A temporary compendium of thyroid hormone target genes in brain

Chatonnet, Fabrice; Flamant, Frédéric; Morte, Beatriz

doi:10.1016/j.bbagrm.2014.05.023

Cited by 85 publications

(90 citation statements)

References 48 publications

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“…Recent reports have shown that several hundred genes are regulated by T 3 at the transcriptional level to varying extends and degrees, and that some of these genes are mutated in autism [67][68][69]. As the most biologically active form of thyroid hormone, T 3 interacts with nuclear receptors to regulate gene expression.…”

Section: Molecular Aspects Of Thyroid Hormone Actionmentioning

confidence: 99%

Maternal Hypothyroxinemia-Induced Neurodevelopmental Impairments in the Progeny

et al. 2015

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Maternal hypothyroxinemia can induce neurodevelopmental impairments in the developing fetus. We here review recent studies on the epidemiology and molecular mechanisms associated with this important public health issue. In 2011, the American Thyroid Association defined maternal hypothyroxinemia as low serum free thyroxine (FT4) levels (<5th or <10th percentile) existing in conjunction with normal serum free triiodothyronine (FT3) or thyroid stimulating hormone (TSH) levels during pregnancy. Compared to clinical or subclinical hypothyroidism, hypothyroxinemia is more commonly found in pregnant women. Hypothyroxinemia usually ensues in response to several factors, such as mild iodine deficiency, environmental endocrine disrupters, or certain thyroid diseases. Unequivocal evidence demonstrates that maternal hypothyroxinemia leads to negative effects on fetal brain development, increasing the risks for cognitive deficits and poor psychomotor development in resulting progeny. In support of this, rodent models provide direct evidence of neurodevelopmental damage induced by maternal hypothyroxinemia, including dendritic and axonal growth limitation, neural abnormal location, and synaptic function alteration. The neurodevelopmental impairments induced by hypothyroxinemia suggest an independent role of T4. Increasing evidence indicates that adequate thyroxine is required for the mothers in order to protect against the abnormal brain development in their progeny.

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Section: Molecular Aspects Of Thyroid Hormone Actionmentioning

confidence: 99%

Maternal Hypothyroxinemia-Induced Neurodevelopmental Impairments in the Progeny

et al. 2015

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“…We summarize in Tables 1–6 a list of relevant genes that have been found to be T3-regulated at the transcriptional level in the rodents cerebral cortex (149, 322), and their human homolog genes (marked in bold) that have been found mutated in ASD patients. The list is far to be exhaustive and, most probably, the overlapping between T3-regulated and ASD-mutated (T3/ASD) genes will increase in the near future.…”

Section: Asd and Thyroid Hormones During Brain Developmentmentioning

confidence: 99%

An Evo-Devo Approach to Thyroid Hormones in Cerebral and Cerebellar Cortical Development: Etiological Implications for Autism

2014

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The morphological alterations of cortical lamination observed in mouse models of developmental hypothyroidism prompted the recognition that these experimental changes resembled the brain lesions of children with autism; this led to recent studies showing that maternal thyroid hormone deficiency increases fourfold the risk of autism spectrum disorders (ASD), offering for the first time the possibility of prevention of some forms of ASD. For ethical reasons, the role of thyroid hormones on brain development is currently studied using animal models, usually mice and rats. Although mammals have in common many basic developmental principles regulating brain development, as well as fundamental basic mechanisms that are controlled by similar metabolic pathway activated genes, there are also important differences. For instance, the rodent cerebral cortex is basically a primary cortex, whereas the primary sensory areas in humans account for a very small surface in the cerebral cortex when compared to the associative and frontal areas that are more extensive. Associative and frontal areas in humans are involved in many neurological disorders, including ASD, attention deficit-hyperactive disorder, and dyslexia, among others. Therefore, an evo-devo approach to neocortical evolution among species is fundamental to understand not only the role of thyroid hormones and environmental thyroid disruptors on evolution, development, and organization of the cerebral cortex in mammals but also their role in neurological diseases associated to thyroid dysfunction.

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“…Subsequent studies in the next two decades identified T 4 in coelomic fluid at 6 weeks gestation (7) and further described the details of TRs and deiodinase activity in early fetal brain (8,9,10). In more recent years, multiple TH responsive genes have been identified (11,12), including genes involved in differentiation, migration, myelination, axonal growth and synapse formation. Thyroid hormone is believed to play a key role in the processes of neuronal migration in the hippocampus and neocortex, development of cortical connections, cytoskeleton assembly, and neuronal development and maturation.…”

Section: Thyroid Hormone and Fetal Brain Developmentmentioning

confidence: 99%

“…In the rat, embryonic day 0 (E0) is the day of conception; birth occurs at E21-E22, while fetal thyroid is functional at E17. [5][6][7][8][9][10][11][12][13][14][15][16][17][18]. Neurogenesis and migration in the rat occur over 10 days, between E11 and E21, and therefore a period of 3 days in rat brain development corresponds roughly to 37-38 days in humans (13).…”

Section: Animal Models Of Imhmentioning

confidence: 99%

MANAGEMENT OF ENDOCRINE DISEASE: Isolated maternal hypothyroxinemia during pregnancy: knowns and unknowns

Dosiou

Medici

2017

European Journal of Endocrinology

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Isolated maternal hypothyroxinemia (IMH) during pregnancy is defined as a low maternal T 4 in the absence of TSH elevation. As IMH is common, with a prevalence of 1-2% in iodine-sufficient populations, and early research has suggested adverse effects on fetal neurodevelopment, it has been the focus of many studies in the last decade. In the current review, we first discuss the significance of IMH based on data from animal models and recent discoveries regarding the role of thyroid hormone on neurodevelopment. We address issues surrounding the definition and prevalence of this entity and discuss new insights into the etiologies, clinical consequences and management of IMH. A number of large cohort studies have investigated the effects of IMH on the risk of various pregnancy complications and child neurodevelopment. We review these studies in detail and describe their limitations. We discuss the available research on management of IMH, including two recent randomized controlled trials (RCTs). Finally, we delineate the remaining uncertainties in this field and emphasize the need for a sufficiently powered, placebo-controlled RCT on the treatment of IMH early in the first trimester of pregnancy.

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A temporary compendium of thyroid hormone target genes in brain

Cited by 85 publications

References 48 publications

Maternal Hypothyroxinemia-Induced Neurodevelopmental Impairments in the Progeny

Maternal Hypothyroxinemia-Induced Neurodevelopmental Impairments in the Progeny

An Evo-Devo Approach to Thyroid Hormones in Cerebral and Cerebellar Cortical Development: Etiological Implications for Autism

MANAGEMENT OF ENDOCRINE DISEASE: Isolated maternal hypothyroxinemia during pregnancy: knowns and unknowns

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