Akademik Veri Yönetim Sistemi
16TH NATIONAL AND 2ND INTERNATIONAL CONGRESS OF HISTOLOGY AND EMBRYOLOGY, Sakarya, Türkiye, 26 - 28 Eylül 2024, ss.54-55
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.