血清β-淀粉样蛋白及可溶性糖基化终末产物受体与新诊断2型糖尿病患者认知功能损害的关系

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目的通过观察2型糖尿病患者血清β-淀粉样蛋白(Aβ)1-42、可溶性糖基化终末产物受体(sRAGE)水平变化,探讨2型糖尿病患者认知功能损害的可能机制。方法选取2014年3—12月于唐山工人医院内分泌二科诊断为2型糖尿病的患者66例为病例组,另同期选取本院体检中心体检健康者50例为对照组。采用自制调查表收集受试者临床资料,采用可重复的成套神经心理状态测量(RBANS)量表评价受试者认知功能,该量表包括即刻记忆、视觉广度、言语功能、注意力、延迟记忆5个分测验,根据受试者不同年龄查表转化为量表分,再统一转化为标准分。抽取受试者空腹肘静脉血5 ml,采用酶联免疫吸附(ELISA)法测定血清Aβ1-42及sRAGE水平。结果病例组RBANS量表即刻记忆、视觉广度、言语功能、注意力、延迟记忆评分及标准分均低于对照组,差异有统计学意义(P<0.05)。病例组Aβ1-42水平高于对照组,sRAGE水平低于对照组,差异均有统计学意义(P<0.05)。病例组患者年龄与RBANS量表各分测验评分及标准分均呈负相关(P<0.05);受教育年限与即刻记忆、视觉广度、注意力、延迟记忆评分及标准分呈正相关,与言语功能评分呈负相关(P<0.05);Aβ1-42水平与RBANS量表各分测验评分及标准分均呈负相关(P<0.05);sRAGE水平与即刻记忆、言语功能、注意力、延迟记忆评分及标准分呈正相关(P<0.05),与视觉广度评分无直线相关性(P>0.05)。调整年龄、受教育年限后,病例组患者Aβ1-42水平与即刻记忆、注意力、延迟记忆评分及标准分呈负相关(r=-0.464、-0.418、-0.384、-0.696,P<0.05);sRAGE水平与即刻记忆、延迟记忆评分及标准分呈正相关(r=0.422、0.394、0.566,P<0.05)。结论 2型糖尿病患者存在认知功能损害,其发生机制可能与血清Aβ1-42水平升高及sRAGE水平降低有关。 Objective To explore the possible mechanism of cognitive impairment in type 2 diabetic patients by observing the changes of serum amyloid β (Aβ) 1-42 and sRAGE levels in patients with type 2 diabetes mellitus. Methods 66 cases of type 2 diabetes mellitus diagnosed as type 2 diabetes in Tangshan Workers Hospital from March to December in 2014 were selected as case group. In the same period, 50 healthy subjects in our hospital were selected as control group. The subjects’ clinical data were collected using a self-made questionnaire, and the cognitive function was assessed using a repeatable set of neurological status measures (RBANS) scale, including immediate memory, visual breadth, speech function, attention, delay Memory 5 sub-test, according to the subjects of different ages look-up table into scores, then unified into standard points. Fasting elbow venous blood samples were drawn 5 ml, serum levels of Aβ1-42 and sRAGE were determined by enzyme-linked immunosorbent assay (ELISA). Results In the case group, RBANS scale immediate memory, visual breadth, verbal function, attention, delayed memory score and standard scores were lower than the control group, the difference was statistically significant (P <0.05). The level of Aβ1-42 in case group was higher than that in control group, and the level of sRAGE was lower than that in control group (P <0.05). There was a negative correlation between the age of the patients and the test score and the standard score of the RBANS scale (P <0.05). The years of education were positively correlated with immediate memory, visual breadth, attention, delayed memory score and standard scores, (P <0.05). The levels of Aβ1-42 were negatively correlated with the scores of the RBANS scale and the standard scores (P <0.05). The level of sRAGE correlated with immediate memory, verbal function, attention, delayed memory score (P <0.05). There was no linear correlation with visual breadth score (P> 0.05). After adjustment for age and years of education, Aβ1-42 levels were negatively correlated with immediate memory, attention, delayed memory score and standard scores (r = -0.464, -0.418, -0.384, -0.696, P <0.05) ; sRAGE level was positively correlated with immediate memory, delayed memory score and standard score (r = 0.422,0.394,0.566, P <0.05). Conclusion There is cognitive impairment in patients with type 2 diabetes mellitus, which may be related to the increase of serum Aβ1-42 level and the decrease of sRAGE level.
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