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Brain Sciences
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New Advances in Neuroimmunology and Neuroinflammation
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New Advances in Neuroimmunology and Neuroinflammation

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 June 2025 | Viewed by 6226

Special Issue Editors

Dr. Junhui Wang

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Guest Editor
Lunenfeld-Tanenbaum Research Institute, Mount Sinai Hospital, Toronto, ON, Canada
Interests: astrocyte; neuroinflammation; mental health; behavioral science; cognitive impairment; Alzheimer's disease
Special Issues, Collections and Topics in MDPI journals
Dr. Xueping Chen

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Guest Editor
Department of Neurology, West China Hospital, Sichuan University, Chengdu 610041, China
Interests: neurodegenerative disease; Alzheimer's disease; Parkinson's disease; amyotrophic lateral sclerosis
Dr. Jing Sun

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Guest Editor
Department of Pathology (Neuropathology), Capital Medical University, Beijing, China
Interests: clinical neuropathology; neuroglial cells; neuroinflammation
Special Issues, Collections and Topics in MDPI journals
Dr. Matheus Uba Chupel

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Guest Editor
Sunnybrook Research Institute, Toronto, ON M4N 3M5, Canada
Interests: exercise; immunology; blood-brain barrier; supplementation; neurotrophic factors; cognition; biostatistics

Special Issue Information

Dear Colleagues,

Increasing evidence points to strong immunological and inflammatory components in various neurological and neuropsychiatric diseases. Understanding the underlying mechanisms and functions of these immune and inflammatory responses is crucial for advancing our knowledge of conditions like Parkinson's disease, Alzheimer's, mental disorders, and amyotrophic lateral sclerosis (ALS). A great number of clinical trails have failed to successfully address the issue of neuroinflammation and its complex orchestrated response that harnesses age-related diseases. Therefore, the exact role of neuroimmunology and neuroinflammation requires extensive investigation.

This Special Issue of Brain Sciences aims to showcase recent advances in neuroimmunology and neuroinflammation research in both preclinical and clinical areas, with a focus on neurodegenerative diseases. We particularly welcome in vivo and in vitro studies on new concepts, technological innovations, and novel models that can be applied to explore the role of neuroimmunology and neuroinflammation in neurological and neuropsychiatric diseases. This includes (but is not limited to), the role of inflammation in blood-brain barrier dysfunction, the effects of new drugs to treat neurodegenerative diseases and their role in the immune response, and the mediating effects of anti-inflammatory therapies in neurodegeneration.

In addition to research articles, reviews and mini-reviews on recent progress in neuroimmunology and neuroinflammation in neurological and neuropsychiatric diseases are encouraged. Submissions of case reports on rare glia-related conditions (neuroinflammation) from clinical settings, including imaging or neuropathology patterns, are also welcome.

Dr. Junhui Wang
Dr. Xueping Chen
Dr. Jing Sun
Dr. Matheus Uba Chupel
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
  • neuroimmunology
  • glia
  • neurodegenerative diseases
  • cytokines
  • chemokines

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Published Papers (6 papers)

