Warren Alpert Medical School of Brown University, Providence, Rhode Island, USA.
Center for Biomedical Informatics, Brown University, Providence, Rhode Island, USA.
J Neuroimaging. 2022 Nov;32(6):1075-1079. doi: 10.1111/jon.13055. Epub 2022 Sep 23.
Subtle cognitive decline represents a stage of cognitive deterioration in which pathological biomarkers may be present, including early cortical atrophy and amyloid deposition. Using individual items from the Montreal Cognitive Assessment and k-modes cluster analysis, we previously identified three clusters of individuals without overt cognitive impairment: (1) High Performing (no deficits in performance), (2) Memory Deficits (lower memory performance), and (3) Compound Deficits (lower memory and executive function performance). In this study, we sought to understand the relationships found in our clusters between cortical atrophy on MR and amyloid burden on PET.
Data were derived from the Alzheimer's Disease Neuroimaging Initiative and comprised individuals from our previous analyses with available MR and amyloid PET scans (n = 272). Using multiple-group structural equation modeling, we regressed amyloid standardized uptake value ratio on volumetric regions to simultaneously evaluate unique associations within each cluster.
In our Compound Deficits cluster, greater whole cerebral amyloid burden was significantly related to right entorhinal cortical and left hippocampal atrophy, r = -.412 (p = .005) and -.304 (p = .049), respectively. Within this cluster, right entorhinal cortical atrophy was significantly related to greater amyloid burden within multiple frontal regions.
The Compound Deficits cluster, which represents a group potentially at higher risk for decline, was observed to have significantly more cortical atrophy, particularly within the entorhinal cortex and hippocampus, associated with whole brain and frontal lobe amyloid burden. These findings point to a pattern of early pathological deterioration that may place these individuals at risk for future decline.
轻微认知衰退代表认知恶化的一个阶段，在此阶段可能存在病理生物标志物，包括早期皮质萎缩和淀粉样蛋白沉积。使用蒙特利尔认知评估的单个项目和 k-模式聚类分析，我们之前确定了三个没有明显认知障碍的个体集群：（1）表现良好（无表现缺陷），（2）记忆缺陷（记忆表现较低），和（3）复合缺陷（记忆和执行功能表现较低）。在这项研究中，我们试图了解我们的聚类中在 MR 上的皮质萎缩和在 PET 上的淀粉样蛋白负担之间发现的关系。
数据来自阿尔茨海默病神经影像学倡议，包括我们之前的分析中具有可用的 MR 和淀粉样蛋白 PET 扫描的个体（n=272）。使用多组结构方程模型，我们回归了淀粉样蛋白标准化摄取比值与容积区域，以同时评估每个聚类中的独特关联。
在我们的复合缺陷集群中，更大的全脑淀粉样蛋白负担与右侧内嗅皮质和左侧海马萎缩显著相关，r=-.412（p=.005）和-.304（p=.049）。在这个集群中，右侧内嗅皮质萎缩与多个额叶区域的更大淀粉样蛋白负担显著相关。
复合缺陷集群，代表一个潜在风险更高的群体，被观察到有显著更多的皮质萎缩，特别是在内嗅皮质和海马体中，与全脑和额叶淀粉样蛋白负担相关。这些发现表明存在早期病理恶化的模式，这可能使这些个体面临未来衰退的风险。
