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Biomolecules
Special Issues
The Role of Microglia in Aging and Neurodegenerative Disease
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The Role of Microglia in Aging and Neurodegenerative Disease

A special issue of Biomolecules (ISSN 2218-273X). This special issue belongs to the section "Molecular Medicine".

Deadline for manuscript submissions: 31 January 2025 | Viewed by 4438

Special Issue Editor

Prof. Dr. Björn Spittau

E-Mail Website
Guest Editor
Medical School OWL, Anatomy and Cell Biology, Bielefeld University, 33615 Bielefeld, Germany
Interests: the mechanisms of TGF-beta-mediated modulation of microglia functions under physiological and pathological conditions; microglia development/maturation, microglia functions during postnatal CNS development, and microglia in the aged and diseased CNS are addressed using transgenic mouse models
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Microglia significantly change their morphological and functional features during aging as well as during the course of neurodegenerative diseases, thereby contributing to the onset and progression of several CNS pathologies. However, whether microglia reactivity has beneficial or detrimental effects and consequences seems to depend on the particular disease. Moreover, the crosstalk with peripheral immune cells and the gut–brain axis involved in the regulation of age-dependent and disease-specific microglia reactions are only partially understood. We aim to elucidate different microglia reaction states found in distinct CNS pathologies and their contribution to disease outcomes.

Major questions include how microglia functions are regulated during aging and neurodegenerative processes and which endogenous and exogenous factors might bear therapeutic potential for the treatment of neurodegenerative diseases. Furthermore, the understanding of how the gut–brain axis and metabolic changes regulate the reactivity of microglia in CNS diseases will be a major purpose of this Special Issue.

Submissions of original research and review manuscripts focusing on microglia activation and the role of microglia in neurodegenerative diseases of the brain and spinal cord are welcome. We hope to comprehensively summarize and elucidate the different microglia activation states related to neurodegeneration and hope to increase the overall understanding of microglia in neurodegenerative diseases.

Prof. Dr. Björn Spittau
Guest Editor

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. Biomolecules 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 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

  • microglia
  • neurodegenerative diseases
  • disease-associated microglia (DAM)
  • microglia activation
  • Alzheimer's disease
  • Parkinson’s disease
  • ischemic stroke

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Published Papers (3 papers)

