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Biomedicines
Special Issues
Neuroinflammation: From Pathophysiologic Mechanisms to Therapeutic Strategies
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Neuroinflammation: From Pathophysiologic Mechanisms to Therapeutic Strategies

A special issue of Biomedicines (ISSN 2227-9059). This special issue belongs to the section "Neurobiology and Clinical Neuroscience".

Deadline for manuscript submissions: closed (31 January 2025) | Viewed by 6181

Special Issue Editor

Dr. Li-Ping Zhou

E-Mail Website
Guest Editor
School of Optometry, The Hong Kong Polytechnic University, Kowloon, Hong Kong
Interests: neurodegenerative disorders; regenerative medicine; aging-related disorder; anti-inflammatory therapy; mitochondrial augmentation

Special Issue Information

Dear Colleagues,

This Special Issue provides a comprehensive overview of the current information in the field of neuroinflammation. Neuroinflammation is a complex process that involves the activation of immune cells in the central nervous system which can contribute to the development and progression of a wide range of neurological disorders, including Alzheimer’s disease, Parkinson’s disease, multiple sclerosis, and stroke.

This Special Issue will cover a wide range of topics related to neuroinflammation, including, but not limited to, the molecular mechanism of neuroinflammation, the process of neuroinflammation, and the potential therapeutic strategies for treating neuroinflammatory diseases. The Special Issue also includes a discussion on the potential of various therapeutic strategies for treating diseases via targeting neuroinflammation, including, but not limited to, anti-inflammatory drugs, immunomodulatory therapies, and stem cell-based therapies.

Overall, this Special Issue provides a valuable resource for researchers and clinicians interested in neuroinflammation, highlighting the importance of continued research in understanding the underlying pathophysiological mechanisms and developing effective therapeutic strategies for neuroinflammatory diseases.

Dr. Li-Ping Zhou
Guest Editor

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 2600 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 mechanism
  • anti-inflammation
  • stem cell-based therapy
  • cell-free stem-cell-based therapy
  • immunomodulation

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Published Papers (4 papers)

