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Advances in Neuroinflammation

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A special issue of Brain Sciences (ISSN 2076-3425). This special issue belongs to the section "Molecular and Cellular Neuroscience".

Deadline for manuscript submissions: 30 April 2024 | Viewed by 13551

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Special Issue Editors

Dr. Junhui Wang

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Guest Editor

Mount Sinai Hospital, 600 University Avenue, Toronto, ON, Canada
Interests: the interactions between neurons and astrocytes; the role of astrocytes in neurodegenerative diseases (especially tauotopathy, lewy body and AD)
Special Issues, Collections and Topics in MDPI journals

Dr. Hongxing Wang

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Guest Editor

Department of Neurology, Xuanwu Hospital of Capital Medical University, Beijing, China
Interests: research is primarily focused on how gut microbiota affect Alzheimer’s disease at molecular level, especially utilizing the translational medicine route to further understand brain dysfunction

Dr. Jing Sun

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Guest Editor

Department of Pathology (Neuropathology), Capital Medical University, Beijing, China
Interests: neuropathology

Special Issue Information

Dear Colleagues,

Background and history of this topic: Neuroinflammation, mediated by the formation of multiple cytokines, chemokines, reactive oxygen species, etc., has been found to be involved in the aetiopathology of a plethora of neurological diseases. Accumulating evidence from clinical and preclinical studies has validated the great potential of neuroinflammation in the research perspective in terms of mechanism and treatment studies.
Aim and scope of the Special Issue: This Special Issue of Brain Sciences aims to present the recent advance in neuroinflammation research on preclinical and clinical areas, especially focusing on but not limited on neurodegenerative diseases.

[*] Cutting-edge research: In vivo and in vitro studies related to the advance on conception, technology renovation, novel models, etc., which could be applied to study the role of neuroinflammation in neurodegenerative diseases are especially welcome.
What kind of papers we are soliciting: In addition to research articles, reviews or mini reviews covering the recent progress of neuroinflammatory role in neurodegenerative diseases are encouraged too. Case reports presenting some rare glia-related conditions (neuroinflammation) from clinical settings with the imaging or neuropathology pattern are also welcome.

Dr. Junhui Wang
Dr. Hongxing Wang
Dr. Jing Sun
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. Brain Sciences is an international peer-reviewed open access monthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2200 CHF (Swiss Francs). 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
neurodegenerative diseases
glia
cytokines
chemokines

Published Papers (8 papers)

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Research

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15 pages, 1843 KiB

Open AccessArticle

EEG Biofeedback Decreases Theta and Beta Power While Increasing Alpha Power in Insomniacs: An Open-Label Study

by Huicong Wang, Yue Hou, Shuqin Zhan, Ning Li, Jianghong Liu, Penghui Song, Yuping Wang and Hongxing Wang

Brain Sci. 2023, 13(11), 1542; https://doi.org/10.3390/brainsci13111542 - 02 Nov 2023

Viewed by 1169

Abstract

Insomnia, often associated with anxiety and depression, is a prevalent sleep disorder. Biofeedback (BFB) treatment can help patients gain voluntary control over physiological events such as by utilizing electroencephalography (EEG) and electromyography (EMG) power. Previous studies have rarely predicted biofeedback efficacy by measuring the changes in relative EEG power; therefore, we investigated the clinical efficacy of biofeedback for insomnia and its potential neural mechanisms. We administered biofeedback to 82 patients with insomnia, of whom 68 completed 10 sessions and 14 completed 20 sessions. The average age of the participants was 49.38 ± 12.78 years, with 26 men and 56 women. Each biofeedback session consisted of 5 min of EMG and 30 min of EEG feedback, with 2 min of data recorded before and after the session. Sessions were conducted every other day, and four scale measures were taken before the first, fifth, and tenth sessions and after the twentieth session. After 20 sessions of biofeedback treatment, scores on the Pittsburgh Sleep Quality Index (PSQI) were significantly reduced compared with those before treatment (−5.5 ± 1.43,t = −3.85, p = 0.006), and scores on the Beck Depression Inventory (BDI-II) (−7.15 ± 2.43, t = −2.94, p = 0.012) and the State-Trait Anxiety Inventory (STAI) (STAI-S: −12.36 ± 3.40, t = −3.63, p = 0.003; and STAI-T: −9.86 ± 2.38, t = −4.41, p = 0.001) were significantly lower after treatment than before treatment. Beta and theta power were significantly reduced after treatment, compared with before treatment (F = 6.25, p = 0.014; and F = 11.91, p = 0.001). Alpha power was increased after treatment, compared with before treatment, but the difference was not prominently significant (p > 0.05). EMG activity was significantly decreased after treatment, compared with before treatment (F = 2.11, p = 0.015). Our findings suggest that BFB treatment based on alpha power and prefrontal EMG relieves insomnia as well as anxiety and depression and may be associated with increased alpha power, decreased beta and theta power, and decreased EMG power. Full article

