背景:内嗅皮层(EC)和irirhinal皮层(PC)易受阿尔茨海默病的影响。触发因素可能是血管功能障碍和tau病理的相互作用。
方法:我们用7T磁共振成像和手动标记的个体血管在100μm3的死后人体组织成像(平均=270片/例)。每个EC子场量化和比较血管密度,在EC和PC之间,与tau和TARDNA结合蛋白43(TDP-43)半定量评分有关。
结果:PC的血管化比EC的血管化程度更高,并且EC后区的血管密度更高。Tau和TDP-43与血管密度密切相关,临床前阶段严重tau的亚区域的血管密度明显高于tau负荷低的亚区域。
结论:这些数据影响脑血管图,子场脉管系统的量化,以及早期血管和病理的相关性。血管密度的有序关联,和tau或TDP-43病理,可以在预测性上下文中利用。
结论:血管密度与内嗅和旁嗅皮层磷酸化tau(p-tau)负荷相关。在阿尔茨海默病的临床前期,毛囊区35和后部内嗅皮质显示出最大的p-tau负荷,但血管密度也最高。我们结合了离体磁共振成像模型和组织病理学,以证明皮质内血管的3D重建及其与病理的空间关系。
The entorhinal cortex (EC) and perirhinal cortex (PC) are vulnerable to Alzheimer\'s disease. A triggering factor may be the interaction of vascular dysfunction and tau pathology.
We imaged post mortem human tissue at 100 μm3 with 7 T magnetic resonance imaging and manually labeled individual blood vessels (mean = 270 slices/case). Vessel density was quantified and compared per EC subfield, between EC and PC, and in relation to tau and TAR DNA-binding protein 43 (TDP-43) semiquantitative scores.
PC was more vascularized than EC and vessel densities were higher in posterior EC subfields. Tau and TDP-43 strongly correlated with vasculature density and subregions with severe tau at the preclinical stage had significantly greater vessel density than those with low tau burden.
These data impact cerebrovascular maps, quantification of subfield vasculature, and correlation of vasculature and pathology at early stages. The ordered association of vessel density, and tau or TDP-43 pathology, may be exploited in a predictive context.
Vessel density correlates with phosphorylated tau (p-tau) burden in entorhinal and perirhinal cortices. Perirhinal area 35 and posterior entorhinal cortex showed greatest p-tau burden but also the highest vessel density in the preclinical phase of Alzheimer\'s disease. We combined an ex vivo magnetic resonance imaging model and histopathology to demonstrate the 3D reconstruction of intracortical vessels and its spatial relationship to the pathology.