Preliminary Study On Changes Of Blood H₂S、BACE1and Aβ42in Diabetic Cognitive Dysfunction

Objective:To observe the association between diabetic cognitivedysfunction and blood H2S，BACE1，Aβ42.Method:Experimental subjects were divided into3groups: blankcontrol group, simple diabetes group, diabetic cognitive dysfunction group,20cases of each group. After demographic statistics，3groups weredetected concentration of H2S in sensitive sulphur electrode method andBACE1、Aβ42in ELISA method.Results:（1）The HbA1c of diabetic cognitive dysfunction group ishigher than the level of simple diabetes group, the difference wasstatistically significant (P<0.05).（2）Cognitive evaluation items of diabeticpatients with cognitive impairment were all lower, in which languageability and delay memory is significant (P<0.05).（3）The LDL、TC ofdiabetic cognitive dysfunction group is higher than the level of simplediabetes group(P<0.05), while its HDL is lower(P<0.05).（4）Theconcentration of H2S in simple diabetes group was significantly lowerthan those in blank control group (P<0.05), and the diabetic cognitivedysfunction group was significantly lower than simple diabetes group (P<0.05); the concentration of Aβ42、BACE1in simple diabetes group andblank control group showed no significant difference (P>0.05), but those indiabetic cognitive dysfunction group increased significantly (P<0.05).Conclusion: cognitive impairment of diabetics is mainly reflected inthe visual space and delayed memory. Poor blood glucose control，increasedLDL、TC，reduced HDL may be risk factors for cognitive dysfunction indiabetics. After exposure to those risk factors, impaired central nervoussystem IGF-1pathway caused down-regulation of H2S, which positiveeffecting on BACE1, up-regulating the expression of APP/Aβ metabolism,leading to the deposition of Aβ42, and resulted in diabetic cognitivedysfunction.