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Cells
Special Issues
Microglia in Neurodegenerative Diseases—Second Edition
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Microglia in Neurodegenerative Diseases—Second Edition

A special issue of Cells (ISSN 2073-4409). This special issue belongs to the section "Cells of the Nervous System".

Deadline for manuscript submissions: closed (30 June 2022) | Viewed by 18645

Special Issue Editor

Dr. Douglas Gordon Walker

E-Mail Website
Guest Editor
School of Life Sciences and Neurodegenerative Disease Research Center, Arizona State University, Tempe, AZ, USA
Interests: human microglia; CD200; CD33; TREM-2; progranulin; autophagy; lysosomal function; amyloid beta; alpha synuclein; anti-inflammatory signaling; microglia phenotyping
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Following the successful publication of a range of significant articles in the first edition of “Microglia in Neurodegenerative Diseases” in 2019, we are inviting submissions to the second edition on this topic. This is timely as the scientific community progresses from the SARS-Cov2/COVID19 pandemic where some recent studies have implicated microglia pathogenesis.

The role of microglia in neurodegenerative diseases has been widely studied in Alzheimer’s disease and Parkinson's disease, the two most common neurodegenerative diseases. There have been a range of discordant studies proposing evidence for and against their significance in driving these diseases.  There is ample room in this issue to discuss controversial issues on this topic. It should be stated that Neurodegenerative Diseases include multiple sclerosis and its animal models, stroke and its animal models, viral infections (including SARS-Cov2), along with AD and PD.

For this new Special Issue, original research articles, review articles and opinion pieces are invited addressing current issues of how understanding microglia will aid in developing new treatments. In my opinion, it is timely for researchers to consider how, and whether, the large amount of gene expression/sequencing studies of microglia or related genes have advanced the field.

Dr. Douglas Gordon Walker
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. Cells is an international peer-reviewed open access semimonthly 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
  • cytokines
  • reactive
  • phagocytosis
  • neurodegenerative diseases

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Related Special Issue

Published Papers (2 papers)

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Research

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33 pages, 12368 KiB  
Article
C9-ALS-Associated Proline-Arginine Dipeptide Repeat Protein Induces Activation of NLRP3 Inflammasome of HMC3 Microglia Cells by Binding of Complement Component 1 Q Subcomponent-Binding Protein (C1QBP), and Syringin Prevents This Effect
by Ru-Huei Fu, Chia-Wen Tsai, Shao-Chih Chiu, Shih-Ping Liu, Yu-Ting Chiang, Yun-Hua Kuo, Woei-Cherng Shyu and Shinn-Zong Lin
Cells 2022, 11(19), 3128; https://doi.org/10.3390/cells11193128 - 5 Oct 2022
Cited by 16 | Viewed by 4008
Abstract
Amyotrophic lateral sclerosis (ALS) is a fatal disease in which motor neurons gradually degenerate. The mutation of the C9orf72 gene is the main genetic cause of ALS (C9-ALS). One of its specific pathological features is the production of proline-arginine (PR) dipeptide repeat protein [...] Read more.
Amyotrophic lateral sclerosis (ALS) is a fatal disease in which motor neurons gradually degenerate. The mutation of the C9orf72 gene is the main genetic cause of ALS (C9-ALS). One of its specific pathological features is the production of proline-arginine (PR) dipeptide repeat protein (DPR). In this study, we developed a PR-DPR (PR50)-expressing human HMC3 microglial cell model. We found that PR50 mainly aggregates into spots in the nucleus and induces significant NLRP3 inflammasome activity. Moreover, mouse NSC-34 motor neuron cells treated with a conditional medium of PR50-expressing HMC3 cells (PR-CM) caused cell damage and apoptosis activity. However, R50-expressing HMC cells treated with MCC950 (an NLRP3 inhibitor) reversed this result. Furthermore, we identified complement component 1 q subcomponent-binding protein (C1QBP) as one of the interaction partners of PR50. The downregulation of C1QBP in HMC3 cells induces NLRP3 inflammasome activity similar to PR50 expression. Finally, we found that syringin can block the interaction between PR50 and C1QBP, and effectively reduce the PR50-induced NLRP3 inflammasome activity in HMC3 cells. This improves the apoptosis of NSC-34 cells caused by PR-CM. This study is the first to link PR50, C1QBP, and NLRP3 inflammasome activity in microglia and develop potential therapeutic strategies for syringin intervention in C9-ALS. Full article
(This article belongs to the Special Issue Microglia in Neurodegenerative Diseases—Second Edition)
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Review

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52 pages, 3719 KiB  
Review
Microglia Phenotypes in Aging and Neurodegenerative Diseases
by Menbere Y. Wendimu and Shelley B. Hooks
Cells 2022, 11(13), 2091; https://doi.org/10.3390/cells11132091 - 30 Jun 2022
Cited by 121 | Viewed by 14168
Abstract
Neuroinflammation is a hallmark of many neurodegenerative diseases (NDs) and plays a fundamental role in mediating the onset and progression of disease. Microglia, which function as first-line immune guardians of the central nervous system (CNS), are the central drivers of neuroinflammation. Numerous human [...] Read more.
Neuroinflammation is a hallmark of many neurodegenerative diseases (NDs) and plays a fundamental role in mediating the onset and progression of disease. Microglia, which function as first-line immune guardians of the central nervous system (CNS), are the central drivers of neuroinflammation. Numerous human postmortem studies and in vivo imaging analyses have shown chronically activated microglia in patients with various acute and chronic neuropathological diseases. While microglial activation is a common feature of many NDs, the exact role of microglia in various pathological states is complex and often contradictory. However, there is a consensus that microglia play a biphasic role in pathological conditions, with detrimental and protective phenotypes, and the overall response of microglia and the activation of different phenotypes depends on the nature and duration of the inflammatory insult, as well as the stage of disease development. This review provides a comprehensive overview of current research on the various microglia phenotypes and inflammatory responses in health, aging, and NDs, with a special emphasis on the heterogeneous phenotypic response of microglia in acute and chronic diseases such as hemorrhagic stroke (HS), Alzheimer’s disease (AD), and Parkinson’s disease (PD). The primary focus is translational research in preclinical animal models and bulk/single-cell transcriptome studies in human postmortem samples. Additionally, this review covers key microglial receptors and signaling pathways that are potential therapeutic targets to regulate microglial inflammatory responses during aging and in NDs. Additionally, age-, sex-, and species-specific microglial differences will be briefly reviewed. Full article
(This article belongs to the Special Issue Microglia in Neurodegenerative Diseases—Second Edition)
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