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In the second study (28), cognitive function was assessed by the Cognitive Failure Questionnaire, which is a cognitive test that has been shown to have limitations for the study of cognitive aging and that is not considered to be a reliable test for measuring cognitive function (40, 41). IOX1 in vivo Thus, five RCTs were considered for the meta-analysis. For one (13) of these, more information was requested from the authors in order to be able to use the data in the meta-analysis in another form than the one provided in the publication. Figure 1 Flowchart of study identification, inclusion and exclusion. Table 1 shows the characteristics extracted from the included trials. These trials included a total of 12?165 participants randomised in intensive groups and 12?132 randomised in standard groups, with sample sizes in individual studies ranging from 135 to 10?320 participants. Baseline mean age of participants at randomisation across studies ranged from 59 to 70 years. The duration of type 2 diabetes mellitus at baseline ranged from 5.4 to 10.8 years, except for one study which included patients with screen-detected type 2 diabetes mellitus (15). Three trials selected participants with a higher risk of cardiovascular events (13, 14, 16). Another trial included elderly patients who were 70 years old on average at randomisation with a relatively well-controlled diabetes (29). In one of the five trials (13), cognition was not a primary outcome. Follow-up periods ranged from 3.3 to 6.2 years. Table 1 Characteristics of the five included studies. In four trials, patients receiving intensive treatment showed similar rates of cognitive decline to those assigned to standard treatment. Oxygenase Only one RCT showed that intensive therapy compared with standard therapy was associated with a slower rate of cognitive decline. Figure 2 shows the forest plot of the effect of intensive glycaemic control on the rate of cognitive decline compared with standard glycaemic control. There was no statistical difference between intensive and standard glycaemic control, and significant heterogeneity was found (SDM 0.02; 95% CI=?0.03 to 0.08; I 2=68%, see more P for heterogeneity=0.01). Figure 2 The effect of intensive vs standard glycaemic control on cognitive decline in type 2 diabetic patients. In sensitivity analysis, the effect of intensive glycaemic control in reducing cognitive decline was assessed based on HbA1c target in the intervention group at baseline. No difference was reported in two trials with HbA1c target below 7% in the intervention group and in three trials with HbA1c target of 7% or higher. Figure 3 shows pooled results of cognitive decline in patients with intensive HbA1c of