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New Advance in Neuroinflammation
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New Advance in Neuroinflammation

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 (30 November 2022) | Viewed by 18378

Special Issue Editor

Dr. Vasileia Ismini Alexaki

E-Mail Website
Guest Editor
Institute of Clinical Chemistry and Laboratory Medicine, University Clinic Carl Gustav Carus and Medical Faculty, Technische Universität Dresden, Dresden, Germany
Interests: macrophage and microglia-mediated inflammation; cellular metabolism (citrate cycle, arginine metabolism, lipid metabolism); adrenal hormones; inflammatory mouse models
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Neuroinflammation is the sensing and reaction to any noxious event in the central nervous system (CNS) such as disease- or aging-related tissue degeneration, infection, trauma, systemic inflammation or stress. It involves the enhanced activation of microglia, which are immune cells with functions specified to the unique CNS environment. These functions include phagocytosis of synapses, dead cells (efferocytosis), cell debris, proteins and other substances; secretion of inflammatory factors; and neurotrophic effects. Astrocytes are another type of glial cell with trophic and inflammatory functions. Given that neuroinflammation is a significant hallmark of neurodegenerative disease, it is important to understand whether, when and through which mechanisms it is protective or destructive. The present Special Issue welcomes papers addressing the development, role and management of neuroinflammation.

Dr. Vasileia Ismini Alexaki
Guest Editor

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
  • central nervous system
  • microglia

Published Papers (5 papers)

