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Neuroinflammation Toxicity and Neuroprotection 2.0

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A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Toxicology".

Deadline for manuscript submissions: closed (20 February 2025) | Viewed by 14815

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Dr. Ming-Chang Chiang

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Guest Editor

Department of Life Science, College of Science and Engineering, Fu Jen Catholic University, New Taipei 242304, Taiwan
Interests: neuroinflammation toxicity and neuroprotection
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Special Issue Information

Dear Colleagues,

This Special Issue is a continuation of our previous Special Issue, “Neuroinflammation Toxicity and Neuroprotection”.

Neuroinflammation is the beginning of all brain lesions. Neuroinflammation is a real risk factor for the development and progression of brain and neurodegenerative diseases. In addition, neuroinflammation has a vital role in developing pathologies resulting from the interaction of neuronal and glial cells. Thus, an extensive literature dataset suggests that inflammation is the cause of neurotoxicity. Many cellular functions are altered during inflammation, such as mitochondrial dysregulation, oxidative stress, ER stress, cell signaling, and other fundamental mechanisms; therefore, authors are invited to publish in vitro and in vivo papers exploring the pathophysiology of neuroinflammatory toxicity in neurodegenerative diseases, stroke, brain tumors, and the role of PM2.5 pollution while discussing neuroprotective effects.

This Special Issue aims to collect the pathological mechanisms of neuroinflammation-induced toxicity in the fields of neurodegenerative diseases, stroke, brain tumors, and PM2.5 air pollution. It will include original research articles or review papers on the molecular mechanisms of cytotoxicity induced by different injuries. Additional potential neuroprotective topics include drugs, natural anti-inflammatory agents, and nanomedicines that may play a key role in developing new strategies for therapeutic drugs in the development of neuroinflammatory symptoms.

Dr. Ming-Chang Chiang
Guest Editor

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Keywords

neuroinflammation neurotoxicity
neurotoxicity
neuroprotection
neurodegenerative diseases
stroke
brain tumors
anti-inflammatory agents

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Published Papers (6 papers)

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Research

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11 pages, 2464 KiB

Open AccessArticle

Administration of Noggin Suppresses Fibrinogen Leakage into the Brain in the Acute Phase After Traumatic Brain Injury in Mice

by Miho Yasunaga, Fuyuko Takata, Takuro Iwao, Junko Mizoguchi, Nanako Tajima and Shinya Dohgu

Int. J. Mol. Sci. 2025, 26(7), 3002; https://doi.org/10.3390/ijms26073002 - 25 Mar 2025

Viewed by 421

Abstract

Traumatic brain injury (TBI) causes neurovascular unit (NVU) dysfunction, including hyperpermeability of the blood–brain barrier to fibrinogen, glial activation, and neuronal damage, possibly leading to secondary brain damage. However, no known substance can inhibit its pathogenesis. In this study, we investigated noggin, a bone morphogenetic protein (BMP) 4 inhibitor, as a TBI pathogenesis-inhibiting substance. We induced acute TBI in C57BL/6J mice through a controlled cortical impact (CCI) and evaluated the effects of noggin on fibrinogen leakage into the brain and NVU-constituting cells, including pericytes, microglia, astrocytes, and neurons. CCI mice showed increased BMP4 levels and extravascular fibrinogen in the hippocampus. Noggin treatment significantly suppressed fibrinogen leakage four days post-CCI in a dose-dependent manner. Immunofluorescence staining revealed that noggin administration did not inhibit the activation of NVU cells such as pericytes, microglia, and astrocytes, which were characterized by increased PDGFRβ, Iba1, and GFAP expression levels, respectively. On postoperative day 4, CCI mice showed neuronal cell and myelinated neuronal fiber loss, which were not significantly affected by noggin administration. In conclusion, noggin administration suppresses fibrinogen leakage into the brain in the acute phase after TBI. However, the suppression of fibrinogen leakage through noggin administration did not alleviate neuronal damage and activation of NVU cells during the acute phase of TBI. Full article

(This article belongs to the Special Issue Neuroinflammation Toxicity and Neuroprotection 2.0)

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16 pages, 5572 KiB

Open AccessArticle

AMPK Phosphorylates LMX1b to Regulate a Brainstem Neurogenic Network Important for Control of Breathing in Neonatal Mice

by Traci L. Marin, Christopher G. Wilson, Miguel Lopez Ramirez, Wei Sun, Atul Malhotra and Brendan Gongol

Int. J. Mol. Sci. 2025, 26(1), 213; https://doi.org/10.3390/ijms26010213 - 30 Dec 2024

