The impact of non-amyloid processes on cognitive aging

描述(由申请人提供)：年龄增长与大脑结构的变化和认知表现的广泛变化有关。至少其中一些差异可归因于阿尔茨海默病(AD)，目前正在进行一项重大努力，以描绘大脑淀粉样蛋白对年龄相关认知变化和痴呆症的影响。然而，在70-79岁认知正常的人中，大约75%的人没有明显的大脑淀粉样蛋白滞留。这些数据表明，淀粉样变性以外的因素与老年人认知能力下降有关。流行病学研究一再表明，脑血管疾病(CVD)是一种非常常见的疾病，它与认知能力下降以及MCI和痴呆的发生有关，与AD的病理无关。对于心血管疾病更为普遍的非洲裔美国人和西班牙裔社区来说，情况尤其如此。心血管疾病相关认知改变的证据导致了一种假设，即通过预防和治疗血管危险因素，与年龄相关的认知下降的人群负担可能会显著减轻。然而，这一假设一直很难评估。阿尔茨海默氏症和脑血管病的病理通常在痴呆症患者的大脑中同时发生，因此很难辨别出每种病理对认知功能下降的独立影响。然而，淀粉样蛋白成像允许测量AD病理的至少一个组成部分，从而创造了评估认知轨迹、大脑差异和无广泛淀粉样变性个体认知功能下降的风险因素的机会。这项研究的前提是，大脑结构的变化，从脑梗塞到WMH，白质完整性的丧失和脑萎缩随着年龄的增长极其常见。此外，这些变化与认知能力下降和痴呆症风险增加有关。因此，在缺乏广泛淀粉样蛋白的情况下，确定脑损伤的程度和后果是至关重要的。为了实现这一目标，我们将在一组不同的老年个体中表征非淀粉样蛋白相关的脑结构和认知轨迹的变化。通过这样做，我们将加深对血管因素对大脑结构和认知的影响的了解，这将为认知老化和 在以社区为基础、种族和种族多元化的队列中，对未来认知障碍的易感性。

DESCRIPTION (provided by applicant): Advancing age is associated with changes in brain structure and widely varying trajectories of cognitive performance. At least some of these differences are attributable to Alzheimer's disease (AD) and a major effort is underway to delineate the effects of brain amyloid on age related cognitive change and incident dementia. However, approximately 75 percent of cognitively normal individuals aged 70-79 do not have significant brain amyloid retention. These data suggest that factors other than amyloidosis are associated with declining cognitive performance amongst older individuals. Epidemiological studies repeatedly show that cerebrovascular disease (CVD) is extremely common and associated with decreased cognitive performance as well as incident MCI and dementia, independent of AD pathology. This is particularly true for African American and Hispanic communities where CVD is more prevalent. Evidence for CVD-related cognitive change has led to the hypothesis that the population burden of age-related cognitive decline may be considerably lessened through prevention and treatment of vascular risk factors. However, this hypothesis has been difficult to assess. Both Alzheimer's and CVD pathologies commonly co-occur in the brains of demented individuals making the independent effects of each pathology on cognitive decline difficult to discern. Amyloid imaging, however, allows for the measure of at least one component of AD pathology thereby creating the opportunity to assess cognitive trajectories, brain differences and risk factors for cognitive decline amongst individuals free of extensive amyloidosis. The premise of this study is that structural brain changes, ranging from infarction to WMH, loss of white matter integrity and brain atrophy are extremely common with aging. Further, these changes are associated with cognitive decline and increased risk for dementia. Therefore, it is critically important to identify the extent and consequences of brain injury in the absence of extensive amyloid. To accomplish this goal, we will characterize non-amyloid related changes in brain structure and cognitive trajectories in a diverse group of older individuals. In so doing, we will advance understanding of the impact of vascular factors on brain structure and cognition that will provide new insights into the course of cognitive aging and susceptibility to future cognitive impairment in a community based, ethnically and racially diverse cohort.