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Immunology of Neuropsychiatric Disorders

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: closed (31 August 2022) | Viewed by 17984

Special Issue Editors


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Guest Editor
McGovern Medical School, University of Texas Health Science Center at Houston, Houston, TX, USA
Interests: Alzheimer’s disease; Huntington’s diseases; neuropsychiatric disorders; brain stimulation
Special Issues, Collections and Topics in MDPI journals

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Guest Editor
Pontifícia Universidade Católica do Rio Grande do Sul, Porto Alegre, Brazil
Interests: Neuroimmunology; Immunopsychiatry; Immunosenescence; Cellular Senescence; Chronic Stress; Early-Life Stress

Special Issue Information

Dear Colleagues,

Neuropsychiatric disorders are among the main causes of disability worldwide. While the development of novel neurotransmitter-based pharmacological strategies to address them has stalled, different target mechanisms have been pursued. Among promising candidates, there is a growing recognition of the role played by immune mechanisms on body homeostasis in general and central nervous system functioning in particular. Understanding the involvement of immune processes in the pathogenesis and pathophysiology of neuropsychiatric disorders opens venues for the investigation of new biomarkers and molecular targets for these conditions. Accordingly, the overall objective of this Special Issue is to provide an overview of the emerging area of immunopsychiatry.

Dr. Antonio L. Teixeira
Prof. Dr. Moises E. Bauer
Guest Editors

Manuscript Submission Information

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Published Papers (4 papers)

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Research

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15 pages, 2769 KiB  
Article
Sensitivity of Rodent Microglia to Kynurenines in Models of Epilepsy and Inflammation In Vivo and In Vitro: Microglia Activation Is Inhibited by Kynurenic Acid and the Synthetic Analogue SZR104
by Noémi Lajkó, Diana Kata, Melinda Szabó, Adrienne Mátyás, Karolina Dulka, Imre Földesi, Ferenc Fülöp, Karoly Gulya, László Vécsei and András Mihály
Int. J. Mol. Sci. 2020, 21(23), 9333; https://doi.org/10.3390/ijms21239333 - 07 Dec 2020
Cited by 8 | Viewed by 2878
Abstract
Kynurenic acid is an endogenous modulator of ionotropic glutamate receptors and a suppressor of the immune system. Since glutamate and microglia are important in the pathogenesis of epilepsy, we investigated the possible action of the synthetic kynurenic acid analogue, SZR104, in epileptic mice [...] Read more.
Kynurenic acid is an endogenous modulator of ionotropic glutamate receptors and a suppressor of the immune system. Since glutamate and microglia are important in the pathogenesis of epilepsy, we investigated the possible action of the synthetic kynurenic acid analogue, SZR104, in epileptic mice and the action of kynurenic acid and SZR104 on the phagocytotic activity of cultured microglia cells. Pilocarpine epilepsy was used to test the effects of SZR104 on morphological microglia transformation, as evaluated through ionized calcium-binding adaptor molecule 1 (Iba1) immunohistochemistry. Microglia-enriched rat secondary cultures were used to investigate phagocytosis of fluorescent microbeads and Iba1 protein synthesis in control and lipopolysaccharide-challenged cultures. SZR104 inhibited microglia transformation following status epilepticus. Kynurenic acid and SZR104 inhibited lipopolysaccharide-stimulated phagocytotic activity of microglia cells. Although kynurenic acid and its analogues proved to be glutamate receptor antagonists, their immunosuppressive action was dominant in epilepsy. The inhibition of phagocytosis in vitro raised the possibility of the inhibition of genes encoding inflammatory cytokines in microglial cells. Full article
(This article belongs to the Special Issue Immunology of Neuropsychiatric Disorders)
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13 pages, 1187 KiB  
Article
Expression and Functionality Study of 9 Toll-Like Receptors in 33 Drug-Naïve Non-Affective First Episode Psychosis Individuals: A 3-Month Study
by Maria Juncal-Ruiz, Laura Riesco-Davila, Javier Vazquez-Bourgon, Victor Ortiz-Garcia de la Foz, Jacqueline Mayoral-Van Son, Rosa Ayesa-Arriola, Esther Setien-Suero, Juan Carlos Leza, Marcos Lopez-Hoyos and Benedicto Crespo-Facorro
Int. J. Mol. Sci. 2020, 21(17), 6106; https://doi.org/10.3390/ijms21176106 - 25 Aug 2020
Cited by 6 | Viewed by 2473
Abstract
Toll-like receptors (TLRs) are a pivotal component of the innate immune system that seem to have a role in the pathogenesis of psychosis. The purpose of this work was to compare the expression and functionality of 9 TLRs in three peripheral blood mononuclear [...] Read more.
Toll-like receptors (TLRs) are a pivotal component of the innate immune system that seem to have a role in the pathogenesis of psychosis. The purpose of this work was to compare the expression and functionality of 9 TLRs in three peripheral blood mononuclear cells (PBMCs) (monocytes, B cells, and T cells) between 33 drug-naïve first-episode psychosis (FEP) individuals and 26 healthy volunteers, at baseline and after 3-month of antipsychotic treatment. The expression of TLRs 1–9 were assessed by flow cytometry. For the assessment of the TLR functionality, cells collected in sodium heparin tubes were polyclonally stimulated for 18 h, with different agonists for human TLR1–9. The results of our study highlight the role that TLR5 and TLR8 might play in the pathophysiology of psychosis. We found a lower expression of these receptors in FEP individuals, regarding healthy volunteers at baseline and after 3-month of treatment on the three PBMCs subsets. Most TLRs showed a lower functionality (especially reduced intracellular levels of TNF-α) in patients than in healthy volunteers. These results, together with previous evidence, suggest that individuals with psychosis might show a pattern of TLR expression that differs from that of healthy volunteers, which could vary according to the intensity of immune/inflammatory response. Full article
(This article belongs to the Special Issue Immunology of Neuropsychiatric Disorders)
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Review

