Abstract
Background: Today, according to various studies, the gut microbiome is closely linked to various diseases such as cardiovascular disease, metabolic disorders, and neurological disorders like Alzheimer's disease (AD). Objectives: The primary purpose of this investigation was to evaluate the quality and quantity of the gut microbiota in a mouse model of AD. Methods: The mice were randomly divided into either an AD group injected with streptozotocin (STZ, 3 mg/kg) or a control group. After 16 - 17 days, the mice were evaluated for their memory capacity and learning, using the Morris water maze (MWM) and passive avoidance response tests. Specific primers were designed to target the 16S rRNA genes of Enterobacter, Clostridium, Lactobacillus, and Bifidobacterium species in the fecal samples of mice by real‐time PCR assay. Results: The MWM and passive avoidance tests confirmed that STZ caused AD in the mouse model. According to the results of real-time PCR assays, unlike Lactobacillus, Clostridium, and Enterobacter, the population of Bifidobacterium decreased significantly in mice after AD in day 28 (P < 0.05). In other words, mean difference of Bifidobacterium CFU between AD group in day 28 and control group was -5.680 (95% CI: -11.3826 to -0.0174). Conclusions: Restructuring the gut microbiota using personalized dietary approaches or targeted interventions aimed at beneficial microbiota can potentially modify the composition of microbial communities and their metabolic byproducts, offering novel therapeutic possibilities for AD.