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Advanced Research in Neuroinflammation
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Advanced Research in Neuroinflammation

A special issue of Current Issues in Molecular Biology (ISSN 1467-3045). This special issue belongs to the section "Molecular Medicine".

Deadline for manuscript submissions: closed (31 August 2024) | Viewed by 16498

Special Issue Editors

Dr. Giovanna Rigillo

E-Mail Website
Guest Editor
Department of Biomedical, Metabolic and Neural Sciences, University of Modena and Reggio Emilia, 41125 Modena, Italy
Interests: neuropharmacology; molecular pharmacology; epigenetics; natural products; muscle-brain axis
Dr. Silvia Alboni

E-Mail Website
Guest Editor
Department of Life Sciences, University of Modena and Reggio Emilia, 41121 Modena, Italy
Interests: neuropharmacology; psychoneuroimmunoendocrinology; environmental neuroscience; glial cells; metabolomic
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Neuroinflammation is currently considered a hallmark of a broad range of neurological disorders, including neurodegenerative and neuropsychiatric diseases; it is an essential topic in disease prevention and the development of disease-modifying treatments. It is well-established that neuroinflammation plays a key pathogenetic role in brain-affecting disorders; however, the complex dynamic mechanism activated during neuroinflammation and the communication between glial cells and neurons remains to be fully understood. Indeed, all the cells in the central nervous system are connected in an intricate network, resulting in a mutual influence and interdependencies where intercellular interactions may represent links and nodes. Therefore, a deep knowledge of these networks, including the mechanisms that promote collective responses to different challenges in both healthy and pathological conditions, could help to elucidate important aspects of neuroinflammation.

This Special Issue aims to collect new research that can increase knowledge on different aspects, including the following:

  • Cellular and molecular mechanisms of the neuroinflammation processes;
  • Cellular interaction during neuroinflammation;
  • Identification of biomarkers useful for the stratification of patients, for tracking disease progression, for prognosis, and for monitoring of the effects of therapies;
  • The molecular effect of new or already used compounds on neuroinflammation.

You are warmly invited to submit original research and review articles related to any of these aspects.

Dr. Giovanna Rigillo
Dr. Silvia Alboni
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. Current Issues in Molecular Biology 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
  • molecular pharmacology
  • neurodegenerative disease
  • neuropsychiatric disease
  • neuroprotection
  • intercellular communication
  • neuroimmunology
  • cellular mechanisms

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Published Papers (9 papers)

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Editorial

Jump to: Research, Review

3 pages, 178 KiB  
Editorial
Exploring the Frontiers of Neuroinflammation: New Horizons in Research and Treatment
by Giovanna Rigillo and Silvia Alboni
Curr. Issues Mol. Biol. 2024, 46(10), 11665-11667; https://doi.org/10.3390/cimb46100692 - 19 Oct 2024
Viewed by 342
Abstract
The Special Issue “Advanced Research in Neuroinflammation” offers a rich and diverse collection of studies that deepen our understanding of how inflammatory mediators are involved in various neurological conditions [...] Full article
(This article belongs to the Special Issue Advanced Research in Neuroinflammation)

