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Molecular Research on Mental Disorders 2.0
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Molecular Research on Mental Disorders 2.0

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Neurobiology".

Deadline for manuscript submissions: 20 January 2025 | Viewed by 8633

Special Issue Editor

Dr. Magdalena Sowa-Kućma

E-Mail Website
Guest Editor
Department of Human Physiology, Institute of Medical Sciences, Medical College of Rzeszów University, Kopisto 2a, 35-310 Rzeszow, Poland
Interests: antidepressants; glutamate receptors; epigenetics; depression; animal models of depression; oxidative stress; neuroinflammation
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues, 

Mental disorders and substance use disorders affect approximately 13% of the world's population. This number may increase in relation to the COVID-19 pandemic and the resulting changes in human functioning. Mental illnesses, in addition to having a serious impact on health, also have serious social and economic consequences in all countries of the world. There are many types of mental disorders with different presentations. In general, all of them are characterized by a combination of abnormal thoughts, perceptions, behaviors, emotions, and relationships with others. Mental disorders include depression, bipolar disorder, anxiety disorders, schizophrenia and other psychoses, dementia, and developmental disorders (including autism) that vary in their degree of severity. The causal mechanisms underlying mental disorders may contain keys to their effective prevention and treatment, but these remain poorly understood.

The aim of this Special Issue is to collect and disseminate high-quality research articles, as well as review articles, that present the most up-to-date knowledge of the molecular mechanisms involved in the development of mental illnesses and new molecular drug targets in the treatment of mental disorders.

Dr. Patrycja Pańczyszyn-Trzewik is the Guest Editor Assistant of the special issue, she will help manage the special issue with the Guest Editor, Dr. Magdalena Sowa-Kućma.

Dr. Magdalena Sowa-Kućma
Guest Editor

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Keywords

  • mental disorders
  • genetic research
  • epigenetics
  • signal transduction pathways
  • proteomics
  • genomics
  • molecular drug targets

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Published Papers (4 papers)

