目或次级项目工作人员的直接资金。 这个子项目是利用由NIH/NCRR资助的中心拨款提供的资源的许多研究子项目之一。子项目和调查员(PI)可能从另一个NIH来源获得了主要资金，因此可能会出现在其他CRISE条目中。列出的机构是针对中心的，而不一定是针对调查员的机构。心血管健康研究-认知研究(CHS-CS)“轻度认知障碍中阿尔茨海默病(AD)的预测因素”(AG 20098)在过去3年中仔细跟踪了532名非痴呆参与者。这是最初于1992-94年建立的CHS匹兹堡认知研究最初的924名合格参与者中的83%。参与者接受了年度神经心理评估、告密者提供的信息和详细的临床信息。到2006年，32%的正常人(每年约6%)和63%的精神分裂症患者(每年约16%)将患上痴呆症；2006年有359人活着，平均年龄为86岁。这项研究表明，大多数MCI转变为痴呆症，许多正常人非常迅速地转变为痴呆症，MRI表现对于了解风险至关重要，包括脑血管疾病、全局性脑萎缩和局灶性脑异常。拟议的4年续展包括对存活队列进行3年的随访和重复磁共振成像，以评估无痴呆生存的个人的特征，确定风险因素与924名参与者在大约18-20年的随访中MRI变化的关系，分析生活方式、遗传和MRI属性与痴呆症风险、MCI和保持正常的关系。这一拟议后续行动的大部分资源专门用于对核磁共振成像的详细评价、对剩余幸存者的仔细评价和详细的最终分析。这是唯一一项在可预见的未来进行长期随访、重复核磁共振检查和仔细的神经心理学评估的大型人群研究。从这个项目前三年收集的数据中，我们开发了一个中心假设来指导我们的研究问题。具体地说，阿尔茨海默病的病理状态早于痴呆综合征的临床体征/症状发展数年。我们认为MCI是正常认知和坦率痴呆之间的过渡状态，在没有其他共病的情况下，MCI就是AD。在这种背景下，我们对指示神经病变存在的变量(例如，结构和灌注MRI、血浆β-淀粉样蛋白)以及修改风险以表达临床综合征的因素的研究具有额外的重要性。

This subproject is one of many research subprojects utilizing the resources provided by a Center grant funded by NIH/NCRR. Primary support for the subproject and the subproject's principal investigator may have been provided by other sources, including other NIH sources. The Total Cost listed for the subproject likely represents the estimated amount of Center infrastructure utilized by the subproject, not direct funding provided by the NCRR grant to the subproject or subproject staff. 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. The Cardiovascular Health Study-Cognition Study (CHS-CS), "Predictors of Alzheimer's disease (AD) in mild cognitive impairment (MCI)" (AG 20098) has carefully followed 532 non-demented participants over the past 3 years. These were 83% of the 924 eligible participants from the original CHS Pittsburgh cognition study initially established in 1992-94. The participants have been followed with annual neuropsychological evaluations, information from informants and detailed clinical information. By 2006, 32% of the normals (approximately 6% per year) and 63% of the MCIs (approximately 16% per year) will be demented; and 359 are alive in 2006, with a mean age of 86. This study has shown that most MCI convert to dementia, that many normals convert to dementia very rapidly, that the MRI findings are crucial for understanding risk, including vascular disease in the brain, global brain atrophy and focal brain abnormalities. The proposed 4-year renewal includes 3 years of follow up and repeat MRIs for the surviving cohort in order to evaluate the characteristics of individuals who survive free of dementia to determine the relationship of risk factors and MRI changes over an approximate 18-20 year follow up for the 924 participants, to analyze the relationship of lifestyles, genetic and MRI attributes to the risk of dementia, MCI and remaining normal. Most of the resources in this proposed follow up are dedicated to the detailed evaluation of the MRIs, to careful evaluation of the remaining survivors and for detailed final analysis. This is the only large population-based study for the foreseeable future with long term follow up, repeat MRIs and careful neuropsychological evaluation. From the data gathered in the first 3 years of this project, we have developed a central hypothesis to guide our research questions. Specifically, that the pathological state of AD exists years prior to the development of the clinical signs/symptoms of the dementia syndrome. We view MCI as the transitional state between normal cognition and frank dementia, and that in the absence of other comorbid conditions, MCI is AD. In this context, our study of the variables that indicate the presence of neuropathological change (e.g., structural and perfusion MRI, plasma beta-amyloid) and the factors that modify the risk to express the clinical syndrome takes on an added importance.