Research

Jump to: Editorial, Review

14 pages, 2006 KiB  
Article
Brain Ischemic Tolerance Triggered by Preconditioning Involves Modulation of Tumor Necrosis Factor-α-Stimulated Gene 6 (TSG-6) in Mice Subjected to Transient Middle Cerebral Artery Occlusion
by Chiara Di Santo, Antonio Siniscalchi, Daniele La Russa, Paolo Tonin, Giacinto Bagetta and Diana Amantea
Curr. Issues Mol. Biol. 2024, 46(9), 9970-9983; https://doi.org/10.3390/cimb46090595 - 10 Sep 2024
Viewed by 581
Abstract
Ischemic preconditioning (PC) induced by a sub-lethal cerebral insult triggers brain tolerance against a subsequent severe injury through diverse mechanisms, including the modulation of the immune system. Tumor necrosis factor (TNF)-α-stimulated gene 6 (TSG-6), a hyaluronate (HA)-binding protein, has recently been involved in [...] Read more.
Ischemic preconditioning (PC) induced by a sub-lethal cerebral insult triggers brain tolerance against a subsequent severe injury through diverse mechanisms, including the modulation of the immune system. Tumor necrosis factor (TNF)-α-stimulated gene 6 (TSG-6), a hyaluronate (HA)-binding protein, has recently been involved in the regulation of the neuroimmune response following ischemic stroke. Thus, we aimed at assessing whether the neuroprotective effects of ischemic PC involve the modulation of TSG-6 in a murine model of transient middle cerebral artery occlusion (MCAo). The expression of TSG-6 was significantly elevated in the ischemic cortex of mice subjected to 1 h MCAo followed by 24 h reperfusion, while this effect was further potentiated (p < 0.05 vs. MCAo) by pre-exposure to ischemic PC (i.e., 15 min MCAo) 72 h before. By immunofluorescence analysis, we detected TSG-6 expression mainly in astrocytes and myeloid cells populating the lesioned cerebral cortex, with a more intense signal in tissue from mice pre-exposed to ischemic PC. By contrast, levels of TSG-6 were reduced after 24 h of reperfusion in plasma (p < 0.05 vs. SHAM), but were dramatically elevated when severe ischemia (1 h MCAo) was preceded by ischemic PC (p < 0.001 vs. MCAo) that also resulted in significant neuroprotection. In conclusion, our data demonstrate that neuroprotection exerted by ischemic PC is associated with the elevation of TSG-6 protein levels both in the brain and in plasma, further underscoring the beneficial effects of this endogenous modulator of the immune system. Full article
(This article belongs to the Special Issue Advanced Research in Neuroinflammation)
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15 pages, 949 KiB  
Article
SARS-CoV-2-Induced Type I Interferon Signaling Dysregulation in Olfactory Networks Implications for Alzheimer’s Disease
by George D. Vavougios, Theodoros Mavridis, Triantafyllos Doskas, Olga Papaggeli, Pelagia Foka and Georgios Hadjigeorgiou
Curr. Issues Mol. Biol. 2024, 46(5), 4565-4579; https://doi.org/10.3390/cimb46050277 - 10 May 2024
Cited by 2 | Viewed by 2359
Abstract
Type I interferon signaling (IFN-I) perturbations are major drivers of COVID-19. Dysregulated IFN-I in the brain, however, has been linked to both reduced cognitive resilience and neurodegenerative diseases such as Alzheimer’s. Previous works from our group have proposed a model where peripheral induction [...] Read more.
Type I interferon signaling (IFN-I) perturbations are major drivers of COVID-19. Dysregulated IFN-I in the brain, however, has been linked to both reduced cognitive resilience and neurodegenerative diseases such as Alzheimer’s. Previous works from our group have proposed a model where peripheral induction of IFN-I may be relayed to the CNS, even in the absence of fulminant infection. The aim of our study was to identify significantly enriched IFN-I signatures and genes along the transolfactory route, utilizing published datasets of the nasal mucosa and olfactory bulb amygdala transcriptomes of COVID-19 patients. We furthermore sought to identify these IFN-I signature gene networks associated with Alzheimer’s disease pathology and risk. Gene expression data involving the nasal epithelium, olfactory bulb, and amygdala of COVID-19 patients and transcriptomic data from Alzheimer’s disease patients were scrutinized for enriched Type I interferon pathways. Gene set enrichment analyses and gene–Venn approaches were used to determine genes in IFN-I enriched signatures. The Agora web resource was used to identify genes in IFN-I signatures associated with Alzheimer’s disease risk based on its aggregated multi-omic data. For all analyses, false discovery rates (FDR) <0.05 were considered statistically significant. Pathways associated with type I interferon signaling were found in all samples tested. Each type I interferon signature was enriched by IFITM and OAS family genes. A 14-gene signature was associated with COVID-19 CNS and the response to Alzheimer’s disease pathology, whereas nine genes were associated with increased risk for Alzheimer’s disease based on Agora. Our study provides further support to a type I interferon signaling dysregulation along the extended olfactory network as reconstructed herein, ranging from the nasal epithelium and extending to the amygdala. We furthermore identify the 14 genes implicated in this dysregulated pathway with Alzheimer’s disease pathology, among which HLA-C, HLA-B, HLA-A, PSMB8, IFITM3, HLA-E, IFITM1, OAS2, and MX1 as genes with associated conferring increased risk for the latter. Further research into its druggability by IFNb therapeutics may be warranted. Full article
