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Article ; Online: Metabolic pathways in the periphery and brain: Contribution to mental disorders?

Nagalski, Andrzej / Kozinski, Kamil / Wisniewska, Marta B

The international journal of biochemistry & cell biology

2016 Volume 80, Page(s) 19–30

Abstract: The association between mental disorders and diabetes has a long history. Recent large-scale, well-controlled epidemiological studies confirmed a link between diabetes and psychiatric illnesses. The scope of this review is to summarize our current ... ...

Abstract	The association between mental disorders and diabetes has a long history. Recent large-scale, well-controlled epidemiological studies confirmed a link between diabetes and psychiatric illnesses. The scope of this review is to summarize our current understanding of this relationship from a molecular perspective. We first discuss the potential contribution of diabetes-associated metabolic impairments to the etiology of mental conditions. Then, we focus on possible shared molecular risk factors and mechanisms. Simple comorbidity, shared susceptibility loci, and common pathophysiological processes in diabetes and mental illnesses have changed our traditional way of thinking about mental illness. We conclude that schizophrenia and affective disorders are not limited to an imbalance in dopaminergic and serotoninergic neurotransmission in the brain. They are also systemic disorders that can be considered, to some extent, as metabolic disorders.
MeSH term(s)	Animals ; Brain/metabolism ; Comorbidity ; Diabetes Mellitus, Type 2/epidemiology ; Diabetes Mellitus, Type 2/metabolism ; Glucose/metabolism ; Humans ; Mental Disorders/epidemiology ; Mental Disorders/metabolism ; Metabolic Networks and Pathways
Chemical Substances	Glucose (IY9XDZ35W2)
Language	English
Publishing date	2016-11
Publishing country	Netherlands
Document type	Journal Article ; Review
ZDB-ID	1228429-4
ISSN	1878-5875 ; 1357-2725
ISSN (online)	1878-5875
ISSN	1357-2725
DOI	10.1016/j.biocel.2016.09.012
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Article: Metabolic pathways in the periphery and brain: Contribution to mental disorders?

Nagalski, Andrzej / Kamil Kozinski / Marta B. Wisniewska

international journal of biochemistry & cell biology. 2016 Nov., v. 80

2016

Abstract	The association between mental disorders and diabetes has a long history. Recent large-scale, well-controlled epidemiological studies confirmed a link between diabetes and psychiatric illnesses. The scope of this review is to summarize our current understanding of this relationship from a molecular perspective. We first discuss the potential contribution of diabetes-associated metabolic impairments to the etiology of mental conditions. Then, we focus on possible shared molecular risk factors and mechanisms. Simple comorbidity, shared susceptibility loci, and common pathophysiological processes in diabetes and mental illnesses have changed our traditional way of thinking about mental illness. We conclude that schizophrenia and affective disorders are not limited to an imbalance in dopaminergic and serotoninergic neurotransmission in the brain. They are also systemic disorders that can be considered, to some extent, as metabolic disorders.
Keywords	biochemical pathways ; brain ; comorbidity ; diabetes ; epidemiological studies ; etiology ; loci ; risk factors ; schizophrenia
Language	English
Dates of publication	2016-11
Size	p. 19-30.
Publishing place	Elsevier Ltd
Document type	Article
ZDB-ID	1228429-4
ISSN	1878-5875 ; 1357-2725
ISSN (online)	1878-5875
ISSN	1357-2725
DOI	10.1016/j.biocel.2016.09.012
Database	NAL-Catalogue (AGRICOLA)

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Article ; Online: TCF7L2 regulates postmitotic differentiation programmes and excitability patterns in the thalamus.

