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Neuroglia
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Neuroglia at the Crossroads: Emerging Insights into Neurological Disease Mechanisms
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Neuroglia at the Crossroads: Emerging Insights into Neurological Disease Mechanisms

A special issue of Neuroglia (ISSN 2571-6980).

Deadline for manuscript submissions: 30 June 2026 | Viewed by 2025

Special Issue Editor

Dr. Ruoli Chen

E-Mail Website
Guest Editor
School of Pharmacy and Bioengineering, Keele University, Keele ST5 5BJ, UK
Interests: hypoxia inducible factors; stroke; neuroprotection; blood brain barrier; vascular dementia; neuroinflammation; cerebrospinal fluid
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Glial cells, once regarded as passive support cells in the nervous system, are now recognized as dynamic regulators of brain homeostasis, immunity, synaptic plasticity, and neurovascular integrity. Recent discoveries have highlighted their central role in the pathophysiology of a wide range of neurological diseases, from neurodevelopmental disorders and epilepsy to neurodegeneration, stroke, and neuroinflammation. This Special Issue, “Neuroglia at the Crossroads: Emerging Insights into Neurological Disease Mechanisms”,  aims to capture the rapidly evolving landscape of glial research and provide a curated collection of cutting-edge studies that explore how astrocytes, microglia, oligodendrocytes, and other glial subtypes contribute to disease onset, progression, and potential recovery.

We invite contributions that dissect glial signaling pathways, glia–neuron and glia–vascular interactions, and metabolic and immune functions of glia, as well as studies leveraging omics, imaging, and novel in vitro/in vivo models. Of particular interest are investigations revealing context-dependent glial plasticity, cell-type-specific vulnerabilities, or the therapeutic potential of glia-targeted interventions. Both original research and in-depth reviews will be considered.

By bringing together interdisciplinary insights, “Neuroglia at the Crossroads” will serve as a vital reference point for researchers and clinicians alike—illuminating how decoding glial biology may hold the key to solving some of the most challenging problems in neuroscience today.

Dr. Ruoli Chen
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. Neuroglia is an international peer-reviewed open access quarterly 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 1000 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

  • neuroglia
  • astrocytes
  • microglia
  • oligodendrocytes
  • neuroinflammation
  • glia–neuron interactions
  • neurodegeneration
  • blood–brain barrier
  • glial plasticity

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Published Papers (2 papers)

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20 pages, 1691 KB  
Article
Insights into Parkinson’s Disease Pathology Focusing on Glial Response and Apoptosis in a Classic Rat Model of Dopaminergic Degeneration
by Marco Aurelio M. Freire, Gabriel S. Rocha, Nelson Alessandretti M. Lemos, Rafael R. Lima, Stanley Bittar, Lissandra B. Jenkins, Daniel Falcao, Harry W. M. Steinbusch and Jose Ronaldo Santos
Neuroglia 2025, 6(3), 36; https://doi.org/10.3390/neuroglia6030036 - 18 Sep 2025
Viewed by 745
Abstract
Background/Objectives: Parkinson’s disease (PD) is the second-most prevalent neurodegenerative disorder, characterized by the progressive loss of dopaminergic neurons in the Substantia Nigra pars compacta (SNpc). Experimental models that replicate core features of PD are critical to investigate underlying mechanisms and therapeutic strategies. [...] Read more.
Background/Objectives: Parkinson’s disease (PD) is the second-most prevalent neurodegenerative disorder, characterized by the progressive loss of dopaminergic neurons in the Substantia Nigra pars compacta (SNpc). Experimental models that replicate core features of PD are critical to investigate underlying mechanisms and therapeutic strategies. Here we evaluated the effects of an acute unilateral intrastriatal lesion induced by 6-hydroxydopamine (6-OHDA) on neuronal loss and the associated inflammatory response. Methods: Adult male Wistar rats received an injection of 6-OHDA into the right striatum, while the contralateral side received vehicle. Motor behavior was assessed by cylinder and open field tests on post-lesion days (PLDs) 7 and 14. Brains were analyzed by immunohistochemistry for tyrosine hydroxylase (TH), glial response (GFAP and Iba1), and caspase-3 at PLD +14. Results: A marked reduction in TH-immunoreactivity in the lesioned striatum was observed, with ~40% loss of TH-positive neurons in the ipsilateral SNpc. Surviving neurons displayed a 28% increase in soma size compared to the contralateral side. The lesion was accompanied by robust astrocytic and microglial activation at the injection site, as well as enhanced GFAP immunoreactivity in the ipsilateral SN pars reticulata. Apoptotic profiles emerged in the SNpc at PLD +14. Functionally, these alterations were reflected in significant motor asymmetry and decreased locomotor activity. Conclusions: Our findings demonstrate that neuroinflammation accompanies early dopaminergic degeneration following intrastriatal 6-OHDA administration, contributing to motor deficits. Future studies with older animals and broader behavioral and anatomical assessments—including regions such as the ventral tegmental area and motivational or anxiety-related paradigms—may enhance translational relevance. Full article
(This article belongs to the Special Issue Neuroglia at the Crossroads: Emerging Insights into Neurological Disease Mechanisms)
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Review

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20 pages, 2709 KB  
Review
Pro- and Anti-Inflammatory Neuropeptides and Glia: The Balance Between Neuroprotection and Neuroinflammation
by Eli J. Futran-Sheinberg, Victoria Urbina, Sofia Nava, Daniel Sanchez, Gilberto Guzmán-Valdivia and Mario A. Zetter
Neuroglia 2025, 6(3), 35; https://doi.org/10.3390/neuroglia6030035 - 10 Sep 2025
Viewed by 974
Abstract
Neuropeptides (NPs) are small molecular messengers synthesized in large dense core vesicles (LDCVs) and secreted to the extracellular space. In the central nervous system (CNS), NPs are secreted to the synaptic space, playing crucial roles in modulating neurons, astrocytes, microglia, oligodendrocytes, and other [...] Read more.
Neuropeptides (NPs) are small molecular messengers synthesized in large dense core vesicles (LDCVs) and secreted to the extracellular space. In the central nervous system (CNS), NPs are secreted to the synaptic space, playing crucial roles in modulating neurons, astrocytes, microglia, oligodendrocytes, and other glial cells, through G-protein-coupled receptors, thereby influencing complex multicellular responses. During neuroinflammation, NPs regulate glial and neuronal reactions to inflammatory signals, promoting resolution and preventing chronic, non-resolving inflammation. For example, NPs inhibit apoptosis in neurons and oligodendrocytes while inducing anti-inflammatory effects in microglia and astrocytes, modulating cytokine secretion. Here, we present the notion that neuropeptides could participate in neuroinflammatory progression, altering glial responses, leading to excessive, non-resolutive inflammation when dysregulated. NP signaling—whether excessive or deficient—can disrupt specific cellular processes, leading to pathological inflammation, gliosis, and functional loss—hallmarks of neurodegenerative diseases. Despite their significance, the precise mechanisms underlying NP-mediated effects remain incompletely understood. This review synthesizes experimental and translational evidence highlighting the pivotal role of NPs in resolving neuroinflammation and explores how targeting NPs or their receptors could offer novel therapeutic strategies for neurodegenerative disorders. Further research is needed to elucidate the specific signaling pathways and receptor dynamics involved, which could pave the way for innovative treatments that address the root causes of these debilitating conditions. Full article
(This article belongs to the Special Issue Neuroglia at the Crossroads: Emerging Insights into Neurological Disease Mechanisms)
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