Research Topic

Selenium and Selenoproteins in Brain Development, Function, and Disease

About this Research Topic

Selenium (Se) is an essential micronutrient with important effects on the brain. Its influence is mediated primarily through selenoproteins, a class of proteins characterized by the co-translational incorporation of Se as the amino acid selenocysteine. These proteins play fundamental roles in redox signaling and include the glutathione peroxidases, thioredoxin reductases, and iodothyronine deiodinases. The human genome encodes 25 distinct selenoproteins, along with a host of additional Se-related proteins involved in selenoprotein biosynthesis and Se metabolism. Many of these are highly expressed in brain, and mouse knockout studies have shown that several are indispensable for neurodevelopment. Specifically, selenoproteins are required for the functionality of parvalbumin-expressing interneurons, a class of GABAergic neurons characterized by high rates of metabolism. Furthermore, humans with rare mutations in selenoprotein biosynthesis genes exhibit neurological problems that parallel those detailed in knockout mice, including deficits in cognition and motor function, seizures, hearing loss, and altered thyroid metabolism.

The goal of this Research Topic is to assemble a collection of state-of-the-art articles pertaining to the influence of selenium and/or selenoproteins on brain development, function, and disease. We aim to have tentative abstracts from all willing participants by August 1st and complete manuscripts submitted by December 1st.

We are soliciting both Original Research and Review articles of high quality from respected authorities in the Selenium field. All topics should be brain-related in some regard. Specific topics can include, but are not limited to:
1) Roles of individual selenoproteins and/or Se-related proteins in brain
2) Influence of Se-deficiency and/or Se-toxicity on brain function
3) Human mutations and/or polymorphisms in selenoproteins and/or Se-related genes that impact brain function
4) Se levels and speciation in brain and/or CSF in the context of development, aging, and/or disease
5) Influence of Se/selenoproteins on thyroid metabolism in brain
6) Cell-type specific and/or regional influence of Se/selenoproteins in brain
7) Transport, metabolism, and retention of Se in brain

Topic Editor Lutz Schomburg holds shares in selenOmed GmbH, a company involved in selenium status assessment and supplementation. The rest of Topic Editors declare no competing interests with regards to the Research Topic.


Keywords: Selenium, Selenoprotein, Brain, Oxidative Stress, Neurodevelopment


Important Note: All contributions to this Research Topic must be within the scope of the section and journal to which they are submitted, as defined in their mission statements. Frontiers reserves the right to guide an out-of-scope manuscript to a more suitable section or journal at any stage of peer review.

Selenium (Se) is an essential micronutrient with important effects on the brain. Its influence is mediated primarily through selenoproteins, a class of proteins characterized by the co-translational incorporation of Se as the amino acid selenocysteine. These proteins play fundamental roles in redox signaling and include the glutathione peroxidases, thioredoxin reductases, and iodothyronine deiodinases. The human genome encodes 25 distinct selenoproteins, along with a host of additional Se-related proteins involved in selenoprotein biosynthesis and Se metabolism. Many of these are highly expressed in brain, and mouse knockout studies have shown that several are indispensable for neurodevelopment. Specifically, selenoproteins are required for the functionality of parvalbumin-expressing interneurons, a class of GABAergic neurons characterized by high rates of metabolism. Furthermore, humans with rare mutations in selenoprotein biosynthesis genes exhibit neurological problems that parallel those detailed in knockout mice, including deficits in cognition and motor function, seizures, hearing loss, and altered thyroid metabolism.

The goal of this Research Topic is to assemble a collection of state-of-the-art articles pertaining to the influence of selenium and/or selenoproteins on brain development, function, and disease. We aim to have tentative abstracts from all willing participants by August 1st and complete manuscripts submitted by December 1st.

We are soliciting both Original Research and Review articles of high quality from respected authorities in the Selenium field. All topics should be brain-related in some regard. Specific topics can include, but are not limited to:
1) Roles of individual selenoproteins and/or Se-related proteins in brain
2) Influence of Se-deficiency and/or Se-toxicity on brain function
3) Human mutations and/or polymorphisms in selenoproteins and/or Se-related genes that impact brain function
4) Se levels and speciation in brain and/or CSF in the context of development, aging, and/or disease
5) Influence of Se/selenoproteins on thyroid metabolism in brain
6) Cell-type specific and/or regional influence of Se/selenoproteins in brain
7) Transport, metabolism, and retention of Se in brain

Topic Editor Lutz Schomburg holds shares in selenOmed GmbH, a company involved in selenium status assessment and supplementation. The rest of Topic Editors declare no competing interests with regards to the Research Topic.


Keywords: Selenium, Selenoprotein, Brain, Oxidative Stress, Neurodevelopment


Important Note: All contributions to this Research Topic must be within the scope of the section and journal to which they are submitted, as defined in their mission statements. Frontiers reserves the right to guide an out-of-scope manuscript to a more suitable section or journal at any stage of peer review.

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Submission Deadlines

11 January 2021 Manuscript

Participating Journals

Manuscripts can be submitted to this Research Topic via the following journals:

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Topic Editors

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Submission Deadlines

11 January 2021 Manuscript

Participating Journals

Manuscripts can be submitted to this Research Topic via the following journals:

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