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Research

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18 pages, 6710 KiB  
Article
Papain Affects the Percentage and Morphology of Microglia in Hippocampal Neuron–Glial Cultures
by Ivan A. Tumozov, Valentina N. Mal’tseva, Sergei A. Maiorov, Artem M. Kosenkov and Sergei G. Gaidin
Brain Sci. 2025, 15(5), 442; https://doi.org/10.3390/brainsci15050442 - 24 Apr 2025
Viewed by 215
Abstract
Background. Microglia, accounting for 5–15% of total brain cells, represent an essential population of glial cells in the cultures used for modeling neuroinflammation in vitro. However, microglia proliferation is poor in neuron–glial cultures. Here, we studied the population composition of rat hippocampal neuron–glial [...] Read more.
Background. Microglia, accounting for 5–15% of total brain cells, represent an essential population of glial cells in the cultures used for modeling neuroinflammation in vitro. However, microglia proliferation is poor in neuron–glial cultures. Here, we studied the population composition of rat hippocampal neuron–glial cell cultures prepared utilizing papain (PAP cultures) and trypsin (TRY cultures) as proteolytic enzymes for cell isolation. Methods. To evaluate the percentage and morphology of microglia in TRY and PAP cultures and cultures incubated in the presence of TGFβ+MCSF+cholesterol, which should enhance microglia proliferation, we used an immunostaining and calcium imaging approach in combination with staining using the recently developed vital microglia fluorescent probe CDr20. Results. We have shown that the microglia percentage in PAP cultures was higher than in TRY cultures. Microglia in PAP cultures are predominantly polarized, while bushy morphology was more characteristic of TRY cultures. We have also demonstrated that the TGFβ+MCSF+cholesterol combination increases the microglia number both in PAP and TRY cultures (up to 25–30%) and promotes the appearance of ameboid microglia characterized by high mobility. However, the significant appearance of ameboid microglia was observed already at the early stages of cultivation (2 DIV) in TRY cultures, while in PAP cultures, the described transformation was observed at 7 DIV. Based on the absence of the ATP-induced Ca2+ response, round shape, significant proliferation, and high mobility, we have suggested that ameboid microglia are reactive. Conclusions. Thus, our results demonstrate that papain is a more suitable proteolytic enzyme for preparing mixed hippocampal neuron–glial cultures with a higher percentage of heterogeneous microglia and functional neurons and astrocytes (tricultures). Full article
(This article belongs to the Special Issue New Advances in Neuroimmunology and Neuroinflammation)
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21 pages, 4112 KiB  
Article
Enhanced Interleukin 6 Trans-Signaling Modulates Disease Process in Amyotrophic Lateral Sclerosis Mouse Models
by Carol Milligan, Dale O. Cowley, William Stewart, Alyson M. Curry, Elizabeth Forbes, Brian Rector, Annette Hastie, Liang Liu and Gregory A. Hawkins
Brain Sci. 2025, 15(1), 84; https://doi.org/10.3390/brainsci15010084 - 17 Jan 2025
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Abstract
Background/Objectives: Charcot first described ALS in 1869, but the specific mechanisms that mediate the disease pathology are still not clear. Intense research efforts have provided insight into unique neuroanatomical regions, specific neuronal populations and genetic associations for ALS and other neurodegenerative diseases; however, [...] Read more.
Background/Objectives: Charcot first described ALS in 1869, but the specific mechanisms that mediate the disease pathology are still not clear. Intense research efforts have provided insight into unique neuroanatomical regions, specific neuronal populations and genetic associations for ALS and other neurodegenerative diseases; however, the experimental results also suggest a convergence of these events to common toxic pathways. We propose that common toxic pathways can be therapeutically targeted, and this intervention will be effective in slowing progression and improving patient quality of life. Here, we focus on understanding the role of IL6 trans-signaling in ALS disease processes. Methods: We leveraged unique mouse models of IL6 trans-signaling that we developed that recapitulate the production of active sIL6R in a genotypic and quantitative fashion observed in humans. Given that the SOD1 transgenic mouse is one of the most highly studied and characterized models of ALS, we bred SOD1G93A mice with IL6R trans-signaling mice to determine how enhanced trans-signaling influenced symptom onset and pathological processes, including neuromuscular junction (NMJ) denervation, glial activation and motoneuron (MN) survival. Results: The results indicate that in animals with enhanced trans-signaling, symptom onset and pathological processes were accelerated, suggesting a role in disease modification. Administration of an IL6R functional blocking antibody failed to alter accelerated symptom onset and disease progression. Conclusions: Future work to investigate the site-specific influence of enhanced IL6 trans-signaling and the tissue-specific bioavailability of potential therapeutics will be necessary to identify targets for precise therapeutic interventions that may limit disease progression in the 60% of ALS patients who inherit the common Il6R Asp358Ala variant. Full article
(This article belongs to the Special Issue New Advances in Neuroimmunology and Neuroinflammation)
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18 pages, 11130 KiB  