Viewed by 850

Abstract

Ventilatory drive is modulated by a variety of neurochemical inputs that converge on spatially oriented clusters of cells within the brainstem. This regulation is required to maintain energy homeostasis and is essential to sustain life across all mammalian organisms. Therefore, the anatomical orientation of these cellular clusters during development must have a defined mechanistic basis with redundant genomic variants. Failure to completely develop these features causes several conditions including apnea of prematurity (AOP) and sudden infant death syndrome (SIDS). AOP is associated with many adverse outcomes including increased risk of interventricular hemorrhage. However, there are no pharmacological interventions that reduce SIDS and AOP prevalence by promoting brainstem development. AMP-activated protein kinase (AMPK) is a kinase that regulates ventilatory control to maintain homeostasis. This study identifies a signaling axis in which the pharmacological activation of AMPK in vivo via metformin in brainstem ventilatory control centers results in the phosphorylation of LIM homeobox transcription factor 1-beta (Lmx1b), a key player in dorsal–ventral patterning during fetal development. The phosphorylation of Lmx1b transactivates a neurogenic interactome important for the development and regulation of ventilatory control centers. These findings highlight the potential for metformin in the treatment and prevention of AOP. Full article

(This article belongs to the Special Issue Neuroinflammation Toxicity and Neuroprotection 2.0)

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19 pages, 2849 KiB

Open AccessArticle

Positive Effects of Argon Inhalation After Traumatic Brain Injury in Rats

by Viktoriya V. Antonova, Denis N. Silachev, Egor Y. Plotnikov, Irina B. Pevzner, Mikhail E. Ivanov, Ekaterina A. Boeva, Sergey N. Kalabushev, Mikhail Ya. Yadgarov, Rostislav A. Cherpakov, Oleg A. Grebenchikov and Artem N. Kuzovlev

Int. J. Mol. Sci. 2024, 25(23), 12673; https://doi.org/10.3390/ijms252312673 - 26 Nov 2024

Viewed by 1042

Abstract

The noble gas argon is one of the most promising neuroprotective agents for hypoxic-reperfusion injuries of the brain. However, its effect on traumatic injuries has been insufficiently studied. The aim of this study was to analyze the effect of the triple inhalation of the argon-oxygen mixture Ar 70%/O₂ 30% on physical and neurological recovery and the degree of brain damage after traumatic brain injury and to investigate the possible molecular mechanisms of the neuroprotective effect. The experiments were performed in male Wistar rats. A controlled brain injury model was used to investigate the effects of argon treatment and the underlying molecular mechanisms. The results of the study showed that animals with craniocerebral injuries that were treated with argon inhalation exhibited better physical recovery rates, better neurological status, and less brain damage. Argon treatment significantly reduced the expression of the proinflammatory markers TNFα and CD68 caused by TBI, increased the expression of phosphorylated protein kinase B (pAKT), and promoted the expression of the transcription factor Nrf2 in intact animals. Treatment with an argon-oxygen breathing mixture after traumatic brain injury has a neuroprotective effect by suppressing the inflammatory response and activating the antioxidant and anti-ischemic system. Full article

(This article belongs to the Special Issue Neuroinflammation Toxicity and Neuroprotection 2.0)

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21 pages, 7677 KiB

Open AccessArticle

Fermented Protaetia brevitarsis Larvae Improves Neurotoxicity in Chronic Ethanol-Induced-Dementia Mice via Suppressing AKT and NF-κB Signaling Pathway

by Hyo Lim Lee, Jong Min Kim, Min Ji Go, Han Su Lee, Ju Hui Kim and Ho Jin Heo

Int. J. Mol. Sci. 2024, 25(5), 2629; https://doi.org/10.3390/ijms25052629 - 23 Feb 2024