Lipiec, Marcin Andrzej / Bem, Joanna / Koziński, Kamil / Chakraborty, Chaitali / Urban-Ciećko, Joanna / Zajkowski, Tomasz / Dąbrowski, Michał / Szewczyk, Łukasz Mateusz / Toval, Angel / Ferran, José Luis / Nagalski, Andrzej / Wiśniewska, Marta Barbara

Development (Cambridge, England)

2020 Volume 147, Issue 16

Abstract: Neuronal phenotypes are controlled by terminal selector transcription factors in invertebrates, but only a few examples of such regulators have been provided in vertebrates. We hypothesised that TCF7L2 regulates different stages of postmitotic ... ...

Abstract	Neuronal phenotypes are controlled by terminal selector transcription factors in invertebrates, but only a few examples of such regulators have been provided in vertebrates. We hypothesised that TCF7L2 regulates different stages of postmitotic differentiation in the thalamus, and functions as a thalamic terminal selector. To investigate this hypothesis, we used complete and conditional knockouts of
MeSH term(s)	Animals ; Cell Differentiation ; Gene Expression Regulation, Developmental ; Mice ; Mice, Knockout ; Mitosis ; Synaptic Transmission ; Thalamus/cytology ; Thalamus/embryology ; Transcription Factor 4/genetics ; Transcription Factor 4/metabolism
Chemical Substances	Tcf4 protein, mouse ; Transcription Factor 4
Language	English
Publishing date	2020-08-25
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	90607-4
ISSN	1477-9129 ; 0950-1991
ISSN (online)	1477-9129
ISSN	0950-1991
DOI	10.1242/dev.190181
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Article ; Online: Fizjologia i molekularny mechanizm działania glikokortykoidów.

Nagalski, Andrzej / Kiersztan, Anna

Postepy higieny i medycyny doswiadczalnej (Online)

2010 Volume 64, Page(s) 133–145

Abstract: Endogenous glucocorticoids (GCs) are secreted into the systemic circulation from the adrenal cortex. This release is under the control of the circadian clock and can be enhanced at any time in response to a stressor. The levels of circulating GC are ... ...

Title translation	Physiology and molecular mechanism of glucocorticoid action.
Abstract	Endogenous glucocorticoids (GCs) are secreted into the systemic circulation from the adrenal cortex. This release is under the control of the circadian clock and can be enhanced at any time in response to a stressor. The levels of circulating GC are regulated systemically by the hypothalamo-pituitary-adrenal axis and locally by access to target cells and pre-receptor metabolism by 11beta-hydroxysteroids dehydrogenase enzymes. GCs mediate their genomic action by binding to two different ligand-inducible transcription factors: high-affinity mineralocorticoid receptor (MR) and 10-fold lower affinity glucocorticoid receptors (GRs). Responses to GCs vary among individuals, cells, and tissues. The diversity and specificity in the steroid hormone's response in the cell is controlled at different levels, including receptor translocation, interaction with specific transcription factors and coregulators, and the regulation of receptor protein levels by microRNA. Moreover, multiple GR isoforms are generated from one single GR gene by alternative splicing and alternative translation initiation. These isoforms all have unique tissue distribution patterns and transcriptional regulatory profiles. Furthermore, each is subjected to various post-translational modifications that affect receptor function. Deciphering the molecular mechanisms of GC action is further complicated by the realization that GCs can induce rapid, non-genomic effects within the cytoplasm. A tight regulation of GC secretion and their cell-specific activity is essential for proper organism function. This is particularly seen under conditions of GC deficiency or excess, as in Addison's disease and Cushing's syndrome, respectively.
MeSH term(s)	11-beta-Hydroxysteroid Dehydrogenases ; Addison Disease/physiopathology ; Circadian Rhythm/physiology ; Cushing Syndrome/physiopathology ; Glucocorticoids/metabolism ; Glucocorticoids/pharmacology ; Humans ; Receptors, Glucocorticoid/metabolism
Chemical Substances	Glucocorticoids ; Receptors, Glucocorticoid ; 11-beta-Hydroxysteroid Dehydrogenases (EC 1.1.1.146)
Language	Polish
Publishing date	2010-03-18
Publishing country	Poland
Document type	English Abstract ; Journal Article ; Review
ZDB-ID	418865-2
ISSN	1732-2693 ; 0032-5449
ISSN (online)	1732-2693
ISSN	0032-5449
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Article ; Online: Wnt/β-catenin signaling in brain development and mental disorders: keeping TCF7L2 in mind.