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Research

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12 pages, 2492 KiB  
Article
The Ketogenic Diet and Neuroinflammation: The Action of Beta-Hydroxybutyrate in a Microglial Cell Line
by Rita Polito, Maria Ester La Torre, Fiorenzo Moscatelli, Giuseppe Cibelli, Anna Valenzano, Maria Antonietta Panaro, Marcellino Monda, Antonietta Messina, Vincenzo Monda, Daniela Pisanelli, Francesco Sessa, Giovanni Messina and Chiara Porro
Int. J. Mol. Sci. 2023, 24(4), 3102; https://doi.org/10.3390/ijms24043102 - 4 Feb 2023
Cited by 11 | Viewed by 3961
Abstract
The ketogenic diet (KD), a diet high in fat and protein but low in carbohydrates, is gaining much interest due to its positive effects, especially in neurodegenerative diseases. Beta-hydroxybutyrate (BHB), the major ketone body produced during the carbohydrate deprivation that occurs in KD, [...] Read more.
The ketogenic diet (KD), a diet high in fat and protein but low in carbohydrates, is gaining much interest due to its positive effects, especially in neurodegenerative diseases. Beta-hydroxybutyrate (BHB), the major ketone body produced during the carbohydrate deprivation that occurs in KD, is assumed to have neuroprotective effects, although the molecular mechanisms responsible for these effects are still unclear. Microglial cell activation plays a key role in the development of neurodegenerative diseases, resulting in the production of several proinflammatory secondary metabolites. The following study aimed to investigate the mechanisms by which BHB determines the activation processes of BV2 microglial cells, such as polarization, cell migration and expression of pro- and anti-inflammatory cytokines, in the absence or in the presence of lipopolysaccharide (LPS) as a proinflammatory stimulus. The results showed that BHB has a neuroprotective effect in BV2 cells, inducing both microglial polarization towards an M2 anti-inflammatory phenotype and reducing migratory capacity following LPS stimulation. Furthermore, BHB significantly reduced expression levels of the proinflammatory cytokine IL-17 and increased levels of the anti-inflammatory cytokine IL-10. From this study, it can be concluded that BHB, and consequently the KD, has a fundamental role in neuroprotection and prevention in neurodegenerative diseases, presenting new therapeutic targets. Full article
(This article belongs to the Special Issue New Advance in Neuroinflammation)
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16 pages, 5036 KiB  
Article
Effects of Apamin on MPP+-Induced Calcium Overload and Neurotoxicity by Targeting CaMKII/ERK/p65/STAT3 Signaling Pathways in Dopaminergic Neuronal Cells
by Jihyun Park, Kyung Mi Jang and Kwan-Kyu Park
Int. J. Mol. Sci. 2022, 23(23), 15255; https://doi.org/10.3390/ijms232315255 - 3 Dec 2022
Cited by 5 | Viewed by 2357
Abstract
Parkinson’s disease (PD), a neurodegenerative disorder, is characterized by the loss of dopaminergic (DA) neurons. The pathogenesis of PD is associated with several factors including oxidative stress, inflammation, and mitochondrial dysfunction. Ca2+ signaling plays a vital role in neuronal signaling and altered [...] Read more.
Parkinson’s disease (PD), a neurodegenerative disorder, is characterized by the loss of dopaminergic (DA) neurons. The pathogenesis of PD is associated with several factors including oxidative stress, inflammation, and mitochondrial dysfunction. Ca2+ signaling plays a vital role in neuronal signaling and altered Ca2+ homeostasis has been implicated in many neuronal diseases including PD. Recently, we reported that apamin (APM), a selective antagonist of the small-conductivity Ca2+-activated K+ (SK) channel, suppresses neuroinflammatory response. However, the mechanism(s) underlying the vulnerability of DA neurons were not fully understood. In this study, we investigated whether APM affected 1-methyl-4-phenyl pyridinium (MPP+)-mediated neurotoxicity in SH-SY5Y cells and rat embryo primary mesencephalic neurons. We found that APM decreased Ca2+ overload arising from MPP+-induced neurotoxicity response through downregulating the level of CaMKII, phosphorylation of ERK, and translocation of nuclear factor NFκB/signal transducer and activator of transcription (STAT)3. Furthermore, we showed that the correlation of MPP+-mediated Ca2+ overload and ERK/NFκB/STAT3 in the neurotoxicity responses, and dopaminergic neuronal cells loss, was verified through inhibitors. Our findings showed that APM might prevent loss of DA neurons via inhibition of Ca2+-overload-mediated signaling pathway and provide insights regarding the potential use of APM in treating neurodegenerative diseases. Full article
(This article belongs to the Special Issue New Advance in Neuroinflammation)
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14 pages, 3186 KiB  
Article
Pial Vessel-Associated Microglia/Macrophages Increase in Female Dahl-SS/Jr Rats Independent of Pregnancy History
by Junie P. Warrington, Qingmei Shao, Ahsia M. Clayton, Kenji J. Maeda, Ashtin G. Beckett, Michael R. Garrett and Jennifer M. Sasser
Int. J. Mol. Sci. 2022, 23(6), 3384; https://doi.org/10.3390/ijms23063384 - 21 Mar 2022
Cited by 3 | Viewed by 2157
Abstract
As the resident immune cells of the central nervous system, microglia have a wide range of functions such as surveillance, phagocytosis, and signaling through production of chemokines and cytokines. Recent studies have identified and characterized macrophages residing at the meninges, a series of [...] Read more.
As the resident immune cells of the central nervous system, microglia have a wide range of functions such as surveillance, phagocytosis, and signaling through production of chemokines and cytokines. Recent studies have identified and characterized macrophages residing at the meninges, a series of layers surrounding the brain and spinal cord. While perivascular microglia within the brain parenchyma increase following chronic hypertension, there are no reports of changes at the meninges, and specifically, associated with the pial vasculature. Thus, we used female Sprague Dawley and Dahl salt-sensitive (SS/Jr) rat brains, stained for ionized calcium-binding adapter molecule (Iba1), and characterized microglia/macrophages associated with pial vessels in the posterior brain. Results indicate that Iba1+ pial vessel-associated microglia (PVAM) completely surrounded the vessels in brains from the Dahl-SS/Jr rats. PVAM density was significantly higher and distance between PVAMs lower in Dahl-SS/Jr compared to the Sprague Dawley rat brains. Pregnancy history did not affect these findings. While the functional role of these cells are not known, we contextualize our novel findings with that of other studies assessing or characterizing myeloid cells at the borders of the CNS (meninges and choroid plexus) and perivascular macrophages and propose their possible origin in the Dahl-SS/Jr model of chronic hypertension. Full article
(This article belongs to the Special Issue New Advance in Neuroinflammation)
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Review