Cited by 6 | Viewed by 1770

Abstract

This study was investigated to examine the neuroprotective effect of fermented Protaetia brevitarsis larvae (FPB) in ethanol-induced-dementia mice. Consumption of FPB by mice resulted in improved memory dysfunction in the Y-maze, passive avoidance, and Morris water maze tests. FPB significantly decreased oxidative stress by regulating levels of malondialdehyde (MDA), superoxide dismutase (SOD), and reduced glutathione (GSH) in brain tissues. In addition, FPB restored cerebral mitochondrial dysfunction by modulating levels of reactive oxygen species (ROS), mitochondrial membrane potential (MMP), and ATP. In addition, FPB enhanced the cholinergic system via the regulation of acetylcholine (ACh) content, acetylcholinesterase (AChE) activity, and expressions of AChE and choline acetyltransferase (ChAT) in brain tissues. FPB ameliorated neuronal apoptosis through modulation of the protein kinase B (AKT)/B-cell lymphoma (BCL)-2 signaling pathway. Also, FPB improved inflammation response by down-regulating the toll-like receptor (TLR)-4/nuclear factor (NF)-κB pathway. Additionally, FPB ameliorated synaptic plasticity via the increase of the expressions of synaptophysin (SYP), postsynaptic density protein (PSD)-95, and growth-associated protein (GAP)-43. Treatment with FPB also reinforced the blood–brain barrier by increasing tight junctions including zonula occludens (ZO)-1, occludin, and claudin-1. In conclusion, these results show that FPB can improve cognitive impairment via AKT/NF-κB pathways in ethanol-induced-dementia mice. Full article

(This article belongs to the Special Issue Neuroinflammation Toxicity and Neuroprotection 2.0)

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Review

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25 pages, 691 KiB

Open AccessReview

A Review of the Neuroprotective Properties of Exosomes Derived from Stem Cells and Exosome-Coated Nanoparticles for Treating Neurodegenerative Diseases and Stroke

by Yu-Ping Yang, Christopher J. B. Nicol and Ming-Chang Chiang

Int. J. Mol. Sci. 2025, 26(8), 3915; https://doi.org/10.3390/ijms26083915 - 21 Apr 2025

Viewed by 660

Abstract

Neurological diseases, including neurodegenerative disorders and stroke, represent significant medical challenges due to their complexity and the limitations of current treatment approaches. This review explores the potential of stem cell (SC)-derived exosomes (Exos) as a transformative therapeutic strategy for these diseases. Exos, especially those derived from SCs, exhibit natural targeting ability, biocompatibility, and the capacity to cross the blood–brain barrier (BBB), making them ideal vehicles for drug delivery. This review provides an in-depth discussion of the properties and advantages of SC-Exos. It highlights their potential synergistic benefits in therapeutic approaches to treat neurological diseases. This article discusses the mechanisms of action of SC-Exos, highlighting their ability to target specific cells, modulate disease pathways, and provide controlled release of therapeutic agents. Applications in specific neurological disorders have been investigated, demonstrating the potential to improve outcomes in conditions such as Alzheimer’s Disease (AD), Parkinson’s Disease (PD), and stroke. Moreover, Exos-coated nanoparticles (NPs) combine the natural properties of Exos with the multifunctionality of NPs. This integration takes advantage of exosome membrane biocompatibility and targeting capabilities while preserving NPs’ beneficial features, such as drug loading and controlled release. As a result, Exos-coated NPs may enhance the precision, efficacy, and safety of therapeutic interventions. In conclusion, SC-Exos represent a promising and innovative approach to treating neurological diseases. Full article

(This article belongs to the Special Issue Neuroinflammation Toxicity and Neuroprotection 2.0)

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29 pages, 3702 KiB

Open AccessReview

Neuroinflammation in Neurodegenerative Disorders: Current Knowledge and Therapeutic Implications

by Paras Mani Giri, Anurag Banerjee, Arpita Ghosal and Buddhadev Layek

Int. J. Mol. Sci. 2024, 25(7), 3995; https://doi.org/10.3390/ijms25073995 - 3 Apr 2024

Cited by 33 | Viewed by 8689

Abstract

Neurodegenerative disorders (NDs) have become increasingly common during the past three decades. Approximately 15% of the total population of the world is affected by some form of NDs, resulting in physical and cognitive disability. The most common NDs include Alzheimer’s disease, Parkinson’s disease, amyotrophic lateral sclerosis, and Huntington’s disease. Although NDs are caused by a complex interaction of genetic, environmental, and lifestyle variables, neuroinflammation is known to be associated with all NDs, often leading to permanent damage to neurons of the central nervous system. Furthermore, numerous emerging pieces of evidence have demonstrated that inflammation not only supports the progression of NDs but can also serve as an initiator. Hence, various medicines capable of preventing or reducing neuroinflammation have been investigated as ND treatments. While anti-inflammatory medicine has shown promising benefits in several preclinical models, clinical outcomes are often questionable. In this review, we discuss various NDs with their current treatment strategies, the role of neuroinflammation in the pathophysiology of NDs, and the use of anti-inflammatory agents as a potential therapeutic option. Full article

(This article belongs to the Special Issue Neuroinflammation Toxicity and Neuroprotection 2.0)

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