Diabetes, Prediabetes, and Brain Volumes and Subclinical Cerebrovascular Disease on MRI: The Atherosclerosis Risk in Communities Neurocognitive Study (ARIC-NCS).
Diabetes, Prediabetes, and Brain Volumes and Subclinical Cerebrovascular Disease on MRI: The Atherosclerosis Risk in Communities Neurocognitive Study (ARIC-NCS).
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DOI：
10.2337/dc17-1185
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发表时间：
2017-11
期刊：
影响因子：
16.2
通讯作者：
Gottesman RF
中科院分区：
文献类型：
--
作者：
Schneider ALC;Selvin E;Sharrett AR;Griswold M;Coresh J;Jack CR Jr;Knopman D;Mosley T;Gottesman RF
旨在通过脑 MRI 检查糖尿病前期、糖尿病和糖尿病严重程度（通过 HbA1c 和糖尿病持续时间评估）与脑容量和血管病理学的关联，并评估糖尿病与脑容量的关联是否由脑血管病理学介导。对 1,713 名社区神经认知动脉粥样硬化风险研究 (ARIC-NCS) 参与者（平均年龄 75 岁，60% 女性，27% 黑人，30% 糖尿病前期，35% 糖尿病）进行的横断面研究，这些参与者在 2011 年至 2013 年期间接受了 3T 脑部 MRI 扫描。根据糖尿病-HbA1c 状态将参与者分为无糖尿病（<5.7% [参考]）、糖尿病前期（5.7% 至 <6.5%）和糖尿病（[定义为既往诊断或 HbA1c ≥6.5%] <7.0% 与 ≥7.0%），并根据糖尿病病程进一步分层（<10 年与 ≥10 年）。在调整分析中，与非糖尿病且 HbA1c <5.7% 的参与者相比，糖尿病前期和糖尿病且 HbA1c <7.0% 的参与者的脑容量或血管病理学没有显着差异（均 P > 0.05），但患有糖尿病且 HbA1c ≥7.0% 的参与者的总脑容量较小（β -0.20 SDs，95% CI） -0.31，-0.09），区域脑体积较小（包括额叶、颞叶、枕叶和顶叶；深部灰质；阿尔茨海默病特征区域；和海马体[所有 P < 0.05]），以及白质高信号（WMH）负担增加（P = 0.016）。在糖尿病患者中，与 HbA1c <7.0% 的患者相比，HbA1c ≥7.0% 的患者总脑容量和区域脑容量较小，WMH 负担增加（均 P < 0.05）。同样，与糖尿病病程<10年的参与者相比，糖尿病病程较长（≥10年）的参与者脑容量较小，腔隙负担较高（均P<0.05）。通过结构方程模型，我们没有发现 WMH 在糖尿病与脑容量较小之间发挥中介作用的证据（所有 P > 0.05）。较严重的糖尿病（定义为较高的 HbA1c 和较长的病程）与脑体积较小和脑血管病理负担增加相关，但糖尿病前期或较轻的糖尿病则不然。没有证据表明糖尿病与脑容量较小的关联是由脑血管病理学介导的，这表明其他机制可能是造成这些关联的原因。
To examine the associations of prediabetes, diabetes, and diabetes severity (as assessed by HbA1c and diabetes duration) with brain volumes and vascular pathology on brain MRI and to assess whether the associations of diabetes with brain volumes are mediated by brain vascular pathology. Cross-sectional study of 1,713 participants in the Atherosclerosis Risk in Communities Neurocognitive Study (ARIC-NCS) (mean age 75 years, 60% female, 27% black, 30% prediabetes, and 35% diabetes) who underwent 3T brain MRI scans in 2011–2013. Participants were categorized by diabetes-HbA1c status as without diabetes (<5.7% [reference]), with prediabetes (5.7 to <6.5%), and with diabetes ([defined as prior diagnosis or HbA1c ≥6.5%] <7.0% vs. ≥7.0%), with further stratification by diabetes duration (<10 vs. ≥10 years). In adjusted analyses, compared with participants without diabetes and HbA1c <5.7%, participants with prediabetes and those with diabetes and HbA1c <7.0% did not have significantly different brain volumes or vascular pathology (all P > 0.05), but those with diabetes and HbA1c ≥7.0% had smaller total brain volume (β −0.20 SDs, 95% CI −0.31, −0.09), smaller regional brain volumes (including frontal, temporal, occipital, and parietal lobes; deep gray matter; Alzheimer disease signature region; and hippocampus [all P < 0.05]), and increased burden of white matter hyperintensities (WMH) (P = 0.016). Among participants with diabetes, those with HbA1c ≥7.0% had smaller total and regional brain volumes and an increased burden of WMH (all P < 0.05) compared with those with HbA1c <7.0%. Similarly, participants with longer duration of diabetes (≥10 years) had smaller brain volumes and higher burden of lacunes (all P < 0.05) than those with a diabetes duration <10 years. We found no evidence for mediation by WMH in associations of diabetes with smaller brain volumes by structural equation models (all P > 0.05). More-severe diabetes (defined by higher HbA1c and longer disease duration) but not prediabetes or less-severe diabetes was associated with smaller brain volumes and an increased burden of brain vascular pathology. No evidence was found that associations of diabetes with smaller brain volumes are mediated by brain vascular pathology, suggesting that other mechanisms may be responsible for these associations.
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16.2
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