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Neuroinflammation in Brain Health and Diseases
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Neuroinflammation in Brain Health and Diseases

A special issue of Cells (ISSN 2073-4409). This special issue belongs to the section "Cells of the Nervous System".

Deadline for manuscript submissions: 25 July 2025 | Viewed by 4442

Special Issue Editors

Dr. Debashis Dutta

E-Mail Website
Guest Editor
Department of Pediatrics, Darby’s Children Research Institute, Medical University of South Carolina, Charleston, SC, USA
Interests: neuroinflammation; neurodegeneration; proteinopathy; microglia; oligodendrocytes
Dr. Nemil Bhatt

E-Mail Website
Guest Editor
1. Neurology Department, University of Texas Medical Branch, Galveston, TX, USA
2. Mitchell Center for Neurodegenerative Disease, University of Texas Medical Branch, Galveston, TX, USA
Interests: neurodegeneration; protein aggregation; Alzheimer's disease; neuroinflammation

Special Issue Information

Dear Colleagues,

The inflammatory response induced in the central nervous system by infections, brain injury, aging-associated neurodegeneration, or any other acute/chronic stress is called neuroinflammation. Neuroinflammation can be instrumental in both positive and negative aspects of brain physiology and functioning, where acute and transient neuroinflammatory responses are essential for removing pathogens, tissue repair, brain development, and chronic and persistent induction of neuroinflammation results in debilitating outcomes on neuronal functions, causing progressive neurodegeneration. It suggests that the impact of neuroinflammatory molecules must be context and time-dependent. Although microglia, the innate immune cell in the brain, is the central player in neuroinflammation, other cells including astrocytes, endothelial cells, and the infiltrated adaptive immune cells, significantly contribute to this process. Currently, studies on neuroinflammation garner special emphasis in the fields of neurodegenerative diseases, genetic neurological disorders, brain injury, and pathogen-induced encephalitis. It has been demonstrated that inhibiting critical neuroinflammatory pathways by anti-inflammatory molecules can attenuate neuronal loss and improve CNS functions. This Special Issue on ‘Neuroinflammation’ aims to showcase the recent investigations addressing the critical inflammatory pathways governing brain physiology and functions in health and diseases. This will highlight the potential neuroinflammatory pathways that can be considered for future drug development.

Dr. Debashis Dutta
Dr. Nemil Bhatt
Guest Editors

Manuscript Submission Information

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Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2700 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
  • gliosis
  • inflammasome
  • neurodegeneration
  • neurotherapeutics

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Published Papers (4 papers)