Article
First Description of the Role of the Relationship Between Serum Amyloid P Components and Nuclear Factors/Pro-Cytokines During Critical Periods of Toxoplasmic Encephalitis
by Gungor Cagdas Dincel, Hasan Tarik Atmaca and Saeed El-Ashram
Brain Sci. 2024, 14(12), 1298; https://doi.org/10.3390/brainsci14121298 - 23 Dec 2024
Viewed by 1344
Abstract
Background/Objectives: Toxoplasma gondii (T. gondii), an obligate food-borne intracellular parasite, causes severe neuropathology by establishing a persistent infection in the host brain. We have previously shown that T. gondii infection induces severe neuropathology in the brain manifested by increased nitric [...] Read more.
Background/Objectives: Toxoplasma gondii (T. gondii), an obligate food-borne intracellular parasite, causes severe neuropathology by establishing a persistent infection in the host brain. We have previously shown that T. gondii infection induces severe neuropathology in the brain manifested by increased nitric oxide production, oxidative stress, glial activation/BBB damage, increased pro-inflammatory cytokine glia maturation factor-beta and induced apoptosis. Methods: The aim of this experimental study was to investigate the serum amyloid P (SAP) components, nuclear factor kappa B (NF-κB), interleukin-1 beta (IL-1β), caspase 1 (Casp 1), tumor necrosis factor-alpha (TNF-α) and complement 3 (C3) gene expressions on the 10th, 20th and 30th days after infection with T. gondii in the neuroimmunopathogenesis of toxoplasmic encephalitis (TE) in mouse brains by real-time quantitative polymerase chain reaction. The study also aimed to determine whether there was a correlation between the markers included in the study on these critical days, which had not previously been investigated. The mRNA expression levels of SAP components, NF-κB, IL-1β, Casp 1, TNF-α and C3 were examined. Results: The most notable outcome of this investigation was the observation that SAP components exhibited a 13.9-fold increase on day 10 post-infection, followed by a rapid decline in the subsequent periods. In addition, IL-1β expression increased 20-fold, while SAP components decreased 13-fold on day 20 after infection. Additionally, the TNF-α, Casp 1 and NF-κB expression levels were consistently elevated to above normal levels at each time point. Conclusions: This study identified SAP components, NF-κB, IL-1β, Casp 1 and TNF-α expressions as playing critical roles in TE neuroimmunopathogenesis. Furthermore, to the best of our knowledge, this is the first study to investigate SAP components during the transition from acute systemic infection to early/medium chronic and chronic infection and to explore the relationship between SAP components and other nuclear factors/pro-cytokines. Full article
(This article belongs to the Special Issue New Advances in Neuroimmunology and Neuroinflammation)
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9 pages, 542 KiB  
Article
Early Diagnosis of CNS Virus Infections from Neurological Autoimmune Diseases: A Cross-Sectional Study from China in ER Setting
by Daiquan Gao, Xue Lv, Zuoyao Shen, Huicong Wang, Wenfeng Zhao, Huang Wang, Xiukun Jin, Liuchen Tan, Lu Yin, Junhui Wang, Weihua Yue and Hongxing Wang
Brain Sci. 2024, 14(9), 888; https://doi.org/10.3390/brainsci14090888 - 30 Aug 2024
Viewed by 1245
Abstract
It is challenging to differentiate between central nervous system (CNS) virus infections and neurological autoimmune diseases in the emergency department. Considering their different pathogenesis, we assume they differ in neuropsychiatric symptoms and laboratory results. A total of 80 patients were included in this [...] Read more.
It is challenging to differentiate between central nervous system (CNS) virus infections and neurological autoimmune diseases in the emergency department. Considering their different pathogenesis, we assume they differ in neuropsychiatric symptoms and laboratory results. A total of 80 patients were included in this study, 50 with CNS virus infections and 30 with CNS autoimmune diseases, confirmed by a polymerase chain reaction (PCR) of cerebrospinal fluid (CSF). A binary logistic regression model and receiver operating characteristic (ROC) curve were employed to examine the discrimination between the two types of diseases based on neuropsychiatric symptoms and laboratory results. Compared to patients with neurological autoimmune diseases, patients with CNS virus infections had a higher incidence of abnormal behavior (p = 0.026) and abnormal sensation/thought (p = 0.029); higher total (p = 0.005), direct (p = 0.004), and indirect bilirubin (p = 0.004); and increased CSF cell (p = 0.01) and CSF white cell counts (p = 0.01). Patients with disturbance of consciousness and abnormal sensation/thought were 7.79-fold and 5.07-fold more likely to be diagnosed with CNS virus infections (OR = 7.79, p = 0.008; OR = 5.07, p = 0.032). Each unit increase in blood indirect bilirubin concentration and CSF white cell counts increased the risk of developing CNS virus infections by 1.25-fold and 1.01-fold (OR = 1.25, p = 0.016; OR = 1.01, p = 0.011). ROC analysis showed that the area under the curve was 88.0% (p < 0.001). Our study found that patients with CNS viral infections tend to have higher blood indirect bilirubin concentration, CSF leukocyte count, frequency of disorders of consciousness, and abnormal sensation and thought, which may help differentiate them from those with neurological autoimmune diseases. Full article
(This article belongs to the Special Issue New Advances in Neuroimmunology and Neuroinflammation)
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Review

