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Role of Glia in Human Health and Disease
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Role of Glia in Human Health and Disease

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: 20 September 2025 | Viewed by 608

Special Issue Editors

Dr. Daniele Lana

E-Mail Website
Guest Editor
Department of Health Sciences, University of Florence, 50134 Florence, Italy
Interests: neuropharmacology; neurodegeneration; neuroinflammation; glia; microbiota; neurodegenerative diseases; hippocampus; behaviour
Special Issues, Collections and Topics in MDPI journals
Prof. Dr. Hajime Hirase

E-Mail Website
Guest Editor
Center for Translational Neuromedicine, Faculty of Medical and Health Sciences, University of Copenhagen, 1172 Copenhagen, Denmark
Interests: astrocytic signaling; neural circuit; behavioral performance

Special Issue Information

Dear Colleagues,

The majority of brain cells are glia, and yet, over a century after their discovery, their real functions have still not been fully unraveled. Currently, our understanding of the role of glia in central nervous system (CNS) physiology and in neurodevelopmental, neurodegenerative, and demyelinating pathology is rapidly progressing. Glia, with their multiple functions, maintain the homeostasis of the CNS. Astrocytes are the most numerous and ubiquitous glial cells in the CNS and have many housekeeping functions; they bind the grey matter and enwrap synapses, maintain ion and neurotransmitter homeostasis, and regulate synaptogenesis. Microglia, the primary immune cells of the central nervous system, dynamically and continuously survey brain parenchyma to detect and eliminate debris from damaged neurons via phagocytosis and participate in shaping synaptic connectivity in the developing brain. Oligodendrocytes and Schwann cells myelinate axons, shaping the connectome.

Glia are vital, as their interactions with neurons determine the operation of the brain in health and disease states. These interactions form the basis of networks that show morphological and functional reciprocal reliance and dependency.

Alterations affecting one cell population reverberate and affect the others, favoring or dysregulating their activities. Glial cell phenomic dysfunction, whether in the form of atrophy with loss of function or reactivity, is associated with brain diseases, such as Alzheimer’s disease, Parkinson’s disease, multiple sclerosis, and glioblastoma, as well as autism and psychiatric disorders. Understanding the roles of glia will allow us to assess how their interactions can influence the state and progression of diseases and will be critical in identifying therapeutic strategies.

This Special Issue will comprise an in-depth analysis of how different types of glia participate in the physiological and pathological mechanisms behind CNS function and contribute to the onset or progression of brain diseases. In this regard, investigators are invited to contribute original research articles and reviews to improve our understanding of the role of glia in health and disease.

Dr. Daniele Lana
Prof. Dr. Hajime Hirase
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. 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

  • astrocytes
  • microglia
  • oligodendrocytes
  • Schwann cells
  • neurodegeneration

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Published Papers (2 papers)

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Research

17 pages, 9996 KiB  
Article
Activity of Human-Specific Interlaminar Astrocytes in a Chimeric Mouse Model of Fragile X Syndrome
by Alexandria Anding, Baiyan Ren, Ragunathan Padmashri, Maria Burkovetskaya and Anna Dunaevsky
Int. J. Mol. Sci. 2025, 26(13), 6510; https://doi.org/10.3390/ijms26136510 - 6 Jul 2025
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Abstract
Astrocytes, a subtype of glial cells, have multiple roles in regulating neuronal development and homeostasis. In addition to the typical mammalian astrocytes, in the primate cortex, interlaminar astrocytes are located in the superficial layer and project long processes traversing multiple layers of the [...] Read more.
Astrocytes, a subtype of glial cells, have multiple roles in regulating neuronal development and homeostasis. In addition to the typical mammalian astrocytes, in the primate cortex, interlaminar astrocytes are located in the superficial layer and project long processes traversing multiple layers of the cerebral cortex. Previously, we described a human stem cell based chimeric mouse model where interlaminar astrocytes develop. Here, we utilized this model to study the calcium signaling properties of interlaminar astrocytes. To determine how interlaminar astrocytes could contribute to neurodevelopmental disorders, we generated a chimeric mouse model for Fragile X syndrome (FXS). We report that FXS interlaminar astrocytes exhibit hyperexcitable calcium signaling and are associated with dendritic spines with increased turnover rate. Full article
(This article belongs to the Special Issue Role of Glia in Human Health and Disease)
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21 pages, 6059 KiB  
Article
Chronic Chemogenetic Activation of Astrocytes in the Murine Mesopontine Region Leads to Disturbances in Circadian Activity and Movement
by Baneen Maamrah, Krisztina Pocsai, Bui Minh Hoang, Ali Abdelhadi, Mustafa Qais Al-Khafaji, Andrea Csemer, Cintia Sokvári, Péter Szentesi and Balázs Pál
Int. J. Mol. Sci. 2025, 26(10), 4793; https://doi.org/10.3390/ijms26104793 - 16 May 2025
Viewed by 311
Abstract
We have previously shown that neuromodulatory actions on astrocytes can elicit metabotropic glutamate- and N-methyl-D-aspartate receptor-dependent tonic changes in excitability in the mesopontine region. Although in vitro experiments explored robust effects, the in vivo significance of our findings remained unknown. In this project, [...] Read more.
We have previously shown that neuromodulatory actions on astrocytes can elicit metabotropic glutamate- and N-methyl-D-aspartate receptor-dependent tonic changes in excitability in the mesopontine region. Although in vitro experiments explored robust effects, the in vivo significance of our findings remained unknown. In this project, chronic chemogenetic activation of mesopontine astrocytes and its actions on movement, circadian activity, acoustic startle and spatial memory were tested. The control group of young adult male mice where mesopontine astrocytes expressed only the mCherry fluorescent tag was compared to the group expressing the hM3D(Gq) chemogenetic actuator. Chronic chemogenetic astrocyte activation reduced the amplitude of the acoustic startle reflex and increased the locomotion speed in the resting period. Gait alterations were also demonstrated but no change in the spatial memory was explored. As a potential background of these findings, chronic astrocytic activation decreased the cholinergic neuronal number to 54% and reduced the non-cholinergic neuronal number to 76% of the control. In conclusion, chronic astrocytic activation and the consequential decrease in the neuronal number led to disturbances in movement and circadian activity resembling brainstem-related symptoms of progressive supranuclear palsy, raising the possibility that astrocytic overactivation is involved in the pathogenesis of this disease. Full article
(This article belongs to the Special Issue Role of Glia in Human Health and Disease)
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