Effect of C-peptide on Cognitive Dysfunction and Neuronal Apoptosis Caused by beta amyloid 1-42 in Diabetic Rats

Alzheimer disease is characterized by a progressive loss of memory. Its prevalence in diabetic patients is nearly twice in comparison of others. Recent findings suggest that C-peptide replacement in type 1 diabetes exerts beneficial effects on diabetic rats. We examined the effects of C-peptide on cognitive dysfunction and neuronal apoptosis caused by Aβ 1-42 on working memory in Streptozotocin induced diabetic rats. In the present experimental study which was carried out in 2009 at Shiraz University of Medical Sciences, 50 male Sprague Dawley rats (230-300 gr) were divided into five groups: control, type 1 diabetic, diabetic groups receiving C-peptide, diabetic group receiving beta amyloid, diabetic group receiving beta amyloid and c-peptide. The Neuronal apoptosis were assessed with tunnel staining. Diabetes was induced with IV injection of Streptozotocin (60 mg/kg). Twenty six days after the onset of diabetes, behavioral tests were conducted for three days. For data analysis, the Tukey and One way ANOVA tests were used. In comparison to control group, in all diabetic groups working memory impairments was observed (P<0.05), but Aβ 1-42 caused severe deficits in the working memory (P<0.001) and C-peptide could significantly decrease the impairment (P<0.05). Only the diabetic beta amyloid group showed significant amount of tunnel positive neuron (P<0.05) and c-peptide replacement significantly decreased the amount of these cells (P<0.05). C-peptide could significantly decrease memory impairment and neuronal apoptosis among diabetic rats.