(This article belongs to the Special Issue Advances in Neuroinflammation)

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14 pages, 7260 KiB

Open AccessArticle

The Crosstalk between the EGFR and IFN-γ Pathways and Synergistic Roles in Survival Prediction and Immune Escape in Gliomas

by Xingang Zhou, Tingyu Liang, Yulu Ge, Yu Wang and Wenbin Ma

Brain Sci. 2023, 13(9), 1349; https://doi.org/10.3390/brainsci13091349 - 20 Sep 2023

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Abstract

Glioma is the most common primary malignant brain tumor. The poor prognosis of gliomas, especially glioblastoma (GBM), is associated with their unique molecular landscape and tumor microenvironment (TME) features. The epidermal growth factor receptor (EGFR) gene is one of the frequently altered loci in gliomas, leading to the activation of the EGFR signaling pathway and thus, promoting the genesis of gliomas. Whether there exist factors within the TME that can lead to EGFR activation in the context of gliomas is currently unexplored. In total, 702 samples from The Cancer Genome Atlas (TCGA) and 325 samples from The Chinese Glioma Genome Atlas (CGGA) were enrolled in this study. Gene signatures related to EGFR signaling and interferon-γ (IFN-γ) response were established via the LASSO-COX algorithm. Gene Set Enrichment Analysis (GSEA) and Gene Ontology (GO) analysis were applied for function exploration. Kaplan–Meier (KM) curves and single sample GSEA (ssGSEA) of immune cell subpopulations were performed to analyze the prognosis and TME characteristics of different subgroups. Moreover, Western blotting (WB) and flow cytometry (FCM) demonstrated the correlation between IFN-γ and EGFR signaling activation and the subsequent induction of programmed death ligand 1 (PD-L1) expression. An EGFR signaling-related risk score was established, and a higher score was correlated with poorer prognosis and a more malignant phenotype in gliomas. Biological function analysis revealed that a higher EGFR-related score was significantly associated with various cytokine response pathways, especially IFN-γ. Long-term (7 days) exposure to IFN-γ (400 ng/mL) induced the activation of EGFR signaling in the u87 cell line. Next, an IFN-γ response-related risk score was established; the combination of these two scores could be used to further reclassify gliomas into subtypes with different clinical features and TME features. Double high-risk samples tended to have a poorer prognosis and more immunosuppressive TME. Additionally, FCM discovered that the activation of EGFR signaling via EGF (100 ng/mL) could trigger PD-L1 protein expression. This research indicates that IFN-γ, an inflammatory cytokine, can activate the EGFR pathway. The combination of EGFR signaling and IFN-γ response pathway can establish a more precise classification of gliomas. Full article

(This article belongs to the Special Issue Advances in Neuroinflammation)

