Effect of Vortioxetine on Cognitive Functions in an Amyloid β1–42 induced Rat Model of Alzheimer's Disease

Aim: This study aimed to examine whether vortioxetine can improve cognitive performance in a rat model of Alzheimer’s disease induced through intrahippocampal administration of Amyloid-β1–42.Material and Methods: An experimental Alzheimer’s disease model was generated via stereotaxic bilateral injections of Amyloid-β1–42 into the hippocampus. Twenty-eight rats were randomly assigned to four groups (n=7 each): Group 1 (control) received only saline; Group 2 was administered beta-amyloid to establish the Alzheimer model; Group 3 received beta-amyloid plus donepezil (reference treatment); and Group 4 received beta-amyloid in combination with vortioxetine for 14 days. Cognitive function was assessed using the passive avoidance paradigm. Upon completion of behavioral evaluations, animals were euthanized, and their brains were collected for histopathological examination.Results: Median latency times in the passive avoidance task were: Group 1, 300 seconds (19.5–300); Group 2, 10.3 seconds (1–300); Group 3, 300 seconds (33.1–300); and Group 4, 300 seconds (8.9–300). Statistical testing revealed a significant difference among groups (p < 0.05). Group 4 exhibited the longest median latency. Groups 1, 3, and 4 showed significantly higher latency scores compared with Group 2. Histopathological findings demonstrated that vortioxetine reduced degenerative changes in hippocampal pyramidal neurons.Conclusion: This work represents the first experimental study to evaluate vortioxetine’s effects on cognition in an Amyloid-β1–42-induced Alzheimer model. The results suggest that vortioxetine may improve cognitive outcomes and may attenuate neuronal injury