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Research

12 pages, 707 KiB  
Article
Cerebrospinal Fluid Calcium Balance in Tick-Borne Encephalitis: A Preliminary Study and Future Research Directions
by Gabriela Trojan, Anna Moniuszko-Malinowska, Karolina Orywal, Ewelina Kruszewska, Barbara Mroczko, Anna Grzeszczuk and Piotr Czupryna
Biomedicines 2025, 13(2), 337; https://doi.org/10.3390/biomedicines13020337 - 2 Feb 2025
Viewed by 449
Abstract
Introduction: Calcium homeostasis is essential for neurophysiological functions, with dysregulation implicated in neurodegenerative diseases. Recent studies suggest that specific viral brain infections, such as tick-borne encephalitis, can initiate neuronal loss and subsequent neurodegenerative changes. This study examines alterations in calcium levels within [...] Read more.
Introduction: Calcium homeostasis is essential for neurophysiological functions, with dysregulation implicated in neurodegenerative diseases. Recent studies suggest that specific viral brain infections, such as tick-borne encephalitis, can initiate neuronal loss and subsequent neurodegenerative changes. This study examines alterations in calcium levels within the cerebrospinal fluid (CSF) of patients with tick-borne encephalitis (TBE). Objectives: To evaluate the concentration of calcium in the CSF of TBE patients and assess its potential as a diagnostic marker for disease severity. Materials and Methods: CSF samples were collected from 42 subjects (11 controls, 20 with TBE, 11 with other forms of meningitis). Calcium levels were measured using the Alinity c analyzer. Statistical analyses included the Shapiro–Wilk test, Mann–Whitney U test, and ROC curve analysis. Results: Calcium levels were significantly lower in TBE patients compared to controls (mean 0.85 mmol/L vs. 0.98 mmol/L). Lower calcium levels were associated with milder cases of TBE. ROC analysis (AUC 0.802, p-value 0.0053) supports the diagnostic utility of calcium concentration in differentiating TBE severity. The optimal cut-off value for calcium was >3.09 mg/dL, with a sensitivity of 84.62% and specificity of 71.43%. These findings further emphasize the potential of calcium as a diagnostic marker for TBEV. Conclusions: The observed differences in CSF calcium levels between mild and severe TBE cases highlight its potential as a diagnostic marker. Further research is warranted to elucidate calcium’s role in TBE, aiming to improve clinical management and reduce complications. We emphasize that this study is one of the first to propose calcium levels as a potential biomarker for assessing the severity of tick-borne encephalitis, offering a new perspective in the diagnostic approach to this infection. Full article
(This article belongs to the Special Issue Neuroinflammation: From Pathophysiologic Mechanisms to Therapeutic Strategies)
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20 pages, 6109 KiB  
Article
Maresin-like 1 Ameliorates Neuropathology of Alzheimer’s Disease in Brains of a Transgenic Mouse Model
by Pallavi Shrivastava, Yan Lu, Shanchun Su, Yuichi Kobayashi, Yuhai Zhao, Nathan Lien, Abdul-Razak Masoud, Walter J. Lukiw and Song Hong
Biomedicines 2024, 12(12), 2865; https://doi.org/10.3390/biomedicines12122865 - 17 Dec 2024
Viewed by 1035
Abstract
(1) Background: Impeded resolution of inflammation contributes substantially to the pathogenesis of Alzheimer’s disease (AD); consequently, resolving inflammation is pivotal to the amelioration of AD pathology. This can potentially be achieved by the treatment with specialized pro-resolving lipid mediators (SPMs), which should resolve [...] Read more.
(1) Background: Impeded resolution of inflammation contributes substantially to the pathogenesis of Alzheimer’s disease (AD); consequently, resolving inflammation is pivotal to the amelioration of AD pathology. This can potentially be achieved by the treatment with specialized pro-resolving lipid mediators (SPMs), which should resolve neuroinflammation in brains. (2) Methods: Here, we report the histological effects of long-term treatment with an SPM, maresin-like 1 (MarL1), on AD pathogenesis in a transgenic 5xFAD mouse model. (3) Results: MarL1 treatment reduced Aβ overload, curbed the loss of neurons in brains especially cholinergic neurons associated with cleaved-caspase-3-associated apoptotic degeneration, reduced microgliosis and the pro-inflammatory M1 polarization of microglia, curbed the AD-associated decline in anti-inflammatory Iba1+Arg-1+-M2 microglia, inhibited phenotypic switching to pro-inflammatory N1 neutrophils, promoted the blood–brain barrier-associated tight-junction protein claudin-5 and decreased neutrophil leakage in 5xFAD brains, and induced the switch of neutrophils toward the inflammation-resolving N2 phenotype. (4) Conclusions: Long-term administration of MarL1 mitigates AD-related neuropathogenesis in brains by curbing neuroinflammation and neurodegeneration, based on the histological results. These findings provide preclinical leads and mechanistic insights for the development of MarL1 into an effective modality to ameliorate AD pathogenesis. Full article
(This article belongs to the Special Issue Neuroinflammation: From Pathophysiologic Mechanisms to Therapeutic Strategies)
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30 pages, 20372 KiB  
Article
Possible Prophylactic Effects of Sulforaphane on LPS-Induced Recognition Memory Impairment Mediated by Regulating Oxidative Stress and Neuroinflammatory Proteins in the Prefrontal Cortex Region of the Brain
