Morphometric analysis of the effects of cortexin on the brain cortex of alzheimer's model rats

Alzheimer's Disease (AD) is a disease characterized by progressive cognitive decline, causing memory impairment, attention deficit and loss of balance in the early stages. Scopolamine (SCP)-induced amnesia is a widely used experimental model to study dementia-related disorders such as AD. This study aimed to examine the morphometric and histopathological effects of Cortexin® (Koptekcnh; Geropharm pharmaceutical company, Saint Petersburg, Russia), which is known to have neuroprotective effects, on AD rat brain tissue. In this study, 28 Sprague Dawley rats were divided into 4 equal groups. The control group received 2 ml/kg saline intraperitoneally (i.p.) every day. In the AD group, 2 mg/kg SCP [Skopolamin hidrobromür, Sigma-Aldrich Chemical Co.'dan (St Louis, MO, USA)] was dissolved in 2 ml saline and given i.p , the treatment group received 2 mg/kg SCP, and 2 mg/kg Cortexin® (Koptekcnh; Geropharm pharmaceutical company, Saint Petersburg, Russia) dissolved in 2 ml saline i.p.; Cortexin group received 2 mg/kg Cortexin dissolved in 2ml saline i.p every day. The volumes of cortex cerebri areas and cerebellum in rats were measured stereologically. MDA, TAS, TOS, Serotonin, Dopamine in serum; Caspase-3, Serotonin, Dopamine, pTAU, Cortactin Binding Protein 2 (CTTNBP2) values were examined in the tissue. While the volumes of many anatomical areas, including the cerebellum, hippocampus, and amygdala, decreased in the AH group compared to the control group, a significant increase was observed in the AH+C group compared to the AH group. According to the analysis results, while serum MDA and TOS levels increased in the AH group; TAS, Serotonin and Dopamine levels decreased. While pTAU, Caspase-3 immunoreactivity increased in the tissue, Serotonin, Dopamine and CTTNBP2 immune reactivity decreased. These data; It shows that Cortexin has an antioxidant and neuroprotective effect on the brain and cerebellum tissue in AD. We believe that our findings will contribute to the clinic and the literature with more comprehensive studies on AD and Cortexin.