ArticlePloS one2019
Intracerebroventricular administration of the thyroid hormone analog TRIAC increases its brain content in the absence of MCT8.
Article in PloS one, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 15 citations in OpenAlex.
- Triiodothyroacetic acid exerts tissue-specific thyromimetic effects without tachycardia and hyperthermia in male mice.European thyroid journal · 2026Article
- TRIAC disrupts cerebral thyroid hormone action via negative feedback and heterogenous distribution among organs.iScience · 2023Article
- Maternal Administration of the CNS-Selective Sobetirome Prodrug Sob-AM2 Exerts Thyromimetic Effects in Murine MCT8-Deficient Fetuses.Thyroid : official journal of the American Thyroid Association · 2023Article
- Triac Treatment Prevents Neurodevelopmental and Locomotor Impairments in Thyroid Hormone Transporter Mct8/Oatp1c1 Deficient Mice.International journal of molecular sciences · 2023Article
- Gene therapy targeting the blood-brain barrier improves neurological symptoms in a model of genetic MCT8 deficiency.Brain : a journal of neurology · 2022Article
- AAV9-MCT8 Delivery at Juvenile Stage Ameliorates Neurological and Behavioral Deficits in a Mouse Model of MCT8-Deficiency.Thyroid : official journal of the American Thyroid Association · 2022Article
- Thyroid Hormone and Neural Stem Cells: Repair Potential Following Brain and Spinal Cord Injury.Frontiers in neuroscience · 2020Review
- MCT8 Deficiency: The Road to Therapies for a Rare Disease.Frontiers in neuroscience · 2020Review
Corrections and comments
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Authors and funding
5 authors at 3 institutions in 2 countries.
Funding
Abstract
Patients lacking the thyroid hormone (TH) transporter MCT8 present abnormal serum levels of TH: low thyroxine and high triiodothyronine. They also have severe neurodevelopmental defects resulting from cerebral hypothyroidism, most likely due to impaired TH transport across the brain barriers. The use of TH analogs, such as triiodothyroacetic acid (TRIAC), that can potentially access the brain in the absence of MCT8 and restore at least a subset of cerebral TH actions could improve the neurological defects in these patients. We hypothesized that direct administration of TRIAC into the brain by intracerebroventricular delivery to mice lacking MCT8 could bypass the restriction at the brain barriers and mediate TH action without causing hypermetabolism. We found that intracerebroventricular administration of therapeutic doses of TRIAC does not increase further plasma triiodothyronine or further decrease plasma thyroxine levels and does not alter TH content in the cerebral cortex. Although TRIAC content increased in the brain, it did not induce TH-mediated actions on selected target genes. Our data suggest that intracerebroventricular delivery of TRIAC has the ability to target the brain in the absence of MCT8 and should be further investigated to address its potential therapeutic use in MCT8 deficiency.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.