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Research

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29 pages, 3304 KiB  
Article
Inhibition of Indoleamine 2,3-Dioxygenase Exerts Antidepressant-like Effects through Distinct Pathways in Prelimbic and Infralimbic Cortices in Rats under Intracerebroventricular Injection with Streptozotocin
by Yu Qin, Xiao Hu, Hui-Ling Zhao, Nurhumar Kurban, Xi Chen, Jing-Kun Yi, Yuan Zhang, Su-Ying Cui and Yong-He Zhang
Int. J. Mol. Sci. 2024, 25(13), 7496; https://doi.org/10.3390/ijms25137496 - 8 Jul 2024
Cited by 1 | Viewed by 1487
Abstract
The application of intracerebroventricular injection of streptozotocin (ICV-STZ) is considered a useful animal model to mimic the onset and progression of sporadic Alzheimer’s disease (sAD). In rodents, on day 7 of the experiment, the animals exhibit depression-like behaviors. Indoleamine 2,3-dioxygenase (IDO), a rate-limiting [...] Read more.
The application of intracerebroventricular injection of streptozotocin (ICV-STZ) is considered a useful animal model to mimic the onset and progression of sporadic Alzheimer’s disease (sAD). In rodents, on day 7 of the experiment, the animals exhibit depression-like behaviors. Indoleamine 2,3-dioxygenase (IDO), a rate-limiting enzyme catalyzing the conversion of tryptophan (Trp) to kynurenine (Kyn), is closely related to depression and AD. The present study aimed to investigate the pathophysiological mechanisms of preliminary depression-like behaviors in ICV-STZ rats in two distinct cerebral regions of the medial prefrontal cortex, the prelimbic cortex (PrL) and infralimbic cortex (IL), both presumably involved in AD progression in this model, with a focus on IDO-related Kyn pathways. The results showed an increased Kyn/Trp ratio in both the PrL and IL of ICV-STZ rats, but, intriguingly, abnormalities in downstream metabolic pathways were different, being associated with distinct biological effects. In the PrL, the neuroprotective branch of the Kyn pathway was attenuated, as evidenced by a decrease in the kynurenic acid (KA) level and Kyn aminotransferase II (KAT II) expression, accompanied by astrocyte alterations, such as the decrease in glial fibrillary acidic protein (GFAP)-positive cells and increase in morphological damage. In the IL, the neurotoxicogenic branch of the Kyn pathway was enhanced, as evidenced by an increase in the 3-hydroxy-kynurenine (3-HK) level and kynurenine 3-monooxygenase (KMO) expression paralleled by the overactivation of microglia, reflected by an increase in ionized calcium-binding adaptor molecule 1 (Iba1)-positive cells and cytokines with morphological alterations. Synaptic plasticity was attenuated in both subregions. Additionally, microinjection of the selective IDO inhibitor 1-Methyl-DL-tryptophan (1-MT) in the PrL or IL alleviated depression-like behaviors by reversing these different abnormalities in the PrL and IL. These results suggest that the antidepressant-like effects linked to Trp metabolism changes induced by 1-MT in the PrL and IL occur through different pathways, specifically by enhancing the neuroprotective branch in the PrL and attenuating the neurotoxicogenic branch in the IL, involving distinct glial cells. Full article
(This article belongs to the Special Issue Molecular Research on Mental Disorders 2.0)
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17 pages, 2980 KiB  
Article
Chronic Variable Stress and Cafeteria Diet Combination Exacerbate Microglia and c-fos Activation but Not Experimental Anxiety or Depression in a Menopause Model
by Nelly Maritza Vega-Rivera, Erika Estrada-Camarena, Gabriel Azpilcueta-Morales, Nancy Cervantes-Anaya, Samuel Treviño, Enrique Becerril-Villanueva and Carolina López-Rubalcava
Int. J. Mol. Sci. 2024, 25(3), 1455; https://doi.org/10.3390/ijms25031455 - 25 Jan 2024
Cited by 1 | Viewed by 1780
Abstract
The menopause transition is a vulnerable period for developing both psychiatric and metabolic disorders, and both can be enhanced by stressful events worsening their effects. The present study aimed to evaluate whether a cafeteria diet (CAF) combined with chronic variable stress (CVS) exacerbates [...] Read more.
The menopause transition is a vulnerable period for developing both psychiatric and metabolic disorders, and both can be enhanced by stressful events worsening their effects. The present study aimed to evaluate whether a cafeteria diet (CAF) combined with chronic variable stress (CVS) exacerbates anxious- or depressive-like behavior and neuronal activation, cell proliferation and survival, and microglia activation in middle-aged ovariectomized (OVX) rats. In addition, body weight, lipid profile, insulin resistance, and corticosterone as an index of metabolic changes or hypothalamus–pituitary–adrenal (HPA) axis activation, and the serum pro-inflammatory cytokines IL-6, IL-β, and TNFα were measured. A CAF diet increased body weight, lipid profile, and insulin resistance. CVS increased corticosterone and reduced HDL. A CAF produced anxiety-like behaviors, whereas CVS induced depressive-like behaviors. CVS increased serum TNFα independently of diet. A CAF and CVS separately enhanced the percentage of Iba-positive cells in the hippocampus; the combination of factors further increased Iba-positive cells in the ventral hippocampus. A CAF and CVS increased the c-fos-positive cells in the hippocampus; the combination of factors increased the number of positive cells expressing c-fos in the ventral hippocampus even more. The combination of a CAF and CVS generates a slight neuroinflammation process and neuronal activation in a hippocampal region-specific manner and differentially affects the behavior. Full article
(This article belongs to the Special Issue Molecular Research on Mental Disorders 2.0)
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Review