Bem, Joanna / Brożko, Nikola / Chakraborty, Chaitali / Lipiec, Marcin A / Koziński, Kamil / Nagalski, Andrzej / Szewczyk, Łukasz M / Wiśniewska, Marta B

FEBS letters

2019 Volume 593, Issue 13, Page(s) 1654–1674

Abstract: Canonical Wnt signaling, which is transduced by β-catenin and lymphoid enhancer factor 1/T cell-specific transcription factors (LEF1/TCFs), regulates many aspects of metazoan development and tissue renewal. Although much evidence has associated canonical ...

Abstract	Canonical Wnt signaling, which is transduced by β-catenin and lymphoid enhancer factor 1/T cell-specific transcription factors (LEF1/TCFs), regulates many aspects of metazoan development and tissue renewal. Although much evidence has associated canonical Wnt/β-catenin signaling with mood disorders, the mechanistic links are still unknown. Many components of the canonical Wnt pathway are involved in cellular processes that are unrelated to classical canonical Wnt signaling, thus further blurring the picture. The present review critically evaluates the involvement of classical Wnt/β-catenin signaling in developmental processes that putatively underlie the pathology of mental illnesses. Particular attention is given to the roles of LEF1/TCFs, which have been discussed surprisingly rarely in this context. Highlighting recent discoveries, we propose that alterations in the activity of LEF1/TCFs, and particularly of transcription factor 7-like 2 (TCF7L2), result in defects previously associated with neuropsychiatric disorders, including imbalances in neurogenesis and oligodendrogenesis, the functional disruption of thalamocortical circuitry and dysfunction of the habenula.
MeSH term(s)	Animals ; Brain/cytology ; Brain/growth & development ; Brain/metabolism ; Brain/pathology ; Humans ; Mental Disorders/metabolism ; Mental Disorders/pathology ; Neurogenesis ; Transcription Factor 7-Like 2 Protein/metabolism ; Wnt Signaling Pathway
Chemical Substances	Transcription Factor 7-Like 2 Protein
Language	English
Publishing date	2019-06-30
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	212746-5
ISSN	1873-3468 ; 0014-5793
ISSN (online)	1873-3468
ISSN	0014-5793
DOI	10.1002/1873-3468.13502
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Article ; Online: ST8SIA2 promotes oligodendrocyte differentiation and the integrity of myelin and axons.

Szewczyk, Lukasz Mateusz / Brozko, Nikola / Nagalski, Andrzej / Röckle, Iris / Werneburg, Sebastian / Hildebrandt, Herbert / Wisniewska, Marta Barbara / Kuznicki, Jacek

Glia

2017 Volume 65, Issue 1, Page(s) 34–49

Abstract: ST8SIA2 is a polysialyltransferase that attaches polysialic acid to the glycoproteins NCAM1 and CADM1. Polysialylation is involved in brain development and plasticity. ST8SIA2 is a schizophrenia candidate gene, and ... ...

Abstract	ST8SIA2 is a polysialyltransferase that attaches polysialic acid to the glycoproteins NCAM1 and CADM1. Polysialylation is involved in brain development and plasticity. ST8SIA2 is a schizophrenia candidate gene, and St8sia2
Language	English
Publishing date	2017-01
Publishing country	United States
Document type	Journal Article
ZDB-ID	639414-0
ISSN	1098-1136 ; 0894-1491
ISSN (online)	1098-1136
ISSN	0894-1491
DOI	10.1002/glia.23048
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Article ; Online: Physiology and molecular mechanism of glucocorticoid action

