Endocrine Abstracts

Objective: This study analyzes impairments occurred in local thyroid hormones metabolism and their connection to decreased glucose uptake, amyloid-β accumulation and apoptosis of neurons in pharmacologically induced animal model of Alzheimer’s disease.

Methods: Spectrophotometry, immunoassay, morphological studies including immunohistochemistry, rat Scopolamine-induced Alzheimer’s disease model (WAG male rats).

Results: The conducted study showed that local hypothyroidism in brain cortex is observed despite euthyroid status of the organism. We believe that abnormal thyroxin deiodination can be the reason of these impairments due to increased glutamate content and its exitotoxic properties.

It was reported that thyroid hormones determine basal metabolic rate due to their influence on mRNA synthesis. Hypothyroidism, as observed in our study, could influence both amount and activity of enzymes that take part in glucose metabolism. We have observed significant increase in pyruvate dehydrogenase activity and decrease in the citric acid cycle key enzymes. These changes indicate diminished glucose metabolism in brain cortex tissue.

Another aspect of local hypothyroidism is that thyroid hormones are known to potentiate the impact of catecholamines on heat shock proteins synthesis which play a pivotal role in cell reparation. Thus, lipid peroxidation activation can lead to apoptosis activation.

Conclusion: As a consequence of local hypothyroidism, glucose utilization was diminished and this leaded to decreased ATP content, amyloid-β accumulation in brain cortex tissue and cell death.

Figure 1 The role of neurotransmitting, endocrine and metabolic factors in Alzheimer’s disease development in rats.