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Cells
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Glia in Neurodegenerative Diseases
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Glia in Neurodegenerative Diseases

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 (31 December 2021) | Viewed by 18395

Special Issue Editors

Prof. Dr. S. Thameem Dheen

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Guest Editor
Department of Anatomy, Yong Loo Lin School of Medicine, National University of Singapore, Singapore 117594, Singapore
Interests: neurodevelopmental disorders; microglia-mediated neuroinflammation; neuropathology
Special Issues, Collections and Topics in MDPI journals
Dr. Jai Santosh Polepalli

E-Mail
Co-Guest Editor
Department of Anatomy Yong Loo Lin School of Medicine, NUS Principal Investigator, LSI Neurobiology Programme, National University of Singapore, Singapore, Singapore

Special Issue Information

Dear Colleagues,

Increasing evidence indicates that glial cell dysfunction contributes to neurodegenerative disorders, including Alzheimer’s disease, Parkinson’s disease, dementia, etc. In particular, microglia and astrocytes, which are the predominant glial cells of the central nervous system, perform seminal roles in the healthy brain and neuropathology. In neuropathological conditions, microglia and astrocyte elicit an inflammatory response which involves the release of proinflammatory cytokines and chemokines, as well as growth factors that aid in tissue regeneration and repair. However, chronic activation of these cells has been shown to contribute to neuropathology. Hence, it is important to understand the role of these cells in a healthy and pathological brain in order to maintain the healthy status of the brain and develop therapeutic strategies to treat neurodegenerative diseases.

In this Special Issue, we propose to publish original research articles and reviews in the area of complex biology of glia cells and their roles in neurodegenerative diseases. This will be helpful for future translational research that unravels mechanisms by which glial cells dysfunction contribute to neurodegenerative diseases.

Dr. S. Thameem Dheen
Dr. Jai Santosh Polepalli
Guest Editors

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
  • Astrocytes
  • Glioma
  • Neurodegenerative diseases
  • Cognitive impairment

Published Papers (4 papers)

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Research

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20 pages, 2384 KiB  
Article
BASHY Dye Platform Enables the Fluorescence Bioimaging of Myelin Debris Phagocytosis by Microglia during Demyelination
by Maria V. Pinto, Fábio M. F. Santos, Catarina Barros, Ana Rita Ribeiro, Uwe Pischel, Pedro M. P. Gois and Adelaide Fernandes
Cells 2021, 10(11), 3163; https://doi.org/10.3390/cells10113163 - 13 Nov 2021
Cited by 8 | Viewed by 3435
Abstract
Multiple sclerosis (MS) is a demyelinating disease of the central nervous system that is characterized by the presence of demyelinated regions with accumulated myelin lipid debris. Importantly, to allow effective remyelination, such debris must be cleared by microglia. Therefore, the study of microglial [...] Read more.
Multiple sclerosis (MS) is a demyelinating disease of the central nervous system that is characterized by the presence of demyelinated regions with accumulated myelin lipid debris. Importantly, to allow effective remyelination, such debris must be cleared by microglia. Therefore, the study of microglial activity with sensitive tools is of great interest to better monitor the MS clinical course. Using a boronic acid-based (BASHY) fluorophore, specific for nonpolar lipid aggregates, we aimed to address BASHY’s ability to label nonpolar myelin debris and image myelin clearance in the context of demyelination. Demyelinated ex vivo organotypic cultures (OCSCs) and primary microglia cells were immunostained to evaluate BASHY’s co-localization with myelin debris and also to evaluate BASHY’s specificity for phagocytosing cells. Additionally, mice induced with experimental autoimmune encephalomyelitis (EAE) were injected with BASHY and posteriorly analyzed to evaluate BASHY+ microglia within demyelinated lesions. Indeed, in our in vitro and ex vivo studies, we showed a significant increase in BASHY labeling in demyelinated OCSCs, mostly co-localized with Iba1-expressing amoeboid/phagocytic microglia. Most importantly, BASHY’s presence was also found within demyelinated areas of EAE mice, essentially co-localizing with lesion-associated Iba1+ cells, evidencing BASHY’s potential for the in vivo bioimaging of myelin clearance and myelin-carrying microglia in regions of active demyelination. Full article
(This article belongs to the Special Issue Glia in Neurodegenerative Diseases)
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19 pages, 5787 KiB  
Article
Morpho-Functional Consequences of Swiss Cheese Knockdown in Glia of Drosophila melanogaster
by Elena V. Ryabova, Pavel A. Melentev, Artem E. Komissarov, Nina V. Surina, Ekaterina A. Ivanova, Natalia Matiytsiv, Halyna R. Shcherbata and Svetlana V. Sarantseva
Cells 2021, 10(3), 529; https://doi.org/10.3390/cells10030529 - 2 Mar 2021
Cited by 8 | Viewed by 3218
Abstract
Glia are crucial for the normal development and functioning of the nervous system in many animals. Insects are widely used for studies of glia genetics and physiology. Drosophila melanogaster surface glia (perineurial and subperineurial) form a blood–brain barrier in the central nervous system [...] Read more.
Glia are crucial for the normal development and functioning of the nervous system in many animals. Insects are widely used for studies of glia genetics and physiology. Drosophila melanogaster surface glia (perineurial and subperineurial) form a blood–brain barrier in the central nervous system and blood–nerve barrier in the peripheral nervous system. Under the subperineurial glia layer, in the cortical region of the central nervous system, cortex glia encapsulate neuronal cell bodies, whilst in the peripheral nervous system, wrapping glia ensheath axons of peripheral nerves. Here, we show that the expression of the evolutionarily conserved swiss cheese gene is important in several types of glia. swiss cheese knockdown in subperineurial glia leads to morphological abnormalities of these cells. We found that the number of subperineurial glia nuclei is reduced under swiss cheese knockdown, possibly due to apoptosis. In addition, the downregulation of swiss cheese in wrapping glia causes a loss of its integrity. We reveal transcriptome changes under swiss cheese knockdown in subperineurial glia and in cortex + wrapping glia and show that the downregulation of swiss cheese in these types of glia provokes reactive oxygen species acceleration. These results are accompanied by a decline in animal mobility measured by the negative geotaxis performance assay. Full article
(This article belongs to the Special Issue Glia in Neurodegenerative Diseases)
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Review

