ArticleMetabolic brain disease2019
Bipolar limbic expression of auto-immune thyroid targets: thyroglobulin and thyroid-stimulating hormone receptor.
Article in Metabolic brain disease, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed, 10 citations in OpenAlex.
- Thyroid-stimulating hormone receptor mediates peripheral-central neuroimmune crosstalk in autoimmune thyroid diseases.BMC medicine · 2026Article
- The impact of autoimmune thyroid disease on cognitive and psychiatric disorders: focus on clinical, pre-clinical and molecular studies.European thyroid journal · 2025Review
- Primary Hypothyroidism and Alzheimer's Disease: A Tale of Two.Cellular and molecular neurobiology · 2023Review
- Prevalence and Factors Associated with Subclinical Hypothyroidism in Major Depressive Disorder Patients with Dyslipidemia.Neuropsychiatric disease and treatment · 2023Article
- Effects of the LHPP gene polymorphism on the functional and structural changes of gray matter in major depressive disorder.Quantitative imaging in medicine and surgery · 2020Article
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
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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