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Neuroinflammation Toxicity and Neuroprotection 2.0
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Neuroinflammation Toxicity and Neuroprotection 2.0

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: 31 July 2024 | Viewed by 2167

Special Issue Editor

Dr. Ming-Chang Chiang

E-Mail Website
Guest Editor
Department of Life Science, College of Science and Engineering, Fu Jen Catholic University, New Taipei 242304, Taiwan
Interests: neuroinflammation toxicity and neuroprotection
Special Issues, Collections and Topics in MDPI journals

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

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. International Journal of Molecular Sciences is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. There is an Article Processing Charge (APC) for publication in this open access journal. For details about the APC please see here. 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 neurotoxicity
  • neurotoxicity
  • neuroprotection
  • neurodegenerative diseases
  • stroke
  • brain tumors
  • anti-inflammatory agents

Published Papers (2 papers)

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Research

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21 pages, 7677 KiB  
Article
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
Viewed by 601
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 [...] Read more.
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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29 pages, 3702 KiB  
Review
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 - 03 Apr 2024
Viewed by 1018
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, [...] Read more.
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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