RAGE and AGEs in Mild Cognitive Impairment of Diabetic Patients: A Cross-Sectional Study.
RAGE and AGEs in Mild Cognitive Impairment of Diabetic Patients: A Cross-Sectional Study.
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RAGE 和 AGE 在糖尿病患者轻度认知障碍中的作用：一项横断面研究
DOI：
10.1371/journal.pone.0145521
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发表时间：
2016
期刊：
影响因子：
3.7
通讯作者：
Wang S
中科院分区：
文献类型：
--
作者：
Wang P;Huang R;Lu S;Xia W;Cai R;Sun H;Wang S
晚期糖基化终末产物（AGE；RAGE）的受体与 AGE 和淀粉样β 肽结合。 RAGE 与 2 型糖尿病和阿尔茨海默病的慢性并发症有关。我们的目的是研究 RAGE、AGEs 和 RAGE Gly82Ser 多态性在 2 型糖尿病患者轻度认知障碍 (MCI) 中的作用。在招募的 167 名住院 2 型糖尿病患者中，82 名满足 MCI 的诊断标准，85 名匹配的对照个体被归类为非 MCI。收集人口统计数据，并检查可溶性RAGE（sRAGE）浓度、血清AGE-肽（AGE-P）水平、RAGE Gly82Ser基因型和神经心理学测试结果。与对照组相比，MCI组sRAGE水平降低（0.87±0.35 vs. 1.05±0.52 ng/ml，p<0.01），血清AGE-P水平升高（3.54±1.27 vs. 2.71±1.18 U/ml，p<0.01）。 Logistic回归分析表明，sRAGE浓度每降低一个单位，2型糖尿病患者的MCI风险就会增加54%（OR 0.46[95% CI 0.22-0.96]，p = 0.04），AGE-P水平每增加一个单位，2型糖尿病患者的MCI风险就会增加72%（OR 1.72[95% CI 1.31-2.28]，p = 0.04）。 p<0.01）。血清sRAGE水平与试验B（TMT-B）得分呈负相关（r = -0.344，p = 0.002），这表明与糖尿病相关的早期认知缺陷。此外，AGE-P水平与多个认知领域呈正相关（均p<0.05）。不同 RAGE 基因型之间的神经心理学测试结果或血清 RAGE 浓度或 MCI 组和对照组之间的 RAGE 基因型频率没有显着差异（均 p>0.05）。 RAGE 通路部分介导糖尿病患者中 AGE 诱导的 MCI。血清AGE-P水平可能作为这些个体MCI的血清生物标志物，而sRAGE代表2型糖尿病患者早期认知能力下降的预测因子，甚至是潜在的干预目标。高级糖基化终产物诱导糖尿病认知障碍：BDNF 信号介导的海马神经发生 ChiCTR-OCC-15006060
Receptor for advanced glycation end products (AGEs; RAGE) binds to both AGEs and amyloid-beta peptides. RAGE is involved in chronic complications of type 2 diabetes and Alzheimer’s disease. We aimed to investigate the roles of RAGE, AGEs and the Gly82Ser polymorphism of RAGE in mild cognitive impairment (MCI) among type 2 diabetes patients. Of the 167 hospitalized type 2 diabetes patients recruited, 82 satisfied the diagnostic criteria for MCI, and 85 matched control individuals were classified as non-MCI. Demographic data were collected, and the soluble RAGE (sRAGE) concentrations, serum AGE-peptide (AGE-P) levels, RAGE Gly82Ser genotype and neuropsychological test results were examined. The MCI group exhibited a decreased sRAGE level (0.87±0.35 vs. 1.05±0.52 ng/ml, p<0.01) and an increased serum AGE-P level (3.54±1.27 vs. 2.71±1.18 U/ml, p<0.01) compared with the control group. Logistic regression analysis indicated that each unit reduction in the sRAGE concentration increased the MCI risk by 54% (OR 0.46[95% CI 0.22–0.96], p = 0.04) and that each unit increase in the AGE-P level increased the MCI risk by 72% in the type 2 diabetes patients (OR 1.72[95% CI 1.31–2.28], p<0.01). The serum sRAGE level was negatively correlated with the score on the trail making test-B (TMT-B) (r = -0.344, p = 0.002), which indicates early cognitive deficits related to diabetes. Moreover, the AGE-P level was positively correlated with multiple cognitive domains (all p<0.05). No significant differences in the neuropsychological test results or serum RAGE concentrations between the different RAGE genotypes or in the RAGE genotype frequencies between the MCI and control groups were identified (all p>0.05). The RAGE pathway partially mediates AGE-induced MCI in diabetic patients. The serum AGE-P level may serve as a serum biomarker of MCI in these individuals, and sRAGE represents a predictor and even a potential intervention target of early cognitive decline in type 2 diabetes patients. Advanced Glycation End Products Induced Cognitive Impairment in Diabetes: BDNF Signal Meditated Hippocampal Neurogenesis ChiCTR-OCC-15006060