Interaction of APOE e4 and poor glycemic control predicts white matter hyperintensity growth from 73 to 76.
Interaction of APOE e4 and poor glycemic control predicts white matter hyperintensity growth from 73 to 76.
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DOI：
10.1016/j.neurobiolaging.2017.02.014
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发表时间：
2017-06
影响因子：
4.2
通讯作者：
Deary IJ
中科院分区：
文献类型：
--
作者：
Cox SR;Ritchie SJ;Dickie DA;Pattie A;Royle NA;Corley J;Aribisala BS;Harris SE;Valdés Hernández M;Gow AJ;Muñoz Maniega S;Starr JM;Bastin ME;Wardlaw JM;Deary IJ
我们研究了载脂蛋白E(APOE)状态是否与血管风险因素(VRF)相互作用，以预测老年痴呆风险增加时脑部MRI扫描上白质高信号(WMH)的进展。在73岁时，通过自我报告的糖尿病、高血压、吸烟和高胆固醇血症病史，以及通过客观测量血液HbA1c、体重指数、舒张压和收缩压以及血液高密度脂蛋白与总胆固醇(HDL)的比率来评估基线VRF。ApoE e4等位基因编码为存在或不存在。在同一年出生的队列中，434名老年人在3年多的时间里通过MRI测量了WMH的进展。有糖尿病自我诊断的载脂蛋白E e4携带者(β=0.160，p=0.002)或糖化血红蛋白水平较高(β=0.114，p=0.014)的携带者表现出更大的WMH进展，前者在多次检测的校正后存活。所有其他apoe-vrf交互作用均不显著(β交互作用0.056，p>；0.228)。结果表明，携带载脂蛋白E“风险”e4等位基因的人，在八十岁的早期阶段，如果血糖控制较差，则会增加与年龄相关的WMH进展的风险。这种相互作用对共同发生的VRF的影响很强，这表明这可能是缓解这个年龄段大脑和认知衰老的一个目标。
We examined whether apolipoprotein E (APOE) status interacts with vascular risk factors (VRFs) to predict the progression of white matter hyperintensities (WMHs) on brain MRI scans over a specific period of life in older age when the risk of dementia increases. At age 73 years, baseline VRFs were assessed via self-reported history of diabetes, hypertension, smoking, and hypercholesterolemia, and via objective measures of blood HbA1c, body mass index, diastolic and systolic blood pressure, and blood high-density lipoprotein to total cholesterol (HDL) ratio. APOE e4 allele was coded as either present or absent. WMH progression was measured on MRI over 3 years in 434 older adults, in a same-year-of-birth cohort. APOE e4 carriers with either a self-reported diagnosis of diabetes (β = 0.160, p = 0.002) or higher glycated hemoglobin levels (β = 0.114, p = 0.014) exhibited greater WMH progression, and the former survived correction for multiple testing. All other APOE-VRF interactions were nonsignificant (βinteraction < 0.056, p > 0.228). The results suggest that carrying the APOE “risk” e4 allele increases the risk of greater age-related WMH progression over the early part of the eighth decade of life, when combined with poorer glycemic control. The interaction effect was robust to co-occurring VRFs, suggesting a possible target for mitigating brain and cognitive aging at this age.