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Cells
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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 2895

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

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. Cells is an international peer-reviewed open access semimonthly 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 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 (2 papers)

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Research

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
Viewed by 1249
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
Viewed by 1072
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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