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16 pages, 739 KiB  
Review
Immunological Dysfunction in Tourette Syndrome and Related Disorders
by Chia-Jui Hsu, Lee-Chin Wong and Wang-Tso Lee
Int. J. Mol. Sci. 2021, 22(2), 853; https://doi.org/10.3390/ijms22020853 - 16 Jan 2021
Cited by 26 | Viewed by 7167
Abstract
Chronic tic disorder and Tourette syndrome are common childhood-onset neurological diseases. However, the pathophysiology underlying these disorders is unclear, and most studies have focused on the disinhibition of the corticostriatal–thalamocortical circuit. An autoimmune dysfunction has been proposed in the pathogenetic mechanism of Tourette [...] Read more.
Chronic tic disorder and Tourette syndrome are common childhood-onset neurological diseases. However, the pathophysiology underlying these disorders is unclear, and most studies have focused on the disinhibition of the corticostriatal–thalamocortical circuit. An autoimmune dysfunction has been proposed in the pathogenetic mechanism of Tourette syndrome and related neuropsychiatric disorders such as obsessive–compulsive disorder, autism, and attention-deficit/hyperactivity disorder. This is based on evidence from animal model studies and clinical findings. Herein, we review and give an update on the clinical characteristics, clinical evidence, and genetic studies in vitro as well as animal studies regarding immune dysfunction in Tourette syndrome. Full article
(This article belongs to the Special Issue Immunology of Neuropsychiatric Disorders)
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21 pages, 834 KiB  
Review
Neuropsychiatric Disorders Due to Limbic Encephalitis: Immunologic Aspect
by Yu-Chia Kao, Ming-I Lin, Wen-Chin Weng and Wang-Tso Lee
Int. J. Mol. Sci. 2021, 22(1), 389; https://doi.org/10.3390/ijms22010389 - 31 Dec 2020
Cited by 12 | Viewed by 4759
Abstract
Limbic encephalitis (LE) is a rare cause of encephalitis presenting as an acute and subacute onset of neuropsychiatric manifestations, particularly with memory deficits and confusion as core features, along with seizure occurrence, movement disorders, or autonomic dysfunctions. LE is caused by neuronal antibodies [...] Read more.
Limbic encephalitis (LE) is a rare cause of encephalitis presenting as an acute and subacute onset of neuropsychiatric manifestations, particularly with memory deficits and confusion as core features, along with seizure occurrence, movement disorders, or autonomic dysfunctions. LE is caused by neuronal antibodies targeting the cellular surface, synaptic, and intracellular antigens, which alter the synaptic transmission, especially in the limbic area. Immunologic mechanisms involve antibodies, complements, or T-cell-mediated immune responses in different degree according to different autoantibodies. Sensitive cerebrospinal fluid markers of LE are unavailable, and radiographic findings may not reveal a typical mesiotemporal involvement at neurologic presentations; therefore, a high clinical index of suspicions is pivotal, and a neuronal antibody testing is necessary to make early diagnosis. Some patients have concomitant tumors, causing paraneoplastic LE; therefore, tumor survey and treatment are required in addition to immunotherapy. In this study, a review on the molecular and immunologic aspects of LE was conducted to gain awareness of its peculiarity, which we found quite different from our knowledge on traditional psychiatric illness. Full article
(This article belongs to the Special Issue Immunology of Neuropsychiatric Disorders)
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