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14 pages, 6318 KiB  
Review
TREM2 Mediates Microglial Anti-Inflammatory Activations in Alzheimer’s Disease: Lessons Learned from Transcriptomics
by Feng Xue and Heng Du
Cells 2021, 10(2), 321; https://doi.org/10.3390/cells10020321 - 4 Feb 2021
Cited by 25 | Viewed by 4782
Abstract
Alzheimer’s disease (AD) is a lethal neurodegenerative disorder primarily affecting the aged population. The etiopathogenesis of AD, especially that of the sporadic type, remains elusive. The triggering receptor expressed on myeloid cells 2 (TREM2), a member of TREM immunoglobulin superfamily, plays a critical [...] Read more.
Alzheimer’s disease (AD) is a lethal neurodegenerative disorder primarily affecting the aged population. The etiopathogenesis of AD, especially that of the sporadic type, remains elusive. The triggering receptor expressed on myeloid cells 2 (TREM2), a member of TREM immunoglobulin superfamily, plays a critical role in microglial physiology. Missense mutations in human TREM2 are determined as genetic risk factors associated with the development of sporadic AD. However, the roles of TREM2 in the pathogenesis of AD are still to be established. In this review, we outlined the influence of Trem2 on balance of pro- and anti-inflammatory microglial activations from a perspective of AD mouse model transcriptomics. On this basis, we further speculated the roles of TREM2 in different stages of AD, which may shed light to the development of TREM2-targeted strategy for the prevention and treatment of this neurodegenerative disorder. Full article
(This article belongs to the Special Issue Glia in Neurodegenerative Diseases)
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34 pages, 2902 KiB  
Review
In Vivo TSPO Signal and Neuroinflammation in Alzheimer’s Disease
by Benjamin B. Tournier, Stergios Tsartsalis, Kelly Ceyzériat, Valentina Garibotto and Philippe Millet
Cells 2020, 9(9), 1941; https://doi.org/10.3390/cells9091941 - 21 Aug 2020
Cited by 49 | Viewed by 5769
Abstract
In the last decade, positron emission tomography (PET) and single-photon emission computed tomography (SPECT) in in vivo imaging has attempted to demonstrate the presence of neuroinflammatory reactions by measuring the 18 kDa translocator protein (TSPO) expression in many diseases of the central nervous [...] Read more.
In the last decade, positron emission tomography (PET) and single-photon emission computed tomography (SPECT) in in vivo imaging has attempted to demonstrate the presence of neuroinflammatory reactions by measuring the 18 kDa translocator protein (TSPO) expression in many diseases of the central nervous system. We focus on two pathological conditions for which neuropathological studies have shown the presence of neuroinflammation, which translates in opposite in vivo expression of TSPO. Alzheimer’s disease has been the most widely assessed with more than forty preclinical and clinical studies, showing overall that TSPO is upregulated in this condition, despite differences in the topography of this increase, its time-course and the associated cell types. In the case of schizophrenia, a reduction of TSPO has instead been observed, though the evidence remains scarce and contradictory. This review focuses on the key characteristics of TSPO as a biomarker of neuroinflammation in vivo, namely, on the cellular origin of the variations in its expression, on its possible biological/pathological role and on its variations across disease phases. Full article
(This article belongs to the Special Issue Glia in Neurodegenerative Diseases)
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