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Research

15 pages, 548 KiB  
Article
The Role of Cytokine Gene Polymorphisms in Rehabilitation Outcome After Traumatic Brain Injury
by Franca Rosa Guerini, Cristina Agliardi, Milena Zanzottera, Antonio Caronni, Laura Antolini, Chiara Camilla Derchi, Tiziana Atzori, Elisabetta Bolognesi, Jorge Navarro, Mario Clerici and Angela Comanducci
Cells 2025, 14(14), 1056; https://doi.org/10.3390/cells14141056 - 10 Jul 2025
Viewed by 211
Abstract
Traumatic brain injury (TBI) affects millions of people worldwide and often results in long-term disabilities. Clinical outcomes vary widely even among patients with similar injury severity, partly due to systemic neuroinflammatory responses mediated by pro- and anti-inflammatory cytokines. Genetic polymorphisms in cytokine-coding genes [...] Read more.
Traumatic brain injury (TBI) affects millions of people worldwide and often results in long-term disabilities. Clinical outcomes vary widely even among patients with similar injury severity, partly due to systemic neuroinflammatory responses mediated by pro- and anti-inflammatory cytokines. Genetic polymorphisms in cytokine-coding genes may influence cytokine expression, thereby affecting rehabilitation and prognosis. We analyzed genetic polymorphisms in the TNF-α, IL-6, IL-6 receptor, IL-1β, and IL-10 genes in 28 subacute TBI patients undergoing rehabilitation. Clinical outcomes were assessed using the Glasgow Outcome Scale Extended (GOSE) and domain-specific scales for cognitive, motor, and functional recovery. Results were correlated with genetic profiles to identify potential predictive biomarkers. The IL-6-174 (GG) and IL-6R 1073 (AA) genotypes correlated with worse GOSE scores (p = 0.02 and p = 0.01, respectively). Co-segregation of IL-6-174 - IL-6R 1073 G-A alleles was linked to poorer outcomes (p = 0.01). Patients with the TNF-α-308 (GA) genotype showed less improvement in Barthel and Mobility scores (p = 0.001 and p = 0.01, respectively) and had a higher incidence of post-traumatic confusional state after rehabilitation (p = 0.03). Overall, the TNF-α-308(GA), IL-6 -174(GG), and IL-6R 1073(AA) genotypes negatively impact rehabilitation outcomes, likely due to their role in enhancing neuroinflammation. Larger studies are needed to develop personalized therapies tailored to genetic profiles, aiming to improve rehabilitation outcomes for TBI patients. Full article
(This article belongs to the Special Issue Neuroinflammation in Brain Health and Diseases)
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38 pages, 4834 KiB  
Article
Neuro-Inflammatory and Behavioral Changes Are Selectively Reversed by Sceletium tortuosum (Zembrin®) and Mesembrine in Male Rats Subjected to Unpredictable Chronic Mild Stress
by Johané Gericke, Stephan F. Steyn, Francois P. Viljoen and Brian H. Harvey
Cells 2025, 14(13), 1029; https://doi.org/10.3390/cells14131029 - 4 Jul 2025
Viewed by 659
Abstract
Sceletium tortuosum (ST) induces antidepressant and anxiolytic effects, purportedly by monoamine regulation, anti-inflammatory and antioxidant properties, and phosphodiesterase 4 (PDE4) inhibition. These multimodal actions have not been demonstrated in an animal model of major depressive disorder. Wistar rats (both sexes) were subjected to [...] Read more.
Sceletium tortuosum (ST) induces antidepressant and anxiolytic effects, purportedly by monoamine regulation, anti-inflammatory and antioxidant properties, and phosphodiesterase 4 (PDE4) inhibition. These multimodal actions have not been demonstrated in an animal model of major depressive disorder. Wistar rats (both sexes) were subjected to 8-week unpredictable chronic mild stress, subsequently receiving saline, a standardized ST extract, Zembrin® 25 and 12.5 mg/kg (ZEM25 and ZEM12.5), its primary alkaloid mesembrine (MES), or escitalopram (20 mg/kg) for 36 days. Sucrose preference, open field, Barnes maze, and forced swim tests were performed, with cortico-hippocampal monoamines, inflammatory and oxidative stress markers analyzed post-mortem. Male, but not female rats, presented with increased anhedonia and anxiety but not despair. Males presented with increased hippocampal PDE4B expression, increased dopamine metabolites, and decreased cortical serotonin. In males, ZEM12.5 decreased anhedonia- and anxiety-like behavior, decreased cortical and hippocampal PDE4B, and increased plasma interleukin-10. MES induced a transient decrease in anhedonia-like behavior and increased hippocampal serotonergic and cortical dopaminergic activity, whilst decreasing hippocampal PDE4B. ZEM25 increased plasma interleukin-10 but decreased cortical glutathione, indicating paradoxical anti-inflammatory and prooxidant effects. ZEM12.5 and MES more effectively addressed anxious–depressive-like behavior and stress-induced inflammation and monoaminergic alterations, respectively. Multitargeted actions on monoamines, redox-inflammation, and PDE4 may provide ST with antidepressant effects across multiple symptom domains, although mutually synergistic/antagonistic effects of constituent alkaloids should be considered. Full article
(This article belongs to the Special Issue Neuroinflammation in Brain Health and Diseases)
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17 pages, 3346 KiB  
