Cohen Ann D, Bruña Ricardo, Chang Yue-Fang, Cheng Yu, Doman Jack, Huppert Ted, Kim Tae, Maestu Fernando, Roush Rebecca E, Snitz Beth E, Becker James T
Department of Psychiatry, The University of Pittsburgh, Pittsburgh, PA, United States.
Department of Experimental Psychology, Universidad Complutense de Madrid, Pozuelo de Alarcón, Madrid, Spain.
Front Aging Neurosci. 2021 Oct 7;13:669490. doi: 10.3389/fnagi.2021.669490. eCollection 2021.
The natural history of Alzheimer's Disease (AD) includes significant alterations in the human connectome, and this disconnection results in the dementia of AD. The organizing principle of our research project is the idea that the expression of cognitive dysfunction in the elderly is the result of two independent processes - the neuropathology associated with AD, and second the neuropathological changes of cerebrovascular disease. Synaptic loss, senile plaques, and neurofibrillary tangles are the functional and diagnostic hallmarks of AD, but it is the structural changes as a consequence of vascular disease that reduce brain reserve and compensation, resulting in an earlier expression of the clinical dementia syndrome. This work is being completed under the auspices of the Human Connectome Project (HCP). We have achieved an equal representation of Black individuals (vs. White individuals) and enrolled 60% Women. Each of the participants contributes demographic, behavioral and laboratory data. We acquire data relative to vascular risk, and the participants also undergo amyloid imaging, and magnetoencephalography (MEG). All of the data are publicly available under the HCP guidelines using the Connectome Coordinating Facility and the NIMH Data Archive. Locally, we use these data to address specific questions related to structure, function, AD, aging and vascular disease in multi-modality studies leveraging the differential advantages of magnetic resonance imaging (MRI), functional magnetic resonance imaging (fMRI), MEG, and beta amyloid imaging.
阿尔茨海默病（AD）的自然病程包括人类连接组的显著改变，这种连接中断导致了AD痴呆。我们研究项目的组织原则是，老年人认知功能障碍的表现是两个独立过程的结果——与AD相关的神经病理学，以及脑血管疾病的神经病理学变化。突触丧失、老年斑和神经原纤维缠结是AD的功能和诊断标志，但正是血管疾病导致的结构变化降低了大脑储备和代偿能力，从而导致临床痴呆综合征的更早表现。这项工作是在人类连接组计划（HCP）的支持下完成的。我们实现了黑人个体（与白人个体相比）的平等参与，并招募了60%的女性。每位参与者都提供人口统计学、行为学和实验室数据。我们获取与血管风险相关的数据，参与者还接受淀粉样蛋白成像和脑磁图（MEG）检查。所有数据都根据HCP指南，通过连接组协调设施和美国国立精神卫生研究所数据存档公开提供。在本地，我们利用这些数据，在多模态研究中解决与结构、功能、AD、衰老和血管疾病相关的具体问题，充分利用磁共振成像（MRI）、功能磁共振成像（fMRI）、MEG和β淀粉样蛋白成像的不同优势。
