The DOI matches its Crossref record; 17 of the 17 references it cites were found in a registry or an index.
Neurodevelopmental and Neurophysiological Actions of Thyroid Hormone
Open accessAbstract
For over 100 years, thyroid hormones have been known to be essential for neonatal neurodevelopment but whether they are required by the foetal brain remains a matter of controversy. For decades, the prevailing view was that thyroid hormones are not necessary until after birth because circulating levels in the foetus are very low and the placenta forms an efficient barrier to their transfer from the mother. Clinical observations of good neurological outcome following early treatment of congenital hypothyroidism were used to support the view that thyroid hormones are not required early in neurodevelopment. Nevertheless, the issue remained contentious because of findings that the severity of foetal neurological deficit due to maternal iodine deficiency correlated with the degree of maternal thyroxine (T4) deficiency. Furthermore, neurological damage in these cases could be prevented by correction of maternal T4 deficiency before mid‐gestation. This observation led to the opposing view, supported by epidemiological studies of neurological cretinism, that maternal thyroid hormones are important and necessary for early foetal neurodevelopment. It is now clear that thyroid hormones are essential for both foetal and post‐natal neurodevelopment and for the regulation of neuropsychological function in children and adults. In recent years, this controversial subject has progressed very rapidly following remarkable progress in understanding of the molecular mechanisms of thyroid hormone action. This article reviews the contributions of molecular biology and genetics to our new understanding of the physiological effects of thyroid hormones on neurodevelopment and in the adult brain.
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Bianco, A. C., Salvatore, D., Gereben, B., Berry, M. J., & Larsen, P. R. (2002) · Endocrine Reviews · doi:10.1210/edrv.23.1.0455 · Cited by 1,853
Glinoer, D. (1997) · Endocrine Reviews · doi:10.1210/edrv.18.3.0300 · Cited by 1,364
Deiodinases: implications of the local control of thyroid hormone action
Bianco, A. C., & Kim, B. W. (2006) · Journal of Clinical Investigation · doi:10.1172/jci29812 · Cited by 845
Identification of monocarboxylate transporter 8 as a specific thyroid hormone transporter
Friesema, E. C. H., Ganguly, S., Abdalla, A., Fox, J. E. M., Halestrap, A. P., & Visser, T. J. (2003) · Journal of Biological Chemistry · doi:10.1074/jbc.m300909200 · Cited by 725
Friesema, E. C., Grueters, A., Biebermann, H., Krude, H., von Moers, A., Reeser, M., Barrett, T. G., Mancilla, E. E., Svensson, J., Kester, M. H., et al. (2004) · The Lancet · doi:10.1016/s0140-6736(04)17226-7 · Cited by 709
Alexander, E. K., Marqusee, E., Lawrence, J., Jarolim, P., Fischer, G. A., & Larsen, P. R. (2004) · New England Journal of Medicine · doi:10.1056/nejmoa040079 · Cited by 633
Zoeller, R. T., & Rovet, J. (2004) · Journal of Neuroendocrinology · doi:10.1111/j.1365-2826.2004.01243.x · Cited by 605
The type 2 iodothyronine deiodinase is expressed primarily in glial cells in the neonatal rat brain
Guadaño-Ferraz, A., Obregón, M. J., Germain, D. L. S., & Bernal, J. (1997) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.94.19.10391 · Cited by 372
Type 2 iodothyronine deiodinase is the major source of plasma T3 in euthyroid humans
Luiza Maia, A. (2005) · Journal of Clinical Investigation · doi:10.1172/jci25083 · Cited by 360
Abnormal thyroid hormone metabolism in mice lacking the monocarboxylate transporter 8
Trajkovic, M., Visser, T. J., Mittag, J., Horn, S., Lukas, J., Darras, V. M., Raivich, G., Bauer, K., & Heuer, H. (2007) · Journal of Clinical Investigation · doi:10.1172/jci28253 · Cited by 353
Dumitrescu, A. M., Liao, X.-H., Weiss, R. E., Millen, K., & Refetoff, S. (2006) · Endocrinology · doi:10.1210/en.2006-0390 · Cited by 318
Tu, H. M., Kim, S.-W., Salvatore, D., Bartha, T., Legradi, G., Larsen, P. R., & Lechan, R. M. (1997) · Endocrinology · doi:10.1210/endo.138.8.5318 · Cited by 302
Heuer, H., Maier, M. K., Iden, S., Mittag, J., Friesema, E. C. H., Visser, T. J., & Bauer, K. (2005) · Endocrinology · doi:10.1210/en.2004-1179 · Cited by 269
Abel, E. D., Ahima, R. S., Boers, M.-E., Elmquist, J. K., & Wondisford, F. E. (2001) · Journal of Clinical Investigation · doi:10.1172/jci10858 · Cited by 192
Thyroid hormone transporters in health and disease
Jansen, J., Friesema, E. C. H., Milici, C., & Visser, T. J. (2005) · Thyroid · doi:10.1089/thy.2005.15.757 · Cited by 181
Neuroanatomical Pathways for Thyroid Hormone Feedback in the Human Hypothalamus
Alkemade, A., Friesema, E. C., Unmehopa, U. A., Fabriek, B. O., Kuiper, G. G., Leonard, J. L., Wiersinga, W. M., Swaab, D. F., Visser, T. J., & Fliers, E. (2005) · The Journal of Clinical Endocrinology & Metabolism · doi:10.1210/jc.2004-2567 · Cited by 146
Lechan, R. M., Qi, Y., Jackson, I. M., & Mahdavi, V (1994) · Endocrinology · doi:10.1210/endo.135.1.7516871 · Cited by 113
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Brent, G. A. (2012) · Journal of Clinical Investigation · doi:10.1172/jci60047 · Cited by 1,244
Essential metals in health and disease
Jomova, K., Makova, M., Alomar, S. Y., Alwasel, S. H., Nepovimova, E., Kuca, K., Rhodes, C. J., & Valko, M. (2022) · Chemico-Biological Interactions · doi:10.1016/j.cbi.2022.110173 · Cited by 1,121
The Link between Thyroid Function and Depression
Hage, M. P., & Azar, S. T. (2012) · Journal of Thyroid Research · doi:10.1155/2012/590648 · Cited by 549
From cohorts to molecules: adverse impacts of endocrine disrupting mixtures
Caporale, N., Leemans, M., Birgersson, L., Germain, P.-L., Cheroni, C., Borbély, G., Engdahl, E., Lindh, C., Bressan, R. B., Cavallo, F., et al. (2022) · Science · doi:10.1126/science.abe8244 · Cited by 368
Thyroid hormone mimetics: potential applications in atherosclerosis, obesity and type 2 diabetes
Baxter, J. D., & Webb, P. (2009) · Nature Reviews Drug Discovery · doi:10.1038/nrd2830 · Cited by 253
Metadata
- Authors
- Williams, G. R.
- Venue
- Journal of Neuroendocrinology
- Publisher
- Wiley
- Published
- 2008-06
- Volume
- 20
- Issue
- 6
- Pages
- 784-794
- ISSN
- 0953-8194 (ISSN-L)
- 1365-2826
- OpenAlex
- W2002197081
- Cited by
- 559
- References
- 17
- FWCI
- 13.51
- Type
- journal article
- Language
- en
- Open access
- bronze
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