Mechanisms underlying tissue hypothyroidism in the brain during thyroxine substitution therapy


Our aim is to identify the basic cellular and molecular pathways that underlie the symptoms of hypothyroidism in a group of patients who respond poorly to thyroxine (T4) monotherapy. While the therapy is able to normalize the TSH of these patients, they still suffer from symptoms of tissue hypothyroidism that adversely affect cognitive function and regulation of energy homeostasis. We hypothesize that cell-type specific regulation of thyroid hormone (TH) metabolism is predominantly responsible for these phenomena. In this context, we study different mechanisms of cellular and molecular regulation of TH activation. 


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