ReviewEuropean thyroid journal2024
Toward a treatment for thyroid hormone transporter MCT8 deficiency - achievements and challenges.
Review in European thyroid journal, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
4 citing papers in PubMed.
- Triiodothyroacetic acid exerts tissue-specific thyromimetic effects without tachycardia and hyperthermia in male mice.European thyroid journal · 2026Article
- Multi-target-directed drugs: new additions in 2025 and post-marketing safety surveillance of drugs marketed in 2022-2024.Pharmacological reports : PR · 2026Review
- Peripheral manifestations of monocarboxylate transporter 8 deficiency: hepatic and skeletal muscle involvement.Frontiers in pediatrics · 2026Review
- MCT8 Deficiency in Infancy: Opportunities for Early Diagnosis and Screening.International journal of neonatal screening · 2025Article
Corrections and comments
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Authors and funding
3 authors.
Funding
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Abstract
Patients with an inactive thyroid hormone (TH) transporter MCT8 (Allan-Herndon-Dudley Syndrome, AHDS) display severe neurological impairments and motor disabilities, indicating an indispensable function of MCT8 in facilitating TH access to the human brain. Consequently, the CNS of AHDS patients appears to be in a TH deficient state, which greatly compromises proper neural development and function. Another hallmark of this disease is that patients exhibit elevated serum T3 levels, leading to a hyperthyroid situation in peripheral tissues. Several treatment strategies have been developed and evaluated in preclinical mouse models as well as in patients. Here, we discuss these different therapeutic approaches to overcome MCT8 deficiency and summarize the current achievements and challenges in improving brain maturation in the absence of MCT8.
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Registered trials
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