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Erschienen in: Metabolic Brain Disease 5/2019

13.06.2019 | Original Article

Bipolar limbic expression of auto-immune thyroid targets: thyroglobulin and thyroid-stimulating hormone receptor

verfasst von: Meleshni Naicker, Nathlee Abbai, Strinivasen Naidoo

Erschienen in: Metabolic Brain Disease | Ausgabe 5/2019

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Abstract

The associations between thyroid auto-immunity and neuro-psychiatric disorders are well-documented. However, there exists limited literature specifically linking auto-immune thyroid disease (AITD) to bipolar disorder (BD). Thus, we investigated the likely association between Hashimoto’s disease and BD through the extra-thyroidal localisation of thyroid-stimulating hormone receptor (TSH-R) and thyroglobulin (TG) in limbic regions of normal and bipolar human adult brain. Further, we hypothesised that changes in thyroid expression in bipolar limbic cortex may contribute to mood dysregulation associated with BD. Immuno-chemistry and in-situ PCR were used to localise TSH-R/TG within the amygdala, cingulate gyrus and frontal cortex of normal (n = 5) and bipolar (n = 5) brains. Reverse-transcriptase qPCR provided fold-change differences in TSH-R gene expression. The results demonstrated reduced thyroid protein expression in bipolar limbic regions; these novel results correlate with other neuro-imaging reports that describe reduced cortico-limbic tissue volumes and neuro-physiological activity during BD. We also demonstrated TG-like proteins exclusive to bipolar amygdala neurons, and which relates to previous neuro-imaging studies of amygdala hyperactivity and enhanced emotional sensitivity in BD. Indeed, reduced TSH-R/TG in limbic regions may predispose to, or bear relevance in the pathophysiology of mood dysregulation and symptoms of BD. Further, we attribute mood dysregulation in BD to limbic-derived TSH-R, which probably provides potential targets for thyroid auto-immune factors during Hashimoto’s disease. Consequently, this may lead to inactivated and/or damaged neurons. The neuro-pathology of diminished neuronal functioning or neuronal atrophy suggests a novel neuro-degeneration mechanism in BD.
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Zurück zum Zitat Winsberg ME, Sachs N, Tate DL, Adalsteinsson E, Spielman D, Ketter TA (2000) Decreased dorsolateral prefrontal N-acetyl aspartate in bipolar disorder. Biol Psychiatry 47:475–481CrossRefPubMed Winsberg ME, Sachs N, Tate DL, Adalsteinsson E, Spielman D, Ketter TA (2000) Decreased dorsolateral prefrontal N-acetyl aspartate in bipolar disorder. Biol Psychiatry 47:475–481CrossRefPubMed
Zurück zum Zitat Yu F, Gothe S, Wikstrom L, Forest D, Vennstrom B, Larsson L (2000) Effects of thyroid hormone receptor gene disruption on myosin isoform expression in mouse skeletal muscles. Am J Physiol Regul Integr Comp Physiol 278:R1545–R1554CrossRefPubMed Yu F, Gothe S, Wikstrom L, Forest D, Vennstrom B, Larsson L (2000) Effects of thyroid hormone receptor gene disruption on myosin isoform expression in mouse skeletal muscles. Am J Physiol Regul Integr Comp Physiol 278:R1545–R1554CrossRefPubMed
Metadaten
Titel
Bipolar limbic expression of auto-immune thyroid targets: thyroglobulin and thyroid-stimulating hormone receptor
verfasst von
Meleshni Naicker
Nathlee Abbai
Strinivasen Naidoo
Publikationsdatum
13.06.2019
Verlag
Springer US
Erschienen in
Metabolic Brain Disease / Ausgabe 5/2019
Print ISSN: 0885-7490
Elektronische ISSN: 1573-7365
DOI
https://doi.org/10.1007/s11011-019-00437-w

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