Probiotics improve insulin resistance status in an experimental model of Alzheimer’s disease

Background: Nowadays, Alzheimer’s disease (AD) is considered as Type 3 diabetes in which insulin resistance is the common cause of both diseases. Disruption of insulin signaling cascade and insulin resistance can induce AD; and central insulin resistance causes systemic alterations in serum insulin, FBS levels, and lipid profile. Studies have shown that probiotics (Lactobacillus and Bifidobacterium species) can be used as a nutritional approach to improve these metabolic changes. We assessed the probiotic effect (4 species of Lactobacillus and Bifidobacterium) on insulin resistance biomarkers in an experimental model of AD. Methods: A total of 60 rats were divided into 5 groups: (1) a control group without surgical and dietary intervention; (2) a controlprobiotics group receiving probiotics for 8 weeks, but not receiving any surgical intervention; (3) a group receiving a sham operation in which PBS was injected intrahippocampus but without dietary intervention; (4) an Alzheimer group for which Amyloid-ß (Aß) 1- 42 was injected intrahippocampus but without dietary intervention; (5) and an Alzheimer-probiotics group for which Aß1-42 was injected intrahippocampus and given 2g probiotics for 8 weeks. The FBS levels and lipid profile were measured by a calorimetric method, insulin levels were detected by an ELISA kit, and HOMA-IR was calculated using a formula. ANOVA (one way analysis of variance followed by Bonferroni comparisons post hoc) was used to compare all the variables between groups. Results: Serum glucose, insulin levels, and HOMA-IR index increased in the Alzheimer group compared to the control (p<0.001), while probiotics decreased only insulin level and HOMA-IR index in AP group compared to Alzheimer group (p<0.001). Also, TG levels increased in the Alzheimer group (p<0.001), but no significant difference was detected between Alzheimer and Alzheimerprobiotics group. Conclusion: It seems that probiotics play an effective role in controlling glycemic status of Alzheimer’s disease.