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12 pages, 804 KiB  
Review
TREM 2 in Parkinson’s Disease: A Promising Candidate Gene for Disease Susceptibility and Progression
by Paolo Alonge, Carmela Rita Balistreri, Angelo Torrente, Daniele Magro, Elisa Rubino and Roberto Monastero
Brain Sci. 2025, 15(4), 379; https://doi.org/10.3390/brainsci15040379 - 5 Apr 2025
Viewed by 341
Abstract
Background/Objectives: The activation of microglia and the activity of innate immunity have recently been recognized as part of Parkinson’s Disease (PD) pathophysiology. Triggering receptor expressed on myeloid cells 2 (TREM2) is a gene with neuroprotective roles. Its variations are associated with microglial-associated [...] Read more.
Background/Objectives: The activation of microglia and the activity of innate immunity have recently been recognized as part of Parkinson’s Disease (PD) pathophysiology. Triggering receptor expressed on myeloid cells 2 (TREM2) is a gene with neuroprotective roles. Its variations are associated with microglial-associated neurodegeneration. The objective of the present review is to investigate the current evidence on the role of TREM2 in PD pathophysiology. Methods: A comprehensive search was performed using PubMed, Medline, and Web of Science, looking for English papers investigating the role of TREM2 in PD, or more in general, the genetic profile of microglia. Results: Thirty-one papers were considered relevant. Preclinical studies with PD models showed some contradictory results, even if a loss of function of TREM2 is generally associated with a microglial activation in α-synuclein-induced inflammatory processes. The role for TREM2 genetic variations in PD patients should be taken with even more caution. The increase in the soluble extracellular segment of TREM2 (sTREM2) in cerebrospinal fluid of PD patients seems to be associated with increased risk of cognitive decline. Conclusions: There is increasing evidence that TREM2 may have an important role in PD pathophysiology as demonstrated by preclinical and clinical studies. Further investigations are needed to confirm this role and may lead the way for future targeted therapies for different neurodegenerative disorders. Full article
(This article belongs to the Special Issue New Advances in Neuroimmunology and Neuroinflammation)
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19 pages, 1021 KiB  
Review
Hypoxic Neuroinflammation in the Pathogenesis of Multiple Sclerosis
by Bethany Y. A. Hollingworth, Patrick N. Pallier, Stuart I. Jenkins and Ruoli Chen
Brain Sci. 2025, 15(3), 248; https://doi.org/10.3390/brainsci15030248 - 26 Feb 2025
Viewed by 997
Abstract
Multiple sclerosis (MS) is an autoimmune disease that damages the myelin sheath around the central nervous system axons, leading to neurological dysfunction. Although the initial damage is driven by inflammation, hypoxia has been reported in several brain regions of MS patients, but the [...] Read more.
Multiple sclerosis (MS) is an autoimmune disease that damages the myelin sheath around the central nervous system axons, leading to neurological dysfunction. Although the initial damage is driven by inflammation, hypoxia has been reported in several brain regions of MS patients, but the significance of this for prognosis and treatment remains unclear. Neuroinflammation can induce hypoxia, and hypoxia can induce and exacerbate neuroinflammation, forming a vicious cycle. Within MS lesions, demyelination is often followed by remyelination, which may restore neurological function. However, demyelinated axons are vulnerable to damage, which leads to the accumulation of the permanent neurological dysfunction typical in MS, with this vulnerability heightened during hypoxia. Clinically approved therapies for MS are immunomodulatory, which can reduce relapse frequency/severity, but there is a lack of pro-regenerative therapies for MS, for example promoting remyelination. All tissues have protective responses to hypoxia, which may be relevant to MS lesions, especially during remyelinating episodes. When oxygen levels are reduced in the brain, constitutively expressed hypoxia-inducible factors (HIF) are stabilised, upregulating hundreds of genes, including neuroprotective factors. Furthermore, astrocytes upregulate heparin-binding epidermal growth factor (EGF)-like growth factor (HB-EGF) in the early stage of MS. HB-EGF promotes protective mechanisms and induces oligodendrocyte and neuron differentiation and survival. This review article outlines the neuroinflammation and hypoxia cycle in MS pathology and identifies potential therapeutic targets to limit neurodegeneration and/or promote regeneration. Both HIF and HB-EGF signalling pathways induce endogenous protection mechanisms in the CNS, promoting neuroprotection and remyelination directly, but also indirectly by modulating the immune response in MS. Promoting such endogenous protective signalling pathways could be an effective therapy for MS patients. Full article
(This article belongs to the Special Issue New Advances in Neuroimmunology and Neuroinflammation)
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