Akademik Veri Yönetim Sistemi
15. Ulusal / 1. Uluslararası Histoloji ve Embriyoloji Kongresi 26 - 28 MAYIS 2022, Ankara, Türkiye, 26 - 28 Mayıs 2022, ss.76
Introduction: Alzheimer's disease is a cognitive, neuroinflammatory and neurodegenerative disease that is
responsible for a large part of cognitive disorders. Although the pathological changes related to this disease are
not fully known, the most important pathological changes are extracellular plaque deposits of the amyloid beta
(Aβ) proteins and the accumulation of intracellular hyperphosphorylated tau proteins. VDAC1 (Voltage
Dependent Anion Channel-1) is an other multifunctional protein which plays a role in AD progression,
expressed in mitochondria and plasma membrane of cells. Transforming growth factor beta-1 (TGF-β1), an antiinflammatory cytokine, has been reported to have neuroprotective effect in the treatment of neurodegenerative
diseases. While positive effects of TGF-β1 treatment on neuroinflammation were seen, studies about the effects
of this cytokine on amyloid beta 42 (Aβ-42) and VDAC1 expression in the cerebellum and temporal lobe are
limited in the literature. For this purpose, in this study, it was aimed to examine the effect of TGF-β1 on the
expression of amyloid beta-42 and VDAC1 in the cerebellum and temporal lobe of the brain in an experimental
Alzheimer's-like model.
Materials and Methods: 28 Adult Swiss-Albino mice were divided into four groups as control, sham,
experimental and treatment groups. Unlike the control group, sham group received physiological saline
intraperitoneally. Experimental group received Scopolamine Hydrobromide intraperitoneally and treatment
group received TGF-β1 intraperitoneally in addition to Scopolamine Hydrobromide administration. At the end of
the 28th day, the mice were sacrificed and the cerebellum and temporal lobe tissues were analysed by light
microscopic, immunohistochemical and electron microscopic methods.
Results: Immunohistochemically, in the cerebellum tissues of the subjects in experimental group; significant
increase was detected in Aβ-42 expression in perineuronal area when compared to control, sham and treatment
groups. Moreover, VDAC-1 expression were shown to increase in the cerebellum and temporal lobe. In electron
microscopic examination, increased chromatin condensation in the nuclei of neurons at the cerebellum and
temporal lobe and also organelle destruction in the cytoplasm, especially mitochondrial damage were noted in
Scopolamine-treated mice. After the TGF-β1 treatment, decrease in Aβ-42 expression was determined, as well as
decrease the VDAC1 expression were observed. In addition, ultrastructural changes were rarely encountered.
Conclusion: It was concluded that TGF-B1 can prevent Aβ accumulation and reduce mitochondrial damage in an
experimental Alzheimer's-like model by down-regulating Aβ-42 and VDAC1 expression.