Andrzej Nagalski / Anna Kiersztan

Postępy Higieny i Medycyny Doświadczalnej, Vol 64, Iss 840537, Pp 133-

2010 Volume 145

Abstract	Endogenous glucocorticoids (GCs) are secreted into the systemic circulation from the adrenal cortex. This release is under the control of the circadian clock and can be enhanced at any time in response to a stressor. The levels of circulating GC are regulated systemically by the hypothalamo-pituitary-adrenal axis and locally by access to target cells and pre-receptor metabolism by 11β-hydroxysteroids dehydrogenase enzymes. GCs mediate their genomic action by binding to two different ligand-inducible transcription factors: high-affinity mineralocorticoid receptor (MR) and 10-fold lower affinity glucocorticoid receptors (GRs). Responses to GCs vary among individuals, cells, and tissues. The diversity and specificity in the steroid hormone’s response in the cell is controlled at different levels, including receptor translocation, interaction with specific transcription factors and coregulators, and the regulation of receptor protein levels by microRNA. Moreover, multiple GR isoforms are generated from one single GR gene by alternative splicing and alternative translation initiation. These isoforms all have unique tissue distribution patterns and transcriptional regulatory profiles. Furthermore, each is subjected to various post-translational modifications that affect receptor function. Deciphering the molecular mechanisms of GC action is further complicated by the realization that GCs can induce rapid, non-genomic effects within the cytoplasm. A tight regulation of GC secretion and their cell-specific activity is essential for proper organism function. This is particularly seen under conditions of GC deficiency or excess, as in Addison’s disease and Cushing’s syndrome, respectively.
Keywords	glikokortykoidy ; oś podwzgórze-przysadka-kora nadnerczy ; receptor glikokortykoidów ; dehydrogenaza 11β-hydroksysteroidowa ; Choroba Addisona ; zespół Cushinga ; Medicine ; R
Subject code	570
Language	English
Publishing date	2010-03-01T00:00:00Z
Publisher	Sciendo
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: Zastosowanie niacyny w terapii.

Nagalski, Andrzej / Bryła, Jadwiga

Postepy higieny i medycyny doswiadczalnej (Online)

2007 Volume 61, Page(s) 288–302

Abstract: Niacin (nicotinic acid and nicotinamide) is a vitamin used as a source of the NAD+ and NADP+ coenzymes required for many metabolic processes. Its low dietary levels induce the development of pellagra. Niacin has been used for decades in the treatment of ... ...

Title translation	Niacin in therapy.
Abstract	Niacin (nicotinic acid and nicotinamide) is a vitamin used as a source of the NAD+ and NADP+ coenzymes required for many metabolic processes. Its low dietary levels induce the development of pellagra. Niacin has been used for decades in the treatment of patients with disturbed lipid and lipoprotein metabolism, this being the main cause of atherosclerotic changes in cardiovascular diseases. It is still the most efficacious drug in terms of its ability to increase HDL cholesterol content accompanied by a decrease in all atherogenic lipoproteins (VLDL, LDL, and L(a)) as well as fatty acids and triglycerides. Niacin also increases adiponectin level, which might result in additional atheroprotection. There are studies confirming the beneficial action of niacin against migraine and hyperphosphatemia associated with renal failure, ethanol-induced neurodegeneration, and loss of beta-cell function in type 1 diabetes. Moreover, it augments plasma tryptophan concentrations in HIV-infected patients and thyroid radiosensitivity to 131I. Inhibition of the invasion of hepatoma cells has also been proven. However, it is necessary to point out that the currently applied niacin preparations might exhibit such side effects as cutaneous flushing, gastrointestinal disturbances, and hepatotoxicity, particularly during treatment with sustained-release niacin preparations. The recent discovery of the G-protein-coupled receptor GPR109A, which mediates the antilipolytic effects induced by nicotinic acid in adipocytes as well as cutaneous vasodilation, allows the development of new agents interacting with this receptor. In view of these observations, niacin therapy must be accompanied by control of the choice of niacin preparation and its dose in order to eliminate or at least limit its side effects.
MeSH term(s)	Adipocytes/metabolism ; Adiponectin/metabolism ; Animals ; Cholesterol, HDL/drug effects ; Delayed-Action Preparations ; Flushing/prevention & control ; Humans ; Hyperlipidemias/blood ; Hyperlipidemias/drug therapy ; Mice ; Niacin/adverse effects ; Niacin/pharmacology ; Niacin/therapeutic use ; Niacinamide/metabolism ; Nicotinic Acids/metabolism ; Pellagra/diet therapy ; Pellagra/drug therapy ; Pellagra/metabolism ; Rabbits ; Rats ; Receptors, G-Protein-Coupled/metabolism
Chemical Substances	Adiponectin ; Cholesterol, HDL ; Delayed-Action Preparations ; Nicotinic Acids ; Receptors, G-Protein-Coupled ; Niacinamide (25X51I8RD4) ; Niacin (2679MF687A)
Language	Polish
Publishing date	2007-05-15
Publishing country	Poland
Document type	English Abstract ; Journal Article ; Review
ZDB-ID	418865-2
ISSN	1732-2693 ; 0032-5449
ISSN (online)	1732-2693
ISSN	0032-5449
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Article ; Online: Molecular anatomy of the thalamic complex and the underlying transcription factors.