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17 pages, 1171 KiB  
Review
The Impairment of Blood-Brain Barrier in Alzheimer’s Disease: Challenges and Opportunities with Stem Cells
by Adolfo López-Ornelas, Adriana Jiménez, Gilberto Pérez-Sánchez, Citlali Ekaterina Rodríguez-Pérez, Alejandro Corzo-Cruz, Iván Velasco and Enrique Estudillo
Int. J. Mol. Sci. 2022, 23(17), 10136; https://doi.org/10.3390/ijms231710136 - 4 Sep 2022
Cited by 5 | Viewed by 3976
Abstract
Alzheimer’s disease (AD) is the most common neurodegenerative disorder and its prevalence is increasing. Nowadays, very few drugs effectively reduce AD symptoms and thus, a better understanding of its pathophysiology is vital to design new effective schemes. Presymptomatic neuronal damage caused by the [...] Read more.
Alzheimer’s disease (AD) is the most common neurodegenerative disorder and its prevalence is increasing. Nowadays, very few drugs effectively reduce AD symptoms and thus, a better understanding of its pathophysiology is vital to design new effective schemes. Presymptomatic neuronal damage caused by the accumulation of Amyloid β peptide and Tau protein abnormalities remains a challenge, despite recent efforts in drug development. Importantly, therapeutic targets, biomarkers, and diagnostic techniques have emerged to detect and treat AD. Of note, the compromised blood-brain barrier (BBB) and peripheral inflammation in AD are becoming more evident, being harmful factors that contribute to the development of the disease. Perspectives from different pre-clinical and clinical studies link peripheral inflammation with the onset and progression of AD. This review aims to analyze the main factors and the contribution of impaired BBB in AD development. Additionally, we describe the potential therapeutic strategies using stem cells for AD treatment. Full article
(This article belongs to the Special Issue New Advance in Neuroinflammation)
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15 pages, 1181 KiB  
Review
Neuroinflammation in Schizophrenia: The Key Role of the WNT/β-Catenin Pathway
by Alexandre Vallée
Int. J. Mol. Sci. 2022, 23(5), 2810; https://doi.org/10.3390/ijms23052810 - 4 Mar 2022
Cited by 40 | Viewed by 4969
Abstract
Schizophrenia is a very complex syndrome involving widespread brain multi-dysconnectivity. Schizophrenia is marked by cognitive, behavioral, and emotional dysregulations. Recent studies suggest that inflammation in the central nervous system (CNS) and immune dysfunction could have a role in the pathogenesis of schizophrenia. This [...] Read more.
Schizophrenia is a very complex syndrome involving widespread brain multi-dysconnectivity. Schizophrenia is marked by cognitive, behavioral, and emotional dysregulations. Recent studies suggest that inflammation in the central nervous system (CNS) and immune dysfunction could have a role in the pathogenesis of schizophrenia. This hypothesis is supported by immunogenetic evidence, and a higher incidence rate of autoimmune diseases in patients with schizophrenia. The dysregulation of the WNT/β-catenin pathway is associated with the involvement of neuroinflammation in schizophrenia. Several studies have shown that there is a vicious and positive interplay operating between neuroinflammation and oxidative stress. This interplay is modulated by WNT/β-catenin, which interacts with the NF-kB pathway; inflammatory factors (including IL-6, IL-8, TNF-α); factors of oxidative stress such as glutamate; and dopamine. Neuroinflammation is associated with increased levels of PPARγ. In schizophrenia, the expression of PPAR-γ is increased, whereas the WNT/β-catenin pathway and PPARα are downregulated. This suggests that a metabolic-inflammatory imbalance occurs in this disorder. Thus, this research’s triptych could be a novel therapeutic approach to counteract both neuroinflammation and oxidative stress in schizophrenia. Full article
(This article belongs to the Special Issue New Advance in Neuroinflammation)
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