Maintenance of central thyroid status prevents the development of neuroinflammation.
Adult-onset hypothyroidism is associated with learning and cognitive dysfunctions, which may be related to alterations in synaptic plasticity. Local reduced levels of thyroid hormones (THs such as T3) may impair glia morphology and activity in the hippocampus. In a study recently published in IJMS, researchers from NeuroPSI and CNRS UMR 7221 (Molecular Physiology and Adaptation) at MNHN compared the effect of hypothyroid treatment on C57BL/6J and wild-derived WSB/EiJ male mice. Previous data showed that WSB/EiJ mice were resistant to high-fat diet (HFD)-induced obesity, showing no neuroinflammatory response through adaptive abilities, unlike C57BL/6J. As PTU and HFD treatments are known to induce comparable inflammatory responses, the researchers hypothesized that WSB/EiJ mice might also be protected against hypothyroidism-induced neuroinflammation. We showed that hypothyroid WSB/EiJ mice depicted no hippocampal neuroinflammatory response and were able to maintain their hippocampal T3 status despite low circulating TH levels. In contrast, C57BL/6J mice exhibited disturbed hippocampal T3 levels, accompanied by neuroinflammation and memory impairment.
Our results reinforce the preponderance of the hippocampal TH regulatory system over TH circulating levels in the hippocampal glial reactivity. Maintenance of thyroid status in the CNS thus appears to prevent the development of neuroinflammation, and potentially memory deficits.
A Fine Regulation of the Hippocampal Thyroid Signalling Protects Hypothyroid Mice against Glial Cell Activation. Lamis Chamas, Isabelle Seugnet, Roseline Poirier, Marie-Stéphanie Clerget-Froidevaux, and Valérie Enderlin.