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Neuroinflammation and Psychiatric Disorders: From Mechanisms to Therapy Potential
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Neuroinflammation and Psychiatric Disorders: From Mechanisms to Therapy Potential

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Pathology, Diagnostics, and Therapeutics".

Deadline for manuscript submissions: closed (31 December 2018) | Viewed by 29212

Special Issue Editors

Prof. Dr. Romina Mizrahi

E-Mail Website
Guest Editor
Department of Pharmacology and Toxicology, University of Toronto, Toronto, ON M5S 1A8, Canada
Interests: neuroimaging; schziophrenia; psychosis; psychosis risk; neuroinflammation; positron emission tomography; endocannabinoid system; dopaminergic system; stress
Dr. Sina Hafizi

E-Mail Website
Guest Editor
Research Imaging Centre, Centre for Addiction and Mental Health, Toronto, ON M5T 1R8, Canada
Interests: neuroimaging; schziophrenia; psychosis; psychosis risk; neuroinflammation; positron emission tomography

Special Issue Information

Dear Colleagues,

Neuroinflammation and abnormal immune function are suggested to contribute to the development and progression of several psychiatric disorders including (but not limited to) neurodegenerative diseases, autism spectrum disorder and schizophrenia. However, the exact mechanisms underlying the link between these pathophysiological factors and psychiatric disorders are still not clear. Preclinical studies have shown immune abnormalities in animal models of psychiatric disorders. In addition, some immune modulators can induce symptoms resembling psychiatric disorders in animals. Another line of evidence is based on genome-wide association studies showing association between immune-related genes and psychiatric disorders. Supporting this, epidemiological studies have provided evidence for the link between maternal infections during pregnancy and risk of some psychiatric disorders (e.g., autism and schizophrenia) in offspring. One of the most important implications of this research pertains to identification of new targets for novel treatments; as there is a growing body of literature on the role of immune-modulatory medications in prevention and/or treatment of psychiatric disorders. While the role of non-steroidal anti-inflammatory drugs or supplements, such as omega-3 fatty acids is controversial (at best) for neurodegenerative or neurodevelopmental diseases, future studies should aim for more specific therapies. In this Special Issue, we solicit manuscripts that address any aspects of the connection between neuroinflammation and psychiatric disorders; more importantly articles that illustrate how our current understanding of these pathological factors can help in developing novel treatments.

Prof. Dr. Romina Mizrahi
Dr. Sina Hafizi
Guest Editors

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. International Journal of Molecular Sciences is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. There is an Article Processing Charge (APC) for publication in this open access journal. For details about the APC please see here. Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • neuroinflammation
  • cytokines
  • microglia
  • chemokines
  • glia
  • blood-brain barrier
  • immune system
  • diagnosis
  • prevention
  • treatment

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Published Papers (4 papers)