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Research

20 pages, 1999 KiB  
Article
Lipidomics Analysis of Human HMC3 Microglial Cells in an In Vitro Model of Metabolic Syndrome
by Mateusz Chmielarz, Mariusz Aleksander Bromke, Mateusz Olbromski, Kamila Środa-Pomianek, Magdalena Frej-Mądrzak, Piotr Dzięgiel and Beata Sobieszczańska
Biomolecules 2024, 14(10), 1238; https://doi.org/10.3390/biom14101238 - 30 Sep 2024
Viewed by 679
Abstract
Metabolic endotoxemia (ME) is associated with bacterial lipopolysaccharide (LPS, endotoxin) and increased levels of saturated fatty acids (SFAs) in the bloodstream, causing systemic inflammation. ME usually accompanies obesity and a diet rich in fats, especially SFAs. Numerous studies confirm the effect of ME-related [...] Read more.
Metabolic endotoxemia (ME) is associated with bacterial lipopolysaccharide (LPS, endotoxin) and increased levels of saturated fatty acids (SFAs) in the bloodstream, causing systemic inflammation. ME usually accompanies obesity and a diet rich in fats, especially SFAs. Numerous studies confirm the effect of ME-related endotoxin on microglial activation. Our study aimed to assess lipid metabolism and immune response in microglia pre-stimulated with TNFα (Tumor Necrosis Factor α) and then with endotoxin and palmitic acid (PA). Using ELISA, we determined cytokines IL-1β, IL-10, IL-13 (interleukin-1β, -10, -13, and TGFβ (Transforming Growth Factor β) in the culture medium from microglial cells stimulated for 24 h with TNFα and then treated with LPS (10 ng/mL) and PA (200 µM) for 24 h. HMC3 (Human Microglial Cells clone 3) cells produced negligible amounts of IL-1β, IL-10, and IL-13 after stimulation but secreted moderate levels of TGFβ. Changes in lipid metabolism accompanied changes in TREM2 (Triggering Receptor Expressed on Myeloid Cells 2) expression. HMC3 stimulation with endotoxin increased TREM2 expression, while PA treatment decreased it. Endotoxin increased ceramide levels, while PA increased triglyceride levels. These results indicated that pre-stimulation of microglia with TNFα significantly affects its interactions with LPS and PA and modulates lipid metabolism, which may lead to microglial activation silencing and neurodegeneration. Full article
(This article belongs to the Special Issue The Role of Microglia in Aging and Neurodegenerative Disease)
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20 pages, 2345 KiB  
Article
Incretin-Based Multi-Agonist Peptides Are Neuroprotective and Anti-Inflammatory in Cellular Models of Neurodegeneration
by Katherine O. Kopp, Yazhou Li, Elliot J. Glotfelty, David Tweedie and Nigel H. Greig
Biomolecules 2024, 14(7), 872; https://doi.org/10.3390/biom14070872 - 19 Jul 2024
Viewed by 1709
Abstract
Glucagon-like peptide-1 (GLP-1)-based drugs have been approved by the United States Food and Drug Administration (FDA) and are widely used to treat type 2 diabetes mellitus (T2DM) and obesity. More recent developments of unimolecular peptides targeting multiple incretin-related receptors (“multi-agonists”), including the glucose-dependent [...] Read more.
Glucagon-like peptide-1 (GLP-1)-based drugs have been approved by the United States Food and Drug Administration (FDA) and are widely used to treat type 2 diabetes mellitus (T2DM) and obesity. More recent developments of unimolecular peptides targeting multiple incretin-related receptors (“multi-agonists”), including the glucose-dependent insulinotropic polypeptide (GIP) receptor (GIPR) and the glucagon (Gcg) receptor (GcgR), have emerged with the aim of enhancing drug benefits. In this study, we utilized human and mouse microglial cell lines, HMC3 and IMG, respectively, together with the human neuroblastoma SH-SY5Y cell line as cellular models of neurodegeneration. Using these cell lines, we studied the neuroprotective and anti-inflammatory capacity of several multi-agonists in comparison with a single GLP-1 receptor (GLP-1R) agonist, exendin-4. Our data demonstrate that the two selected GLP-1R/GIPR dual agonists and a GLP-1R/GIPR/GcgR triple agonist not only have neurotrophic and neuroprotective effects but also have anti-neuroinflammatory properties, as indicated by the decreased microglial cyclooxygenase 2 (COX2) expression, nitrite production, and pro-inflammatory cytokine release. In addition, our results indicate that these multi-agonists have the potential to outperform commercially available single GLP-1R agonists in neurodegenerative disease treatment. Full article
(This article belongs to the Special Issue The Role of Microglia in Aging and Neurodegenerative Disease)
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18 pages, 6547 KiB  
Article
West Nile Virus-Induced Expression of Senescent Gene Lgals3bp Regulates Microglial Phenotype within Cerebral Cortex
by Artem Arutyunov, Violeta Durán-Laforet, Shenjian Ai, Loris Ferrari, Robert Murphy, Dorothy P. Schafer and Robyn S. Klein
Biomolecules 2024, 14(7), 808; https://doi.org/10.3390/biom14070808 - 8 Jul 2024
Cited by 1 | Viewed by 1495
Abstract
Microglia, the resident macrophages of the central nervous system, exhibit altered gene expression in response to various neurological conditions. This study investigates the relationship between West Nile Virus infection and microglial senescence, focusing on the role of LGALS3BP, a protein implicated in both [...] Read more.
Microglia, the resident macrophages of the central nervous system, exhibit altered gene expression in response to various neurological conditions. This study investigates the relationship between West Nile Virus infection and microglial senescence, focusing on the role of LGALS3BP, a protein implicated in both antiviral responses and aging. Using spatial transcriptomics, RNA sequencing and flow cytometry, we characterized changes in microglial gene signatures in adult and aged mice following recovery from WNV encephalitis. Additionally, we analyzed Lgals3bp expression and generated Lgals3bp-deficient mice to assess the impact on neuroinflammation and microglial phenotypes. Our results show that WNV-activated microglia share transcriptional signatures with aged microglia, including upregulation of genes involved in interferon response and inflammation. Lgals3bp was broadly expressed in the CNS and robustly upregulated during WNV infection and aging. Lgals3bp-deficient mice exhibited reduced neuroinflammation, increased homeostatic microglial numbers, and altered T cell populations without differences in virologic control or survival. These data indicate that LGALS3BP has a role in regulating neuroinflammation and microglial activation and suggest that targeting LGALS3BP might provide a potential route for mitigating neuroinflammation-related cognitive decline in aging and post-viral infections. Full article
(This article belongs to the Special Issue The Role of Microglia in Aging and Neurodegenerative Disease)
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