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19 pages, 8487 KiB

Open AccessArticle

Dexmedetomidine Improves Anxiety-like Behaviors in Sleep-Deprived Mice by Inhibiting the p38/MSK1/NFκB Pathway and Reducing Inflammation and Oxidative Stress

by Jiangjing Li, Heming Zhang, Bin Deng, Xin Wang, Peng Liang, Shenglong Xu, Ziwei Jing, Zhibin Xiao, Li Sun, Changjun Gao, Jin Wang and Xude Sun

Brain Sci. 2023, 13(7), 1058; https://doi.org/10.3390/brainsci13071058 - 11 Jul 2023

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Abstract

(1) Background: Sleep deprivation (SD) triggers a range of neuroinflammatory responses. Dexmedetomidine can improve sleep deprivation-induced anxiety by reducing neuroinflammatory response but the mechanism is unclear; (2) Methods: The sleep deprivation model was established by using an interference rod device. An open field test and an elevated plus maze test were used to detect the emotional behavior of mice. Mouse cortical tissues were subjected to RNA sequence (RNA-seq) analysis. Western blotting and immunofluorescence were used to detect the expression of p38/p-p38, MSK1/p-MSK1, and NFκBp65/p- NFκBp65. Inflammatory cytokines were detected using enzyme-linked immunosorbent assay (ELISA); (3) Results: SD triggered anxiety-like behaviors in mice and was closely associated with inflammatory responses and the MAPK pathway (as demonstrated by transcriptome analysis). SD led to increased expression levels of p-p38, p-MSK1, and p-NFκB. P38 inhibitor SB203580 was used to confirm the important role of the p38/MSK1/NFκB pathway in SD-induced neuroinflammation. Dexmedetomidine (Dex) effectively improves emotional behavior in sleep-deprived mice by attenuating SD-induced inflammatory responses and oxidative stress in the cerebral cortex, mainly by inhibiting the activation of the p38/MSK1/NFκB pathway; (4) Conclusions: Dex inhibits the activation of the p38/MSK1/NFκB pathway, thus attenuating SD-induced inflammatory responses and oxidative stress in the cerebral cortex of mice. Full article

(This article belongs to the Special Issue Advances in Neuroinflammation)

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10 pages, 795 KiB

Open AccessArticle

Clinical and Neurophysiological Follow-Up of Chronic Inflammatory Demyelinating Polyneuropathy Patients Treated with Subcutaneous Immunoglobulins: A Real-Life Single Center Study

by Paolo Alonge, Vincenzo Di Stefano, Antonino Lupica, Massimo Gangitano, Angelo Torrente, Antonia Pignolo, Bruna Maggio, Salvatore Iacono, Francesca Gentile and Filippo Brighina

Brain Sci. 2023, 13(1), 10; https://doi.org/10.3390/brainsci13010010 - 21 Dec 2022

Cited by 2 | Viewed by 1101

Abstract

Background: chronic idiopathic demyelinating polyneuropathy (CIDP) is an acquired, immune-mediated neuropathy characterized by weakness, sensory symptoms and significant reduction or loss of deep tendon reflexes evolving over 2 months at least, associated with electrophysiological evidence of peripheral nerve demyelination. Recently, subcutaneous immunoglobulins (SCIg) have been introduced in clinical practice as a maintenance therapy for CIDP; nevertheless, electrophysiological and efficacy data are limited. Methods: to evaluate SCIg treatment efficacy, we retrospectively reviewed data from 15 CIDP patients referring to our clinic, receiving SCIg treatment and who performed electrophysiological studies (NCS) and clinical scores (MRC sumscore, INCAT disability score and ISS) before starting the treatment and at least one year after. Results: NCS showed no significant changes before and during treatment for all the nerves explored. Clinical scores did not significantly change between evaluations. Correlation analysis evidenced a positive correlation of cMAPs distal amplitude with MRC sumscore and a trend of negative correlation with the INCAT disability score. Conclusions: SCIg maintenance therapy preserves nerve function in CIDP with a good efficacy and safety. Treatment effectiveness can be assessed with ENG, which represents a useful instrument in the follow-up and prognostic assessment of CIDP. Full article