by Noor Ahmed Alzahrani, Khulud Abdullah Bahaidrah, Rasha A. Mansouri, Rahaf Saeed Aldhahri, Gamal S. Abd El-Aziz and Badrah S. Alghamdi
Biomedicines 2024, 12(5), 1107; https://doi.org/10.3390/biomedicines12051107 - 16 May 2024
Cited by 1 | Viewed by 2330
Abstract
Background: Alzheimer’s disease (AD) presents a significant global health concern, characterized by neurodegeneration and cognitive decline. Neuroinflammation is a crucial factor in AD development and progression, yet effective pharmacotherapy remains elusive. Sulforaphane (SFN), derived from cruciferous vegetables and mainly from broccoli, has shown [...] Read more.
Background: Alzheimer’s disease (AD) presents a significant global health concern, characterized by neurodegeneration and cognitive decline. Neuroinflammation is a crucial factor in AD development and progression, yet effective pharmacotherapy remains elusive. Sulforaphane (SFN), derived from cruciferous vegetables and mainly from broccoli, has shown a promising effect via in vitro and in vivo studies as a potential treatment for AD. This study aims to investigate the possible prophylactic mechanisms of SFN against prefrontal cortex (PFC)-related recognition memory impairment induced by lipopolysaccharide (LPS) administration. Methodology: Thirty-six Swiss (SWR/J) mice weighing 18–25 g were divided into three groups (n = 12 per group): a control group (vehicle), an LPS group (0.75 mg/kg of LPS), and an LPS + SFN group (25 mg/kg of SFN). The total duration of the study was 3 weeks, during which mice underwent treatments for the initial 2 weeks, with daily monitoring of body weight and temperature. Behavioral assessments via novel object recognition (NOR) and temporal order recognition (TOR) tasks were conducted in the final week of the study. Inflammatory markers (IL-6 and TNF), antioxidant enzymes (SOD, GSH, and CAT), and pro-oxidant (MDA) level, in addition to acetylcholine esterase (AChE) activity and active (caspase-3) and phosphorylated (AMPK) levels, were evaluated. Further, PFC neuronal degeneration, Aβ content, and microglial activation were also examined using H&E, Congo red staining, and Iba1 immunohistochemistry, respectively. Results: SFN pretreatment significantly improved recognition memory performance during the NOR and TOR tests. Moreover, SFN was protected from neuroinflammation and oxidative stress as well as neurodegeneration, Aβ accumulation, and microglial hyperactivity. Conclusion: The obtained results suggested that SFN has a potential protective property to mitigate the behavioral and biochemical impairments induced by chronic LPS administration and suggested to be via an AMPK/caspase-3-dependent manner. Full article
(This article belongs to the Special Issue Neuroinflammation: From Pathophysiologic Mechanisms to Therapeutic Strategies)
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16 pages, 8262 KiB  
Article
Levosimendan and Dobutamin Attenuate LPS-Induced Inflammation in Microglia by Inhibiting the NF-κB Pathway and NLRP3 Inflammasome Activation via Nrf2/HO-1 Signalling
by Federica Mannino, Valentina Urzì Brancati, Rita Lauro, Igor Pirrotta, Michelangelo Rottura, Natasha Irrera, Gian Maria Cavallini, Giovanni Pallio, Eloisa Gitto and Sara Manti
Biomedicines 2024, 12(5), 1009; https://doi.org/10.3390/biomedicines12051009 - 3 May 2024
Cited by 2 | Viewed by 1797
Abstract
Hypovolemic shock is a circulatory failure, due to a loss in the effective circulating blood volume, that causes tissue hypoperfusion and hypoxia. This condition stimulates reactive oxygen species (ROS) and pro-inflammatory cytokine production in different organs and also in the central nervous system [...] Read more.
Hypovolemic shock is a circulatory failure, due to a loss in the effective circulating blood volume, that causes tissue hypoperfusion and hypoxia. This condition stimulates reactive oxygen species (ROS) and pro-inflammatory cytokine production in different organs and also in the central nervous system (CNS). Levosimendan, a cardioprotective inodilator, and dobutamine, a β1-adrenergic agonist, are commonly used for the treatment of hypovolemic shock, thanks to their anti-inflammatory and antioxidant effects. For this reason, we aimed at investigating levosimendan and dobutamine’s neuroprotective effects in an “in vitro” model of lipopolysaccharide (LPS)-induced neuroinflammation. Human microglial cells (HMC3) were challenged with LPS (0.1 µg/mL) to induce an inflammatory phenotype and then treated with levosimendan (10 µM) or dobutamine (50 µM) for 24 h. Levosimendan and dobutamine significantly reduced the ROS levels and markedly increased Nrf2 and HO-1 protein expression in LPS-challenged cells. Levosimendan and dobutamine also decreased p-NF-κB expression and turned off the NLRP3 inflammasome together with its downstream signals, caspase-1 and IL-1β. Moreover, a reduction in TNF-α and IL-6 expression and an increase in IL-10 levels in LPS-stimulated HMC3 cells was observed following treatment. In conclusion, levosimendan and dobutamine attenuated LPS-induced neuroinflammation through NF-κB pathway inhibition and NLRP3 inflammasome activation via Nrf2/HO-1 signalling, suggesting that these drugs could represent a promising therapeutic approach for the treatment of neuroinflammation consequent to hypovolemic shock. Full article
(This article belongs to the Special Issue Neuroinflammation: From Pathophysiologic Mechanisms to Therapeutic Strategies)
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