Effects of TGF-β1 on Aβ-40 and α- β- γ secretase expression in hippocampus and prefrontal cortex in experimental Alzheimer's disease.

Alzheimer's disease is a chronic complex neurodegenerative disease characterized with amyloid plaques and loss of neurons. TGF-β1 is important growth factor, plays critical roles in cell metabolism, tissue homeostasis, neuronal development, and synaptic plasticity. In this study, we 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 an experimental Scopolamine-induced AD-like model. The subjects were divided into 5 groups such as control, sham, TGF-β1 control, Scopolamin group, TGF-β1 treatment groups.Then all groups were divided into 2 subgroups according to 28th-56th days. Except for Morris water maze (MWM) test, hippocampus and prefrontal cortex tissues were taken for light-electron microscopic, immunohistochemical, and biochemical examinations. It was observed that learning and memory abilities, which decreased in the MWM test of the Scopolamine group, increased in the treatment groups. In addition, α-secretase expression decreased in the Scopolamin group, while it increased in the TGF-β1 treatment group. It was determined that Aβ-40 and caspase-3 immunoreactivity, β and γ-secretase enzyme levels increased in the Scopolamin group and decreased in TGF-β1 treatment group. Cellular degenerations were relatively decreased in TGF-β1 treatment group. 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 AD-like model induced by Scopolamine and also, may be effective preventing neuronal damage by down-regulating caspase-3 expression. When all the findings evaluated together, it was concluded that TGF-β1 could be evaluated as a therapeutic agent in Alzheimer's disease.