Nagalski, Andrzej / Puelles, Luis / Dabrowski, Michal / Wegierski, Tomasz / Kuznicki, Jacek / Wisniewska, Marta B

Brain structure & function

2015 Volume 221, Issue 5, Page(s) 2493–2510

Abstract: Thalamocortical loops have been implicated in the control of higher-order cognitive functions, but advances in our understanding of the molecular underpinnings of neocortical organization have not been accompanied by similar analyses in the thalamus. ... ...

Abstract	Thalamocortical loops have been implicated in the control of higher-order cognitive functions, but advances in our understanding of the molecular underpinnings of neocortical organization have not been accompanied by similar analyses in the thalamus. Using expression-based correlation maps and the manual mapping of mouse and human datasets available in the Allen Brain Atlas, we identified a few individual regions and several sets of molecularly related nuclei that partially overlap with the classic grouping that is based on topographical localization and thalamocortical connections. These new molecular divisions of the adult thalamic complex are defined by the combinatorial expression of Tcf7l2, Lef1, Gbx2, Prox1, Pou4f1, Esrrg, and Six3 transcription factor genes. Further in silico and experimental analyses provided the evidence that TCF7L2 might be a pan-thalamic specifier. These results provide substantial insights into the "molecular logic" that underlies organization of the thalamic complex.
MeSH term(s)	Animals ; Atlases as Topic ; Databases, Chemical ; Eye Proteins/genetics ; Eye Proteins/metabolism ; Gene Expression ; Gene Expression Regulation, Developmental ; Homeodomain Proteins/genetics ; Homeodomain Proteins/metabolism ; Humans ; Lymphoid Enhancer-Binding Factor 1/genetics ; Lymphoid Enhancer-Binding Factor 1/metabolism ; Mice ; Nerve Tissue Proteins/genetics ; Nerve Tissue Proteins/metabolism ; Receptors, Estrogen/genetics ; Receptors, Estrogen/metabolism ; Thalamic Nuclei/metabolism ; Transcription Factor 7-Like 2 Protein/genetics ; Transcription Factor 7-Like 2 Protein/metabolism ; Transcription Factor Brn-3A/genetics ; Transcription Factor Brn-3A/metabolism ; Transcription Factors/genetics ; Transcription Factors/metabolism ; Tumor Suppressor Proteins/genetics ; Tumor Suppressor Proteins/metabolism ; Homeobox Protein SIX3
Chemical Substances	ESRRG protein, human ; Eye Proteins ; GBX2 protein, human ; Homeodomain Proteins ; LEF1 protein, human ; Lymphoid Enhancer-Binding Factor 1 ; Nerve Tissue Proteins ; POU4F1 protein, human ; Receptors, Estrogen ; TCF7L2 protein, human ; Transcription Factor 7-Like 2 Protein ; Transcription Factor Brn-3A ; Transcription Factors ; Tumor Suppressor Proteins ; prospero-related homeobox 1 protein
Language	English
Publishing date	2015-05-12
Publishing country	Germany
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2273162-3
ISSN	1863-2661 ; 1863-2653
ISSN (online)	1863-2661
ISSN	1863-2653
DOI	10.1007/s00429-015-1052-5
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Article ; Online: TCF7L2 mediates the cellular and behavioral response to chronic lithium treatment in animal models.

