Commentary 10.1172/JCI125203

Cognitive function in hypothyroidism: what is that deiodinase again?

Arturo Hernandez

Center for Molecular Medicine, Maine Medical Center Research Institute, Scarborough, Maine, USA. Graduate School for Biomedical Science and Engineering, University of Maine, Orono, Maine, USA. Department of Medicine, Tufts University School of Medicine, Boston, Massachusetts, USA.

Address correspondence to: Arturo Hernandez, Maine Medical Center Research Institute, Scarborough, Maine 04074, USA. Phone: 207.396.8139; E-mail: hernaa@mmc.org.

Find articles by Hernandez, A. in: JCI | PubMed | Google Scholar | Orcid 24x24

First published December 3, 2018 - More info

Published in Volume 129, Issue 1 on January 2, 2019
J Clin Invest. 2019;129(1):55–57. https://doi.org/10.1172/JCI125203.
Copyright © 2019, American Society for Clinical Investigation
First published December 3, 2018 - Version history

Treatment of hypothyroidism involves the endogenous conversion of thyroxine (T4) to 3,5,3′-triiodothyronine (T3) and may not be optimal in some cases when based on T4 alone. In the current issue of the JCI, Jo et al. present results that explain the reduced enzymatic activity of a common genetic variant of the enzyme responsible for this conversion, type 2 deiodinase (DIO2). The authors further explore the functional consequences of this variant on brain T3 activity, endoplasmic reticulum stress in glial cells, and cognitive function. These findings have important implications for the clinical treatment of hypothyroidism and for susceptibility to other neurological and metabolic diseases.

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