(This article belongs to the Special Issue Advances in Neuroinflammation)

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Review

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21 pages, 926 KiB

Open AccessReview

The Diverse Roles of Reactive Astrocytes in the Pathogenesis of Amyotrophic Lateral Sclerosis

by Kangqin Yang, Yang Liu and Min Zhang

Brain Sci. 2024, 14(2), 158; https://doi.org/10.3390/brainsci14020158 - 04 Feb 2024

Cited by 1 | Viewed by 1873

Abstract

Astrocytes displaying reactive phenotypes are characterized by their ability to remodel morphologically, molecularly, and functionally in response to pathological stimuli. This process results in the loss of their typical astrocyte functions and the acquisition of neurotoxic or neuroprotective roles. A growing body of research indicates that these reactive astrocytes play a pivotal role in the pathogenesis of amyotrophic lateral sclerosis (ALS), involving calcium homeostasis imbalance, mitochondrial dysfunction, abnormal lipid and lactate metabolism, glutamate excitotoxicity, etc. This review summarizes the characteristics of reactive astrocytes, their role in the pathogenesis of ALS, and recent advancements in astrocyte-targeting strategies. Full article

(This article belongs to the Special Issue Advances in Neuroinflammation)

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25 pages, 1265 KiB

Open AccessReview

Thirty Risk Factors for Alzheimer’s Disease Unified by a Common Neuroimmune–Neuroinflammation Mechanism

by Donald F. Weaver

Brain Sci. 2024, 14(1), 41; https://doi.org/10.3390/brainsci14010041 - 31 Dec 2023

Cited by 1 | Viewed by 2397

Abstract

One of the major obstacles confronting the formulation of a mechanistic understanding for Alzheimer’s disease (AD) is its immense complexity—a complexity that traverses the full structural and phenomenological spectrum, including molecular, macromolecular, cellular, neurological and behavioural processes. This complexity is reflected by the equally complex diversity of risk factors associated with AD. However, more than merely mirroring disease complexity, risk factors also provide fundamental insights into the aetiology and pathogenesis of AD as a neurodegenerative disorder since they are central to disease initiation and subsequent propagation. Based on a systematic literature assessment, this review identified 30 risk factors for AD and then extended the analysis to further identify neuroinflammation as a unifying mechanism present in all 30 risk factors. Although other mechanisms (e.g., vasculopathy, proteopathy) were present in multiple risk factors, dysfunction of the neuroimmune–neuroinflammation axis was uniquely central to all 30 identified risk factors. Though the nature of the neuroinflammatory involvement varied, the activation of microglia and the release of pro-inflammatory cytokines were a common pathway shared by all risk factors. This observation provides further evidence for the importance of immunopathic mechanisms in the aetiopathogenesis of AD. Full article

(This article belongs to the Special Issue Advances in Neuroinflammation)

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20 pages, 1559 KiB

Open AccessReview

Neuroinflammation and Neurodegenerative Diseases: How Much Do We Still Not Know?

by Carmela Rita Balistreri and Roberto Monastero

Brain Sci. 2024, 14(1), 19; https://doi.org/10.3390/brainsci14010019 - 23 Dec 2023

Cited by 1 | Viewed by 2516

Abstract

The term “neuroinflammation” defines the typical inflammatory response of the brain closely related to the onset of many neurodegenerative diseases (NDs). Neuroinflammation is well known, but its mechanisms and pathways are not entirely comprehended. Some progresses have been achieved through many efforts and research. Consequently, new cellular and molecular mechanisms, diverse and conventional, are emerging. In listing some of those that will be the subject of our description and discussion, essential are the important roles of peripheral and infiltrated monocytes and clonotypic cells, alterations in the gut–brain axis, dysregulation of the apelinergic system, alterations in the endothelial glycocalyx of the endothelial component of neuronal vascular units, variations in expression of some genes and levels of the encoding molecules by the action of microRNAs (miRNAs), or other epigenetic factors and distinctive transcriptional factors, as well as the role of autophagy, ferroptosis, sex differences, and modifications in the circadian cycle. Such mechanisms can add significantly to understanding the complex etiological puzzle of neuroinflammation and ND. In addition, they could represent biomarkers and targets of ND, which is increasing in the elderly. Full article