(This article belongs to the Special Issue Advanced Research in Neuroinflammation)
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13 pages, 2355 KiB  
Article
Expression of G2019S LRRK2 in Rat Primary Astrocytes Mediates Neurotoxicity and Alters the Dopamine Synthesis Pathway in N27 Cells via Astrocytic Proinflammatory Cytokines and Neurotrophic Factors
by Dong Hwan Ho, Hyejung Kim, Daleum Nam, Mi Kyoung Seo, Sung Woo Park and Ilhong Son
Curr. Issues Mol. Biol. 2024, 46(5), 4324-4336; https://doi.org/10.3390/cimb46050263 - 6 May 2024
Cited by 1 | Viewed by 1343
Abstract
Astrocytes in the brain contribute to various essential functions, including maintenance of the neuronal framework, survival, communication, metabolic processes, and neurotransmitter levels. Leucine-rich repeat kinase 2 (LRRK2) is associated with the pathogenesis of Parkinson’s disease (PD). LRRK2 is expressed in neurons, microglia, and [...] Read more.
Astrocytes in the brain contribute to various essential functions, including maintenance of the neuronal framework, survival, communication, metabolic processes, and neurotransmitter levels. Leucine-rich repeat kinase 2 (LRRK2) is associated with the pathogenesis of Parkinson’s disease (PD). LRRK2 is expressed in neurons, microglia, and astrocytes and plays diverse roles in these cell types. We aimed to determine the effects of mutant human G2019S-LRRK2 (GS-hLRRK2) in rat primary astrocytes (rASTROs). Transfection with GS-hLRRK2 significantly decreased cell viability compared to transfection with the vector and wild-type human LRRK2 (WT-hLRRK2). GS-hLRRK2 expression significantly reduced the levels of nerve growth factor and increased the levels of proinflammatory cytokines (interleukin-1β and tumor necrosis factor α) compared to the vector and WT-hLRRK2 expression. Furthermore, GS-hLRRK2 expression in rASTROs promoted astrogliosis, which was characterized by increased expression of glial fibrillary acidic protein and vimentin. Treatment with the conditioned medium of G2019S LRRK2-expressing rASTROs decreased N27 cell viability compared to treatment with that of WT-hLRRK2-expressing rASTROs. Consequently, the regulation of the dopamine synthesis pathway was affected in N27 cells, thereby leading to altered levels of tyrosine hydroxylase, dopamine transporter, Nurr1, and dopamine release. Overall, the G2019S LRRK2 mutation disrupted astrocyte function, thereby aggravating PD progression. Full article
(This article belongs to the Special Issue Advanced Research in Neuroinflammation)
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17 pages, 9619 KiB  
Article
Nicotinamide Riboside Regulates Chemotaxis to Decrease Inflammation and Ameliorate Functional Recovery Following Spinal Cord Injury in Mice
by Yan Li, Chunjia Zhang, Zihan Li, Fan Bai, Yingli Jing, Han Ke, Shuangyue Zhang, Yitong Yan and Yan Yu
Curr. Issues Mol. Biol. 2024, 46(2), 1291-1307; https://doi.org/10.3390/cimb46020082 - 1 Feb 2024
Viewed by 1897
Abstract
Changes in intracellular nicotinamide adenine dinucleotide (NAD+) levels have been observed in various disease states. A decrease in NAD+ levels has been noted following spinal cord injury (SCI). Nicotinamide riboside (NR) serves as the precursor of NAD+. Previous [...] Read more.
Changes in intracellular nicotinamide adenine dinucleotide (NAD+) levels have been observed in various disease states. A decrease in NAD+ levels has been noted following spinal cord injury (SCI). Nicotinamide riboside (NR) serves as the precursor of NAD+. Previous research has demonstrated the anti-inflammatory and apoptosis-reducing effects of NR supplements. However, it remains unclear whether NR exerts a similar role in mice after SCI. The objective of this study was to investigate the impact of NR on these changes in a mouse model of SCI. Four groups were considered: (1) non-SCI without NR (Sham), (2) non-SCI with NR (Sham +NR), (3) SCI without NR (SCI), and (4) SCI with NR (SCI + NR). Female C57BL/6J mice aged 6–8 weeks were intraperitoneally administered with 500 mg/kg/day NR for a duration of one week. The supplementation of NR resulted in a significant elevation of NAD+ levels in the spinal cord tissue of mice after SCI. In comparison to the SCI group, NR supplementation exhibited regulatory effects on the chemotaxis/recruitment of leukocytes, leading to reduced levels of inflammatory factors such as IL-1β, TNF-α, and IL-22 in the injured area. Moreover, NR supplementation notably enhanced the survival of neurons and synapses within the injured area, ultimately resulting in improved motor functions after SCI. Therefore, our research findings demonstrated that NR supplementation had inhibitory effects on leukocyte chemotaxis, anti-inflammatory effects, and could significantly improve the immune micro-environment after SCI, thereby promoting neuronal survival and ultimately enhancing the recovery of motor functions after SCI. NR supplementation showed promise as a potential clinical treatment strategy for SCI. Full article
(This article belongs to the Special Issue Advanced Research in Neuroinflammation)
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Review

