Glial Dynamics in Neurological Disorders: From Molecular Mechanisms to Therapeutic Perspectives

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

Deadline for manuscript submissions: 29 June 2026 | Viewed by 3739

Special Issue Editors


E-Mail Website
Guest Editor
1. Neurophysiology Department, Instituto Nacional de Neurología y Neurocirugía “Manuel Velasco Suárez”, Mexico City 14269, Mexico
2. Psychology Department, Universidad Iberoamericana, Mexico City 01376, Mexico
Interests: glia; astrocytes; microglia; oligodendrocytes; neurodegeneration; neuroinflammation; neurovascular coupling; extracellular matrix; synaptic plasticity; therapeutic targets

E-Mail Website
Guest Editor
Neurophysiology Laboratory, National Institute of Neurology and Neurosurgery MVS, Mexico City 14269, Mexico
Interests: glial biology; cerebellum; epilepsy and neuroinflammation

E-Mail Website
Guest Editor
Departamento de Neurofisiología, Instituto Nacional de Neurología y Neurocirugía, Manuel Velasco Suárez, Ciudad de México 14269, Mexico
Interests: neuroscience research; clinical neuroscience; neuropathology

Special Issue Information

Dear Colleagues,

Glial cells have emerged as central players in the pathophysiology of neurological disorders, challenging the traditional neuron-centric view of brain function and disease. This Special Issue aims to showcase cutting-edge research that illuminates the multifaceted roles of astrocytes, microglia, and oligodendrocytes in neurological conditions ranging from neurodegenerative diseases to neurovascular disorders.

We invite original research articles, comprehensive reviews, and perspectives that address the molecular, cellular, and systems-level contributions of glia to neurological health and disease. Topics of particular interest include:

  • Microglial activation and neuroinflammatory cascades in neurodegenerative diseases (Alzheimer's disease, Huntington's disease, Parkinson's disease);
  • Astrocytic dysfunction in epilepsy, stroke, and neurovascular malformations;
  • Oligodendrocyte biology and myelin dynamics in demyelinating disorders;
  • Glial-neuronal interactions in synaptic plasticity and circuit remodeling;
  • Extracellular matrix remodeling and glial-vascular coupling;
  • Novel therapeutic strategies targeting glial dysfunction;
  • Advanced methodologies for studying glial cells in health and disease.

This Special Issue seeks to foster international collaboration and bring together diverse perspectives from researchers across the Americas, Europe, and beyond. We particularly encourage submissions that integrate molecular mechanisms with translational approaches, offering new insights into how glial biology can inform therapeutic innovation.

By bridging fundamental discoveries with clinical relevance, this collection aims to advance our understanding of glial contributions to neurological disorders and identify novel targets for intervention.

Dr. Héctor Romo-Parra
Dr. Carmen Rubio
Dr. Norma Serrano-García
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 250 words) can be sent to the Editorial Office for assessment.

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 1200 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

  • glia
  • astrocytes
  • microglia
  • oligodendrocytes
  • neurodegeneration
  • neuroinflammation
  • neurovascular coupling
  • extracellular matrix
  • synaptic plasticity
  • therapeutic targets

Benefits of Publishing in a Special Issue

  • Ease of navigation: Grouping papers by topic helps scholars navigate broad scope journals more efficiently.
  • Greater discoverability: Special Issues support the reach and impact of scientific research. Articles in Special Issues are more discoverable and cited more frequently.
  • Expansion of research network: Special Issues facilitate connections among authors, fostering scientific collaborations.
  • External promotion: Articles in Special Issues are often promoted through the journal's social media, increasing their visibility.
  • Reprint: MDPI Books provides the opportunity to republish successful Special Issues in book format, both online and in print.

Further information on MDPI's Special Issue policies can be found here.