Article
Dysregulation of Metabolic Peptides Precedes Hyperinsulinemia and Inflammation Following Exposure to Rotenone in Rats
by Vandana Zaman, Denise Matzelle, Naren L. Banik and Azizul Haque
Cells 2025, 14(2), 124; https://doi.org/10.3390/cells14020124 - 16 Jan 2025
Cited by 1 | Viewed by 1566
Abstract
Rotenone, a naturally occurring compound derived from the roots of tropical plants, is used as a broad-spectrum insecticide, piscicide, and pesticide. It is a classical, high-affinity mitochondrial complex I inhibitor that causes not only oxidative stress, α-synuclein phosphorylation, DJ-1 (Parkinson’s disease protein 7) [...] Read more.
Rotenone, a naturally occurring compound derived from the roots of tropical plants, is used as a broad-spectrum insecticide, piscicide, and pesticide. It is a classical, high-affinity mitochondrial complex I inhibitor that causes not only oxidative stress, α-synuclein phosphorylation, DJ-1 (Parkinson’s disease protein 7) modifications, and inhibition of the ubiquitin-proteasome system but it is also widely considered an environmental contributor to Parkinson’s disease (PD). While prodromal symptoms, such as loss of smell, constipation, sleep disorder, anxiety/depression, and the loss of dopaminergic neurons in the substantia nigra of rotenone-treated animals, have been reported, alterations of metabolic hormones and hyperinsulinemia remain largely unknown and need to be investigated. Whether rotenone and its effect on metabolic peptides could be utilized as a biomarker for its toxic metabolic effects, which can cause long-term detrimental effects and ultimately lead to obesity, hyperinsulinemia, inflammation, and possibly gut–brain axis dysfunction, remains unclear. Here, we show that rotenone disrupts metabolic homeostasis, altering hormonal peptides and promoting infiltration of inflammatory T cells. Specifically, our results indicate a significant decrease in glucagon-like peptide-1 (GLP-1), C-peptide, and amylin. Interestingly, levels of several hormonal peptides related to hyperinsulinemia, such as insulin, leptin, pancreatic peptide (PP), peptide YY (PYY), and gastric inhibitory polypeptide (GIP), were significantly upregulated. Administration of rotenone to rats also increased body weight and activated macrophages and inflammatory T cells. These data strongly suggest that rotenone disrupts metabolic homeostasis, leading to obesity and hyperinsulinemia. The potential implications of these findings are vast, given that monitoring these markers in the blood could not only provide a crucial tool for assessing the extent of exposure and its relevance to obesity and inflammation but could also open new avenues for future research and potential therapeutic strategies. Full article
(This article belongs to the Special Issue Neuroinflammation in Brain Health and Diseases)
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15 pages, 1341 KiB  
Article
Systemic Administration of a Site-Targeted Complement Inhibitor Attenuates Chronic Stress-Induced Social Behavior Deficits and Neuroinflammation in Mice
by Amit Kumar Madeshiya, Brandi Quintanilla, Carl Whitehead, Stephen Tomlinson and Anilkumar Pillai
Cells 2024, 13(23), 1988; https://doi.org/10.3390/cells13231988 - 2 Dec 2024
Cited by 1 | Viewed by 1249
Abstract
Chronic stress, a risk factor for many neuropsychiatric conditions, causes dysregulation in the immune system in both humans and animal models. Additionally, inflammation and synapse loss have been associated with deficits in social behavior. The complement system, a key player of innate immunity, [...] Read more.
Chronic stress, a risk factor for many neuropsychiatric conditions, causes dysregulation in the immune system in both humans and animal models. Additionally, inflammation and synapse loss have been associated with deficits in social behavior. The complement system, a key player of innate immunity, has been linked to social behavior impairments caused by chronic stress. However, it is not known whether complement inhibition can help prevent neuroinflammation and behavioral deficits caused by chronic stress. In this study, we investigated the potential of a site-targeted complement inhibitor to ameliorate chronic stress-induced changes in social behavior and inflammatory markers in the prefrontal cortex (PFC) and hippocampus. Specifically, we investigated the use of C2-Crry, which comprises a natural antibody-derived single-chain antibody (ScFv) targeting domain-designated C2, linked to Crry, a C3 activation inhibitor. The C2 targeting domain recognizes danger-associated molecular patterns consisting of a subset of phospholipids that become exposed following cell stress or injury. We found that systemic administration of C2-Crry attenuated chronic stress-induced social behavioral impairments in mice. Furthermore, C2-Crry administration significantly decreased microglia/macrophage and astrocyte activation markers in the PFC and hippocampus. These findings suggest that site-targeted complement inhibition could offer a promising, safe, and effective strategy for treating chronic stress induced behavioral and immune function disorders. Full article
(This article belongs to the Special Issue Neuroinflammation in Brain Health and Diseases)
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