Misztal, Katarzyna / Brozko, Nikola / Nagalski, Andrzej / Szewczyk, Lukasz M / Krolak, Marta / Brzozowska, Katarzyna / Kuznicki, Jacek / Wisniewska, Marta B

Neuropharmacology

2017 Volume 113, Issue Pt A, Page(s) 490–501

Abstract: The mechanism of lithium's therapeutic action remains obscure, hindering the discovery of safer treatments for bipolar disorder. Lithium can act as an inhibitor of the kinase GSK3α/β, which in turn negatively regulates β-catenin, a co-activator of LEF1/ ... ...

Abstract	The mechanism of lithium's therapeutic action remains obscure, hindering the discovery of safer treatments for bipolar disorder. Lithium can act as an inhibitor of the kinase GSK3α/β, which in turn negatively regulates β-catenin, a co-activator of LEF1/TCF transcription factors. However, unclear is whether therapeutic levels of lithium activate β-catenin in the brain, and whether this activation could have a therapeutic significance. To address this issue we chronically treated mice with lithium. Although the level of non-phospho-β-catenin increased in all of the brain areas examined, β-catenin translocated into cellular nuclei only in the thalamus. Similar results were obtained when thalamic and cortical neurons were treated with a therapeutically relevant concentration of lithium in vitro. We tested if TCF7L2, a member of LEF1/TCF family that is highly expressed in the thalamus, facilitated the activation of β-catenin. Silencing of Tcf7l2 in thalamic neurons prevented β-catenin from entering the nucleus, even when the cells were treated with lithium. Conversely, when Tcf7l2 was ectopically expressed in cortical neurons, β-catenin shifted to the nucleus, and lithium augmented this process. Lastly, we silenced tcf7l2 in zebrafish and exposed them to lithium for 3 days, to evaluate whether TCF7L2 is involved in the behavioral response. Lithium decreased the dark-induced activity of control zebrafish, whereas the activity of zebrafish with tcf7l2 knockdown was unaltered. We conclude that therapeutic levels of lithium activate β-catenin selectively in thalamic neurons. This effect is determined by the presence of TCF7L2, and potentially contributes to the therapeutic response.
MeSH term(s)	Animals ; Brain/cytology ; Brain/drug effects ; Brain/physiology ; Cells, Cultured ; Drug Administration Schedule ; Lithium/administration & dosage ; Locomotion/drug effects ; Locomotion/physiology ; Male ; Mice ; Mice, Inbred C57BL ; Models, Animal ; Neurons/drug effects ; Neurons/physiology ; Rats ; Transcription Factor 7-Like 2 Protein/physiology ; Zebrafish
Chemical Substances	Tcf7l2 protein, mouse ; Transcription Factor 7-Like 2 Protein ; Lithium (9FN79X2M3F)
Language	English
Publishing date	2017-02
Publishing country	England
Document type	Journal Article
ZDB-ID	218272-5
ISSN	1873-7064 ; 0028-3908
ISSN (online)	1873-7064
ISSN	0028-3908
DOI	10.1016/j.neuropharm.2016.10.027
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