INVESTIGATION OF THE RELATIONSHIP BETWEEN NEUROGENESIS AND METABOLIC PARAMETERS IN THE STREPTOZOTOCIN-INDUCED ALZHEIMER'S DISEASE MODEL

Gul Sahika GOKDEMIR, Beran YOKUS

Medical Records - 2026;8(1):1-8

Mardin Artuklu University, Faculty of Medicine, Department of Physiology, Mardin

 

Aim: In this study, we aimed to analyze the interactions between neuroplasticity-related proteins (DCX, EGR1, sFRP3) and metabolic markers (insulin, HbA1c, asprosin) in an STZ-induced Alzheimer's disease model, as well as to evaluate how changes in these parameters affect the pathophysiology of Alzheimer's disease (AD). Material and Methods: 14 male Wistar albino rats, aged 8-10 weeks, weighing 250-300 grams, were used. The animals were randomly assigned to two groups: AD group (n=7) and control group (n=7). The AD model was created by stereotaxic injection of STZ, and the control group was injected with artificial CSF. The animals were monitored for fourteen days after surgery. At the end of the study, serum samples were collected and DCX, EGR1, sFRP3, insulin, gHbA1c, and asprosin levels were analyzed by ELISA. The variables were compared between the groups, and P-values < 0.05 were considered significant. Results: DCX (p=0.056) and EGR1 (p=0.080) levels showed borderline changes without statistical significance, while sFRP3 levels were significantly higher in the AD group (p=0.012). Insulin levels did not differ (p=0.829), but asprosin and gHbA1c levels were significantly higher (p=0.046 and p= 0.000, respectively), indicating metabolic derangement. Correlation analysis showed strong positive correlations between asprosin and gHbA1c (r=0.807, p<0.01) and sFRP3 and EGR1 (r=0.780, p<0.01), suggesting interconnected roles in AD pathophysiology. Conclusion: The findings of our study indicate that both neuroplastic and metabolic parameters are impaired in the STZ-induced Alzheimer's model and that there may be potential interactions between these two systems. Our study has shown the necessity of further investigating the complex relationships between neuroinflammation, metabolic dysregulation and synaptic plasticity in the pathophysiology of AD.