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24 pages, 2187 KiB  
Review
Modulation of Oxidative Stress and Neuroinflammation by Cannabidiol (CBD): Promising Targets for the Treatment of Alzheimer’s Disease
by Jordan P. Hickey, Andrila E. Collins, Mackayla L. Nelson, Helen Chen and Bettina E. Kalisch
Curr. Issues Mol. Biol. 2024, 46(5), 4379-4402; https://doi.org/10.3390/cimb46050266 - 6 May 2024
Cited by 4 | Viewed by 2512
Abstract
Alzheimer’s disease (AD) is a progressive neurodegenerative disease and the most common form of dementia globally. Although the direct cause of AD remains under debate, neuroinflammation and oxidative stress are critical components in its pathogenesis and progression. As a result, compounds like cannabidiol [...] Read more.
Alzheimer’s disease (AD) is a progressive neurodegenerative disease and the most common form of dementia globally. Although the direct cause of AD remains under debate, neuroinflammation and oxidative stress are critical components in its pathogenesis and progression. As a result, compounds like cannabidiol (CBD) are being increasingly investigated for their ability to provide antioxidant and anti-inflammatory neuroprotection. CBD is the primary non-psychotropic phytocannabinoid derived from Cannabis sativa. It has been found to provide beneficial outcomes in a variety of medical conditions and is gaining increasing attention for its potential therapeutic application in AD. CBD is not psychoactive and its lipophilic nature allows its rapid distribution throughout the body, including across the blood–brain barrier (BBB). CBD also possesses anti-inflammatory, antioxidant, and neuroprotective properties, making it a viable candidate for AD treatment. This review outlines CBD’s mechanism of action, the role of oxidative stress and neuroinflammation in AD, and the effectiveness and limitations of CBD in preclinical models of AD. Full article
(This article belongs to the Special Issue Advanced Research in Neuroinflammation)
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29 pages, 1178 KiB  
Review
The Effect of Gut Microbiota-Targeted Interventions on Neuroinflammation and Motor Function in Parkinson’s Disease Animal Models—A Systematic Review
by Paul-Ștefan Panaitescu, Vlad Răzniceanu, Ștefania-Maria Mocrei-Rebrean, Vlad Sever Neculicioiu, Hanna-Maria Dragoș, Carmen Costache and Gabriela Adriana Filip
Curr. Issues Mol. Biol. 2024, 46(5), 3946-3974; https://doi.org/10.3390/cimb46050244 - 26 Apr 2024
Cited by 1 | Viewed by 1522
Abstract
Gut microbiome-targeted interventions such as fecal transplant, prebiotics, probiotics, synbiotics, and antibiotic gut depletion are speculated to be of potential use in delaying the onset and progression of Parkinson’s disease by rebalancing the gut microbiome in the context of the gut–brain axis. Our [...] Read more.
Gut microbiome-targeted interventions such as fecal transplant, prebiotics, probiotics, synbiotics, and antibiotic gut depletion are speculated to be of potential use in delaying the onset and progression of Parkinson’s disease by rebalancing the gut microbiome in the context of the gut–brain axis. Our study aims to organize recent findings regarding these interventions in Parkinson’s disease animal models to identify how they affect neuroinflammation and motor outcomes. A systematic literature search was applied in PubMed, Web of Science, Embase, and SCOPUS for gut microbiome-targeted non-dietary interventions. Studies that investigated gut-targeted interventions by using in vivo murine PD models to follow dopaminergic cell loss, motor tests, and neuroinflammatory markers as outcomes were considered to be eligible. A total of 1335 studies were identified in the databases, out of which 29 were found to be eligible. A narrative systematization of the resulting data was performed, and the effect direction for the outcomes was represented. Quality assessment using the SYRCLE risk of bias tool was also performed. Out of the 29 eligible studies, we found that a significant majority report that the intervention reduced the dopaminergic cell loss (82.76%, 95% CI [64.23%, 94.15%]) produced by the induction of the disease model. Also, most studies reported a reduction in microglial (87.5%, 95% CI [61.65%, 98.45%]) and astrocytic activation (84,62%, 95% CI [54.55%, 98.08%]) caused by the induction of the disease model. These results were also mirrored in the majority (96.4% 95% CI [81.65%, 99.91%]) of the studies reporting an increase in performance in behavioral motor tests. A significant limitation of the study was that insufficient information was found in the studies to assess specific causes of the risk of bias. These results show that non-dietary gut microbiome-targeted interventions can improve neuroinflammatory and motor outcomes in acute Parkinson’s disease animal models. Further studies are needed to clarify if these benefits transfer to the long-term pathogenesis of the disease, which is not yet fully understood. The study had no funding source, and the protocol was registered in the PROSPERO database with the ID number CRD42023461495. Full article
