Danis AYGUN, Mehmet Bulent OZDEMIR, Nuriye KURBETLI
Marmara Medical Journal - 2026;39(2):131-139
Objective: Alzheimer's disease is the most common cause of age-related dementia. This disease is a progressive, degenerative central nervous system disease. Neuron loss is more pronounced in hippocampal pyramidal cells. Although various agents are known for its treatment, a stronger or definitive treatment has not yet been found. Alzheimer's disease is seen in more than half of diabetes mellitus patients. The main similarities between these two diseases are insulin resistance and inflammatory pathways. Therefore, Alzheimer's disease is also called type 3 diabetes. The antidiabetic effect of Ocimum gratissimum (O. gratissimum) extract, commonly known as basil extract are well documented worldwide. However, its behavioral and neuroprotective effects in Alzheimer's disease have not been sufficiently studied yet. Our aim is to demonstrate the anti-apoptotic effect of O. gratissimum on hippocampal pyramidal cells in an experimental rat model of Alzheimer's disease induced by streptozotocin (STZ) and in paralel, to test learning-related behaviors in rats. Materials and Methods: Thirty-three 4-month-old male Wistar rats were used and randomly divided into five groups: control, sham, STZ, O. gratissimum , and O. gratissimum +STZ. The eight-arm radial maze test was taught to all animals that were kept under suitable conditions. Finally, STZ and O. Gratissimum extract were given to rats together intraperitoneally. Blood glucose and the weight of all rats were measured regularly. After the eight-arm radial maze test was performed on the rats in all groups, the rats were decapitated, their brains were sectioned by histological methods, and all apoptotic cells in the hippocampus were counted with TUNEL method. All groups were compared by statistical analysis (ANOV A). Results: In rats whose learning was impaired with STZ, learning behavior improved in a statistically significant way with O. gratissimum extract (p <0.05). In parallel, O. gratissimum significantly reduced neuron loss in CA1, CA2, and CA3 areas of hippocampus when compared to STZ (p <0.05). Behavioral tests show that STZ and O. gratissimum have effects on apoptosis in the brain, especially in the hippocampus. There are also studies in parallel with our study showing that O. gratissimum reduces neuronal atrophy in the CA3 region. In our study, it was observed that the number of apoptotic cells was higher in the STZ group, and there was a corrective effect in the O. gratissimum added group. Conclusion: As a result, O. gratissimum extract showed a neuroprotective effect against the loss of hippocampal neurons caused by STZ, similar to that observed in Alzheimer's disease, and maintained learning behavior accordingly. This study may be an important resource for future molecular and clinical studies on the use of O. gratissimum extract in Alzheimer's disease.