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Research

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20 pages, 10941 KiB  
Article
Lack of Rhes Increases MDMA-Induced Neuroinflammation and Dopamine Neuron Degeneration: Role of Gender and Age
by Giulia Costa, Pier Francesca Porceddu, Marcello Serra, Maria Antonietta Casu, Valentina Schiano, Francesco Napolitano, Annalisa Pinna, Alessandro Usiello and Micaela Morelli
Int. J. Mol. Sci. 2019, 20(7), 1556; https://doi.org/10.3390/ijms20071556 - 28 Mar 2019
Cited by 19 | Viewed by 4368
Abstract
Ras homolog enriched in striatum (Rhes) is a protein that exerts important physiological functions and modulates psychostimulant drug effects. On this basis, the object of this study was to assess 3,4-methylenedioxymethamphetamine (MDMA) effects on microglial (CD11b) and astroglial (GFAP) activation and on dopamine [...] Read more.
Ras homolog enriched in striatum (Rhes) is a protein that exerts important physiological functions and modulates psychostimulant drug effects. On this basis, the object of this study was to assess 3,4-methylenedioxymethamphetamine (MDMA) effects on microglial (CD11b) and astroglial (GFAP) activation and on dopamine neuron degeneration (TH) in wild-type (WT) and Rhes knockout (KO) male and female mice of different ages. Motor activity was also evaluated. Adult (3 months) MDMA-treated mice displayed an increase in GFAP-positive cells in striatum (STR), whereas the substantia nigra pars compacta (SNc) was affected only in male mice. In these mice, the increase of CD11b was more extensive including STR, SNc, motor cortex (CTX), ventral tegmental area (VTA), and nucleus accumbens (NAc). MDMA administration also affected TH immunoreactivity in both STR and SNc of male but not female WT and Rhes KO mice. In middle-aged mice (12 months), MDMA administration further increased GFAP and CD11b and decreased TH immunoreactivity in STR and SNc of all mice. Finally, MDMA induced a higher increase of motor activity in adult Rhes KO male, but not female mice. The results show that Rhes protein plays an important role on MDMA-mediated neuroinflammation and neurodegeneration dependent on gender and age, and confirm the important role of Rhes protein in neuroinflammatory and neurodegenerative processes. Full article
(This article belongs to the Special Issue Neuroinflammation and Psychiatric Disorders: From Mechanisms to Therapy Potential)
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16 pages, 4343 KiB  
Article
Early Hyperbaric Oxygen Treatment Attenuates Burn-Induced Neuroinflammation by Inhibiting the Galectin-3-Dependent Toll-Like Receptor-4 Pathway in a Rat Model
by Zong-Sheng Wu, Jing-Jou Lo, Sheng-Hua Wu, Chau-Zen Wang, Rong-Fu Chen, Su-Shin Lee, Chee-Yin Chai and Shu-Hung Huang
Int. J. Mol. Sci. 2018, 19(8), 2195; https://doi.org/10.3390/ijms19082195 - 27 Jul 2018
Cited by 28 | Viewed by 5473
Abstract
Hyperbaric oxygen (HBO) treatment has been proven to decrease neuroinflammation in rats. This study aimed to determine the potential mechanism underlying the anti-inflammatory effects of HBO treatment on burn-induced neuroinflammation in rats. Thirty-six adult male Sprague-Dawley (SD) rats were randomly assigned to the [...] Read more.
Hyperbaric oxygen (HBO) treatment has been proven to decrease neuroinflammation in rats. This study aimed to determine the potential mechanism underlying the anti-inflammatory effects of HBO treatment on burn-induced neuroinflammation in rats. Thirty-six adult male Sprague-Dawley (SD) rats were randomly assigned to the following six groups (n = 6 per group): (1) sham burn with sham HBO treatment; (2) sham burn with HBO treatment; (3) burn with one-week sham HBO treatment; (4) burn with two-week sham HBO treatment; (5) burn with one-week HBO treatment; and (6) burn with two-week HBO treatment. SD rats that received third-degree burn injury were used as a full-thickness burn injury model. Subsequently, we analyzed the expression of proteins involved in the galectin-3 (Gal-3)-dependent Toll-like receptor-4 (TLR-4) pathway through enzyme-linked immunosorbent assay (ELISA), immunohistochemistry (IHC) analysis, and Western blotting. A behavior test was also conducted, which revealed that HBO treatment significantly suppressed mechanical hypersensitivity in the burn with HBO treatment group compared to the burn with sham HBO treatment group (p < 0.05). ELISA results showed that tumor necrosis factor α (TNF-α) and interleukin 1 beta (IL-1β) levels in the dorsal horn of the spinal cord and the skin significantly decreased in the burn with HBO treatment group compared with the burn with sham HBO treatment group (p < 0.05). Western blotting results demonstrated that HBO treatment significantly reduced the expression of Gal-3 and TLR-4 in the dorsal horn of the spinal cord in the burn with HBO treatment group compared with the burn with sham HBO treatment group (p < 0.05). IHC analysis showed that the expression of Gal-3, TLR-4, CD68 and CD45 in the dorsal horn of the spinal cord was significantly lower in the burn with HBO treatment group than in the burn with sham HBO treatment group (p < 0.05), and the expression of CD68 and macrophage migration inhibitory factor (MIF) in the right hind paw skin was significantly lower. The expression of vimentin and fibroblast growth factor in the right hind paw skin was significantly higher after HBO treatment (p < 0.05). This study proved that early HBO treatment relieves neuropathic pain, inhibits the Gal-3-dependent TLR-4 pathway, and suppresses microglia and macrophage activation in a rat model. Full article
(This article belongs to the Special Issue Neuroinflammation and Psychiatric Disorders: From Mechanisms to Therapy Potential)
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Review

