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Inflammation and Neurological Diseases: Molecular Mechanisms and Therapeutic Implications

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

Deadline for manuscript submissions: 30 May 2024 | Viewed by 1887

Special Issue Editor


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Guest Editor
1. Drug Development Program, Kansas City VA Medical Center, Kansas City, MO 64128, USA
2. Cancer Biology, University of Kansas Medical Center, Kansas City, KS 66160, USA
Interests: breast cancer; pancreatic cancer; non-small cell lung cancer; neuroinflammation; NLRP3; microRNA; inflammasome
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Special Issue Information

Dear Colleagues,

We are pleased to invite you to contribute to our Special Issue of the International Journal of Molecular Sciences (IJMS) entitled “Inflammation and Neurological Diseases: Molecular Mechanisms and Therapeutic Implications”.

In recent years, accumulating evidence suggests that inflammation plays a critical role in the pathogenesis of various neurological diseases, icluding Alzheimer's disease (AD), Parkinson's disease (PD), multiple sclerosis epilepsy, sroke and brain injury. Therefore, a better understanding of the specific mechanisms that play a role in the natural history of diseases is crucial for the development of novel integrated pharmacological approaches to treat these diseases. This Special Issue will focus on elaborating the current findings on the complexities of targeting neuroinflammation as a novel therapy, and its role in the etiopathogenesis of several neurological diseases.

Potential topics include, but are not limited to, the following:

  • NLRP3 inflammasome and neurological diseases;
  • microRNA-based regulation of inflammation;
  • Gut microbiota-mediated inflammation and neurological diseases;
  • Targeting inflammasomes to treat neurological diseases.

Dr. Inamul Haque
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

  • CNS
  • neuroinflammation
  • Alzheimer's disease
  • Parkinson's disease
  • multiple sclerosis
  • epilepsy
  • NLRP3 inflammasome
  • therapeutic
  • microRNA
  • blood–brain barrier

Published Papers (1 paper)

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Research

16 pages, 3642 KiB  
Article
Stimulation of the Pro-Resolving Receptor Fpr2 Reverses Inflammatory Microglial Activity by Suppressing NFκB Activity
by Edward S. Wickstead, Bradley T. Elliott, Sarah Pokorny, Christopher Biggs, Stephen J. Getting and Simon McArthur
Int. J. Mol. Sci. 2023, 24(21), 15996; https://doi.org/10.3390/ijms242115996 - 06 Nov 2023
Cited by 1 | Viewed by 1364
Abstract
Neuroinflammation driven primarily by microglia directly contributes to neuronal death in many neurodegenerative diseases. Classical anti-inflammatory approaches aim to suppress pro-inflammatory mediator production, but exploitation of inflammatory resolution may also be of benefit. A key driver of peripheral inflammatory resolution, formyl peptide receptor [...] Read more.
Neuroinflammation driven primarily by microglia directly contributes to neuronal death in many neurodegenerative diseases. Classical anti-inflammatory approaches aim to suppress pro-inflammatory mediator production, but exploitation of inflammatory resolution may also be of benefit. A key driver of peripheral inflammatory resolution, formyl peptide receptor 2 (Fpr2), is expressed by microglia, but its therapeutic potential in neurodegeneration remains unclear. Here, we studied whether targeting of Fpr2 could reverse inflammatory microglial activation induced by the potent bacterial inflammogen lipopolysaccharide (LPS). Exposure of murine primary or immortalised BV2 microglia to LPS triggered pro-inflammatory phenotypic change and activation of ROS production, effects significantly attenuated by subsequent treatment with the Fpr2 agonist C43. Mechanistic studies showed C43 to act through p38 MAPK phosphorylation and reduction of LPS-induced NFκB nuclear translocation via prevention of IκBα degradation. Here, we provide proof-of-concept data highlighting Fpr2 as a potential target for control of microglial pro-inflammatory activity, suggesting that it may be a promising therapeutic target for the treatment of neuroinflammatory disease. Full article
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