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21 pages, 382 KiB  
Review
New Light on Prions: Putative Role of PrPc in Pathophysiology of Mood Disorders
by Adrian Andrzej Chrobak, Patrycja Pańczyszyn-Trzewik, Patrycja Król, Magdalena Pawelec-Bąk, Dominika Dudek and Marcin Siwek
Int. J. Mol. Sci. 2024, 25(5), 2967; https://doi.org/10.3390/ijms25052967 - 4 Mar 2024
Viewed by 1653
Abstract
Mood disorders are highly prevalent and heterogenous mental illnesses with devastating rates of mortality and treatment resistance. The molecular basis of those conditions involves complex interplay between genetic and environmental factors. Currently, there are no objective procedures for diagnosis, prognosis and personalization of [...] Read more.
Mood disorders are highly prevalent and heterogenous mental illnesses with devastating rates of mortality and treatment resistance. The molecular basis of those conditions involves complex interplay between genetic and environmental factors. Currently, there are no objective procedures for diagnosis, prognosis and personalization of patients’ treatment. There is an urgent need to search for novel molecular targets for biomarkers in mood disorders. Cellular prion protein (PrPc) is infamous for its potential to convert its insoluble form, leading to neurodegeneration in Creutzfeldt-Jacob disease. Meanwhile, in its physiological state, PrPc presents neuroprotective features and regulates neurotransmission and synaptic plasticity. The aim of this study is to integrate the available knowledge about molecular mechanisms underlying the impact of PrPc on the pathophysiology of mood disorders. Our review indicates an important role of this protein in regulation of cognitive functions, emotions, sleep and biological rhythms, and its deficiency results in depressive-like behavior and cognitive impairment. PrPc plays a neuroprotective role against excitotoxicity, oxidative stress and inflammation, the main pathophysiological events in the course of mood disorders. Research indicates that PrPc may be a promising biomarker of cognitive decline. There is an urgent need of human studies to elucidate its potential utility in clinical practice. Full article
(This article belongs to the Special Issue Molecular Research on Mental Disorders 2.0)
22 pages, 940 KiB  
Review
The Importance of α-Klotho in Depression and Cognitive Impairment and Its Connection to Glutamate Neurotransmission—An Up-to-Date Review
by Patrycja Pańczyszyn-Trzewik, Ewelina Czechowska, Katarzyna Stachowicz and Magdalena Sowa-Kućma
Int. J. Mol. Sci. 2023, 24(20), 15268; https://doi.org/10.3390/ijms242015268 - 17 Oct 2023
Cited by 3 | Viewed by 2859
Abstract
Depression is a serious neuropsychiatric disease affecting an increasing number of people worldwide. Cognitive deficits (including inattention, poor memory, and decision-making difficulties) are common in the clinical picture of depression. Cognitive impairment has been hypothesized to be one of the most important components [...] Read more.
Depression is a serious neuropsychiatric disease affecting an increasing number of people worldwide. Cognitive deficits (including inattention, poor memory, and decision-making difficulties) are common in the clinical picture of depression. Cognitive impairment has been hypothesized to be one of the most important components of major depressive disorder (MDD; referred to as clinical depression), although typical cognitive symptoms are less frequent in people with depression than in people with schizophrenia or bipolar disorder (BD; sometimes referred to as manic-depressive disorder). The importance of α-Klotho in the aging process has been well-documented. Growing evidence points to the role of α-Klotho in regulating other biological functions, including responses to oxidative stress and the modulation of synaptic plasticity. It has been proven that a Klotho deficit may contribute to the development of various nervous system pathologies, such as behavioral disorders or neurodegeneration. Given the growing evidence of the role of α-Klotho in depression and cognitive impairment, it is assumed that this protein may be a molecular link between them. Here, we provide a research review of the role of α-Klotho in depression and cognitive impairment. Furthermore, we propose potential mechanisms (related to oxidative stress and glutamatergic transmission) that may be important in α-Klotho-mediated regulation of mental and cognitive function. Full article
(This article belongs to the Special Issue Molecular Research on Mental Disorders 2.0)
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