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29 pages, 328 KiB  
Review
Sex-Dependent Effects of Perinatal Inflammation on the Brain: Implication for Neuro-Psychiatric Disorders
by Maryam Ardalan, Tetyana Chumak, Zinaida Vexler and Carina Mallard
Int. J. Mol. Sci. 2019, 20(9), 2270; https://doi.org/10.3390/ijms20092270 - 8 May 2019
Cited by 60 | Viewed by 7583
Abstract
Individuals born preterm have higher rates of neurodevelopmental disorders such as schizophrenia, autistic spectrum, and attention deficit/hyperactivity disorders. These conditions are often sexually dimorphic and with different developmental trajectories. The etiology is likely multifactorial, however, infections both during pregnancy and in childhood have [...] Read more.
Individuals born preterm have higher rates of neurodevelopmental disorders such as schizophrenia, autistic spectrum, and attention deficit/hyperactivity disorders. These conditions are often sexually dimorphic and with different developmental trajectories. The etiology is likely multifactorial, however, infections both during pregnancy and in childhood have emerged as important risk factors. The association between sex- and age-dependent vulnerability to neuropsychiatric disorders has been suggested to relate to immune activation in the brain, including complex interactions between sex hormones, brain transcriptome, activation of glia cells, and cytokine production. Here, we will review sex-dependent effects on brain development, including glia cells, both under normal physiological conditions and following perinatal inflammation. Emphasis will be given to sex-dependent effects on brain regions which play a role in neuropsychiatric disorders and inflammatory reactions that may underlie early-life programming of neurobehavioral disturbances later in life. Full article
(This article belongs to the Special Issue Neuroinflammation and Psychiatric Disorders: From Mechanisms to Therapy Potential)
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34 pages, 3184 KiB  
Review
From Systemic Inflammation to Neuroinflammation: The Case of Neurolupus
by Mykolas Bendorius, Chrystelle Po, Sylviane Muller and Hélène Jeltsch-David
Int. J. Mol. Sci. 2018, 19(11), 3588; https://doi.org/10.3390/ijms19113588 - 13 Nov 2018
Cited by 55 | Viewed by 11007
Abstract
It took decades to arrive at the general consensus dismissing the notion that the immune system is independent of the central nervous system. In the case of uncontrolled systemic inflammation, the relationship between the two systems is thrown off balance and results in [...] Read more.
It took decades to arrive at the general consensus dismissing the notion that the immune system is independent of the central nervous system. In the case of uncontrolled systemic inflammation, the relationship between the two systems is thrown off balance and results in cognitive and emotional impairment. It is specifically true for autoimmune pathologies where the central nervous system is affected as a result of systemic inflammation. Along with boosting circulating cytokine levels, systemic inflammation can lead to aberrant brain-resident immune cell activation, leakage of the blood–brain barrier, and the production of circulating antibodies that cross-react with brain antigens. One of the most disabling autoimmune pathologies known to have an effect on the central nervous system secondary to the systemic disease is systemic lupus erythematosus. Its neuropsychiatric expression has been extensively studied in lupus-like disease murine models that develop an autoimmunity-associated behavioral syndrome. These models are very useful for studying how the peripheral immune system and systemic inflammation can influence brain functions. In this review, we summarize the experimental data reported on murine models developing autoimmune diseases and systemic inflammation, and we explore the underlying mechanisms explaining how systemic inflammation can result in behavioral deficits, with a special focus on in vivo neuroimaging techniques. Full article
(This article belongs to the Special Issue Neuroinflammation and Psychiatric Disorders: From Mechanisms to Therapy Potential)
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