Published Papers (2 papers)

Order results
Result details
Select all
Export citation of selected articles as:

Review

16 pages, 1156 KB  
Review
The Glymphatic System in Glioblastoma: Emerging Insights into a Hidden Network in Brain Tumor Dynamics
by Enes Demir, Meriem Boukhiam, Mohammad Rashad, Ammar Saloum, Victor Akinyemi, Deondra Montgomery and Michael Karsy
Neuroglia 2026, 7(2), 11; https://doi.org/10.3390/neuroglia7020011 - 1 Apr 2026
Viewed by 859
Abstract
The discovery of the glymphatic system (GS) transformed understanding of central nervous system homeostasis by revealing a brain-wide network that facilitates cerebrospinal and interstitial fluid exchange along perivascular pathways. This system clears metabolic waste and maintains the precise ionic environment required for neuronal [...] Read more.
The discovery of the glymphatic system (GS) transformed understanding of central nervous system homeostasis by revealing a brain-wide network that facilitates cerebrospinal and interstitial fluid exchange along perivascular pathways. This system clears metabolic waste and maintains the precise ionic environment required for neuronal function through the coordinated action of astrocytic aquaporin-4 channels and intact perivascular architecture. Glioblastoma multiforme (GBM), the most aggressive primary brain tumor in adults, alters physiological barriers through pathological angiogenesis, compression of perivascular spaces, depolarization of aquaporin-4 at astrocytic endfeet, and obstruction of venous and lymphatic drainage. This narrative review synthesizes current experimental and clinical literature identified through targeted searches of PubMed and Scopus to examine interactions between glioblastoma, glymphatic system dysfunction, and tumor microenvironmental changes. To minimize selection bias, studies were categorized according to evidence source and experimental design. Evidence from rodent models and advanced imaging demonstrates as tumor growth impairs glymphatic function, the resulting dysfunction promotes tumor progression by enabling accumulation of pro-tumorigenic growth factors, inflammatory mediators, and acidic metabolites, while elevated interstitial fluid pressure limits drug delivery. Impaired antigen drainage further diminishes immune surveillance, contributing to the immunosuppressive microenvironment that limits immunotherapy efficacy. A critical evaluation of these mechanisms highlights how the glymphatic system influences disease progression and suggests novel avenues for diagnostic imaging and therapeutic intervention. Although significant challenges remain in modeling human fluid dynamics, understanding these hidden networks offers a promising frontier for strategies aimed at restoring cerebral clearance and improving clinical outcomes. Full article
Show Figures

Figure 1

19 pages, 2935 KB  
Review
The Double Face of Microglia in the Brain
by Moisés Rubio-Osornio, Carmen Rubio, Maximiliano Ganado and Héctor Romo-Parra
Neuroglia 2026, 7(1), 3; https://doi.org/10.3390/neuroglia7010003 - 2 Jan 2026
Cited by 1 | Viewed by 2335
Abstract
The microglia, first identified by Pío del Río-Hortega, are resident macrophages in the CNS that aid in immune monitoring, synaptic remodeling, and tissue repair. Microglial biology’s dual functions in maintaining homeostasis and contributing to neurodegeneration are examined in this review, with a focus [...] Read more.
The microglia, first identified by Pío del Río-Hortega, are resident macrophages in the CNS that aid in immune monitoring, synaptic remodeling, and tissue repair. Microglial biology’s dual functions in maintaining homeostasis and contributing to neurodegeneration are examined in this review, with a focus on neurodegenerative disease treatment targets. Methods: We reviewed microglial research using single-cell transcriptomics, molecular genetics, and neuroimmunology to analyze heterogeneity and activation states beyond the M1/M2 paradigm. Results: Microglia maintains homeostasis through phagocytosis, trophic factor production, and synaptic pruning. They acquire activated morphologies in pathological conditions, releasing proinflammatory cytokines and reactive oxygen species via NF-κB, MAPK, and NLRP3 signaling. Single-cell investigations show TREM2 and APOE-expressing disease-associated microglia (DAM) in neurodegenerative lesions. Microglial senescence, mitochondrial failure, and chronic inflammation result from Nrf2/Keap1 redox pathway malfunction in ageing. Microglial interactions with astrocytes via IL-1α, TNF-α, and C1q result in neurotoxic or neuroprotective A2 astrocytes, demonstrating linked glial responses. Microglial inflammatory or reparative responses are influenced by epigenetic and metabolic reprogramming, such as regulation of PGC-1α, SIRT1, and glycolytic flux. Microglia are essential to neuroprotection and neurodegeneration. TREM2 agonists, NLRP3 inhibitors, and epigenetic modulators can treat chronic neuroinflammation and restore CNS homeostasis in neurodegenerative illnesses by targeting microglial signaling pathways. Full article
Show Figures

Figure 1

Back to TopTop