(This article belongs to the Special Issue Advances in Neuroinflammation)

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15 pages, 786 KiB

Open AccessReview

Investigation of the Relationship between Apolipoprotein E Alleles and Serum Lipids in Alzheimer’s Disease: A Meta-Analysis

by Huaxue Xu, Jiajia Fu, Risna Begam Mohammed Nazar, Jing Yang, Sihui Chen, Yan Huang, Ting Bao and Xueping Chen

Brain Sci. 2023, 13(11), 1554; https://doi.org/10.3390/brainsci13111554 - 06 Nov 2023

Viewed by 1067

Abstract

Prior studies have yielded mixed findings concerning the association between apolipoprotein E(APOE)-ε4 and serum lipids in patients with Alzheimer’s disease (AD) and healthy individuals. Some studies suggested a relationship between APOEε4 and serum lipids in patients with AD and healthy individuals, whereas others proposed that the APOEε4 allele affects lipids only in patients with AD. Our study aimed to investigate whether APOE alleles have a distinct impact on lipids in AD. We conducted a comprehensive search of the PubMed and Embase databases for all related studies that investigate APOE and serum lipids of AD from the inception to 30 May 2022. Elevated total cholesterol (TC) and low-density lipoprotein (LDL) levels were found in APOEε4 allele carriers compared with non-carriers. No significant differences were found for high-density lipoprotein (HDL) and triglyceride (TG) levels in APOEε4 allele carriers compared to non-carriers. Notably, elevated TC and LDL levels showed considerable heterogeneity between patients with AD and healthy controls. A network meta-analysis did not find a distinct effect of carrying one or two APOEε4 alleles on lipid profiles. Higher TC and LDL levels were found in APOEε4 allele carriers compared with non-carriers, and the difference was more significant in patients with AD than in healthy controls. Full article

(This article belongs to the Special Issue Advances in Neuroinflammation)

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Planned Papers

The below list represents only planned manuscripts. Some of these manuscripts have not been received by the Editorial Office yet. Papers submitted to MDPI journals are subject to peer-review.

Oncology Meets Immunology: Neuroinflammation and Immunotherapy in Glioblastoma

Xiaoqin Zhang and Xin Li

Department of Pathology, School of Medicine, South China University of Technology,

Guangzhou, China

Abstract

Glioblastoma (GBM) is the most common and malignant primary brain tumor with high morbidity and mortality. Despite the optimal treatment, the median survival of GBM patients remains only 12 to 15 months. The standard therapy for newly diagnosed GBM involves surgical resection when feasible, radiotherapy and chemotherapy. However, resistance to treatment, high proliferation rates and aggressive features of tumor cells, lead to its unfavorable prognosis. During the past decades, there have been important advances in the understanding of the molecular pathogenesis of malignant gliomas and progress in treating them. However, most of these studies are tumor cell-centric, which may underestimate the role of tumor microenvironment (TME) in tumor progression. In recent years, TME, including immune cells infiltration, enhanced vascularization and extracellular matrix (ECM), has been increasingly recognized as an important player and therapeutic target in GBM. The complex interactions between the tumor cells and infiltrated immune cells can promote the neuro-inflammatory tumor microenvironment which can impact GMB’s survival, proliferation and invasiveness. There is a great need for a full and integrated understanding of interplay between GBM tumor cells and TME for the development of mor efficient therapies. In this review, we will provide a comprehensive report of the GBM TME, especially the neuroinflammation, in tumor invasion and progression of GBM. We will also discuss the anti-neuroinflammation interventions that can be employed as potential immunotherapy targets.

Key Words: Glioblastoma, Brain tumor, Neuro-inflammation, Tumor microenvironment, Immunotherapy

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