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载脂蛋白 E4 修饰认知健康成年人海马结构与肥胖相关的萎缩。

Apolipoprotein ε4 modifies obesity-related atrophy in the hippocampal formation of cognitively healthy adults.

机构信息

Cardiff University Brain Research Imaging Centre (CUBRIC), School of Psychology, Cardiff University, Maindy Road, Cardiff, UK.

Psychological Medicine and Clinical Neurosciences, School of Medicine, Cardiff University, Cardiff, UK.

出版信息

Neurobiol Aging. 2022 May;113:39-54. doi: 10.1016/j.neurobiolaging.2022.02.004. Epub 2022 Feb 18.

DOI:10.1016/j.neurobiolaging.2022.02.004
PMID:35303671
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9084919/
Abstract

Characterizing age- and risk-related hippocampal vulnerabilities may inform about the neural underpinnings of cognitive decline. We studied the impact of three risk-factors, Apolipoprotein (APOE)-ε4, a family history of dementia, and central obesity, on the CA1, CA2/3, dentate gyrus and subiculum of 158 cognitively healthy adults (38-71 years). Subfields were labelled with the Automatic Segmentation of Hippocampal Subfields and FreeSurfer (version 6) protocols. Volumetric and microstructural measurements from quantitative magnetization transfer and Neurite Orientation Density and Dispersion Imaging were extracted for each subfield and reduced to three principal components capturing apparent myelin/neurite packing, size/complexity, and metabolism. Aging was associated with an inverse U-shaped curve on myelin/neurite packing and affected all subfields. Obesity led to reductions in myelin/neurite packing and size/complexity regardless of APOE and family history of dementia status. However, amongst individuals with a healthy Waist-Hip-Ratio, APOE ε4 carriers showed lower size/complexity than non-carriers. Segmentation protocol type did not affect this risk pattern. These findings reveal interactive effects between APOE and central obesity on the hippocampal formation of cognitively healthy adults.

摘要

描述年龄和风险相关的海马脆弱性可以为认知能力下降的神经基础提供信息。我们研究了三个风险因素(载脂蛋白 E4、痴呆家族史和中心性肥胖)对 158 名认知健康成年人(38-71 岁)的 CA1、CA2/3、齿状回和下托的影响。使用自动分割海马亚区和 FreeSurfer(版本 6)协议对亚区进行标记。从定量磁化传递和神经丝取向密度和分散成像中提取每个亚区的容积和微观结构测量值,并将其简化为三个主成分,以捕获明显的髓鞘/神经丝包裹、大小/复杂性和代谢。衰老与髓鞘/神经丝包裹的倒 U 形曲线相关,并影响所有亚区。肥胖导致髓鞘/神经丝包裹和大小/复杂性降低,而与 APOE 和痴呆家族史无关。然而,在具有健康腰臀比的个体中,APOE ε4 携带者的大小/复杂性低于非携带者。分割协议类型不会影响这种风险模式。这些发现揭示了 APOE 和中心性肥胖对认知健康成年人海马结构的相互作用。

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