Neurosciences - Posters G
Introduction: Alzheimer's disease (AD) is an age-related neurodegenerative disease with
progressive memory decline that may be aggravated by other factors such as abnormalities in
the hypothalamic–pituitary–thyroid (HPT) axis. Transgenic mouse models are promising tools
for understanding the underlying mechanisms.
Aims: During our experiments, we found that male, 6-month-old triple transgenic (3xTg-AD)
mice performed better in food-motivated cognitive tests compared to the control group. In the
background of this, we assumed an imbalance in the HPT axis.
Methods: First blood glucose leves as well as free thyroxine (FT4) and free triiodothyronine
(FT3) level were detected in serum. Then changes in major genes of HPT axis was observed
by qPCR.
Results: The blood glucose level was increased while FT4 showed a decrease compared to
the control group. A significant increase in thyrotropin-releasing hormone mRNA expression
was detected in the paraventricular nucleus of hypothalamus. The thyrotropin-stimulating
hormone mRNA expression level in the pituitary gland did not change compared to the values
of the control mice, while the thyroid hormone β2 receptor mRNA expression decreased
significantly. The mRNA expression levels of the deiodinase enzymes in the pituitary gland
and MBH varied.
Conclusion: In summary, the results of the abnormal HPT axis might be the background for
this „food craving”. Our results further support the idea that AD is a metabolic disease. When
interpreting the outcome of food-driven learning tests, it is also important to examine the
motivation of individuals, including their HPT axis.