Effects of TFG-β1 on Aβ-40 and α- β- γ Secretase Expression in Hippocampus and Prefrontal Cortex in Experimental Alzheimer's Diseases


Creative Commons License

Kara S., Özandaç Polat S., Akıllıoğlu K., Şaker D., Evlice A. T., Sencar L., ...More

16TH NATIONAL AND 2ND INTERNATIONAL CONGRESS OF HISTOLOGY AND EMBRYOLOGY, Sakarya, Turkey, 26 - 28 September 2024, pp.54-55

  • Publication Type: Conference Paper / Summary Text
  • City: Sakarya
  • Country: Turkey
  • Page Numbers: pp.54-55
  • Çukurova University Affiliated: Yes

Abstract

            Introduction: Alzheimer's disease (AD) is a chronic complex neurodegenerative disease characterized amyloid plaques and neurofibrillary tangle formation, loss of neurons and synapses, and marked atrophy in the brain. Transforming growth factor β1 (TGF-β1) is an important growth factor with critical roles in cell metabolism, tissue homeostasis, neuronal development, and synaptic plasticity.

             Aim: This study, it was aimed to examine the effect of TGF-β1 on the regulation of α, β, and γ-secretase enzymes, Aβ-40 accumulation, apoptosis, and neuronal damage in experimental AD-like disease model.

            Material-Method: Eighty-eight male Swiss-Albino mice were randomly divided into 5 groups; the control group without any treatment, the sham group in which only saline as applied, the group in which TGF-β was administered, the experimental group in which Scopolamine was applied for 28 days, and the treatment group in which Scopolamine and TGF-β1 was applied. The mice in the treatment group were also divided into 2 subgroups. To examine the long-term effects of the applied methods, sham, TGF-β1 control, experiment, treatment-1, and treatment-2 groups were followed until the 56th day, and the Moris water maze test (MWM) was applied on the 28th and 56th days, and memory functions were examined. Hippocampus and prefrontal cortex tissues taken from all groups on the 28th and 56th days were examined by light and electron microscopic, immunohistochemical, and biochemical methods.

            Results: In the MWM test, it was observed that memory performance decreased in the experimental groups, while memory performance increased again in the treatment groups. It was observed that Aβ-40 and caspase-3 immunoreactivity increased in the hippocampus and prefrontal cortex on the 28th and 56th days in the experimental group, and immunoreactivity was decreased as a result of TGF-β1 treatment. Structural changes were detected in neurons and glial cells in the experimental groups in light and electron microscopic examinations. It was interesting that cellular changes were relatively decreased in TGF-β1 treatment groups. It was found that α-secretase expression decreased in the experimental groups, while it increased in the treatment groups. It was determined that β and γ-secretase enzyme levels increased in the experimental groups and decreased in the treatment groups. It was thought that TGF-β1 might have a therapeutic effect on Alzheimer's disease by increasing memory performance and preventing Aβ-40 accumulation in the Alzheimer's-like disease model induced by scopolamine and also, it may be effective in preventing neuronal damage by down-regulating caspase-3 expression.

            Conclusion: At the same time, it can be effective in preventing the disease with its regulatory role on α, β, and γ-secretase enzymes. When all the findings were evaluated together, it was concluded that TGF-β1 could be evaluated as a therapeutic agent in Alzheimer's disease.