(This article belongs to the Special Issue Advanced Research in Neuroinflammation)
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12 pages, 891 KiB  
Review
Cannabis, Cannabinoids, and Stroke: Increased Risk or Potential for Protection—A Narrative Review
by Caroline Carter, Lindsay Laviolette, Bashir Bietar, Juan Zhou and Christian Lehmann
Curr. Issues Mol. Biol. 2024, 46(4), 3122-3133; https://doi.org/10.3390/cimb46040196 - 4 Apr 2024
Cited by 1 | Viewed by 2610
Abstract
Worldwide, approximately 15 million people per year suffer from stroke. With about 5 million deaths, stroke is the second most common cause of death and a major cause of long-term disability. It is estimated that about 25% of people older than 85 years [...] Read more.
Worldwide, approximately 15 million people per year suffer from stroke. With about 5 million deaths, stroke is the second most common cause of death and a major cause of long-term disability. It is estimated that about 25% of people older than 85 years will develop stroke. Cannabis sativa and derived cannabinoids have been used for recreational and medical purposes for many centuries. However, due to the legal status in the past, research faced restrictions, and cannabis use was stigmatized for potential negative impacts on health. With the changes in legal status in many countries of the world, cannabis and cannabis-derived substances such as cannabinoids and terpenes have gained more interest in medical research. Several medical effects of cannabis have been scientifically proven, and potential risks identified. In the context of stroke, the role of cannabis is controversial. The negative impact of cannabis use on stroke has been reported through case reports and population-based studies. However, potential beneficial effects of specific cannabinoids are described in animal studies under certain conditions. In this narrative review, the existing body of evidence regarding the negative and positive impacts of cannabis use prior to stroke will be critically appraised. Full article
(This article belongs to the Special Issue Advanced Research in Neuroinflammation)
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24 pages, 1420 KiB  
Review
Nerve Growth Factor and Autoimmune Diseases
by Sergio Terracina, Giampiero Ferraguti, Luigi Tarani, Francesca Fanfarillo, Paola Tirassa, Massimo Ralli, Giannicola Iannella, Antonella Polimeni, Marco Lucarelli, Antonio Greco and Marco Fiore
Curr. Issues Mol. Biol. 2023, 45(11), 8950-8973; https://doi.org/10.3390/cimb45110562 - 10 Nov 2023
Cited by 7 | Viewed by 2472
Abstract
NGF plays a crucial immunomodulatory role and increased levels are found in numerous tissues during autoimmune states. NGF directly modulates innate and adaptive immune responses of B and T cells and causes the release of neuropeptides and neurotransmitters controlling the immune system activation [...] Read more.
NGF plays a crucial immunomodulatory role and increased levels are found in numerous tissues during autoimmune states. NGF directly modulates innate and adaptive immune responses of B and T cells and causes the release of neuropeptides and neurotransmitters controlling the immune system activation in inflamed tissues. Evidence suggests that NGF is involved in the pathogenesis of numerous immune diseases including autoimmune thyroiditis, chronic arthritis, multiple sclerosis, systemic lupus erythematosus, mastocytosis, and chronic granulomatous disease. Furthermore, as NGF levels have been linked to disease severity, it could be considered an optimal early biomarker to identify therapeutic approach efficacy. In conclusion, by gaining insights into how these molecules function and which cells they interact with, future studies can devise targeted therapies to address various neurological, immunological, and other disorders more effectively. This knowledge may pave the way for innovative treatments based on NGF manipulation aimed at improving the quality of life for individuals affected by diseases involving neurotrophins. Full article
(This article belongs to the Special Issue Advanced Research in Neuroinflammation)
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