Journal Description
Neuroglia
Neuroglia
is an international, peer-reviewed, open access journal on Neuroscience published quarterly online by MDPI.
- Open Access— free for readers, with article processing charges (APC) paid by authors or their institutions.
- High Visibility: indexed within Scopus and other databases.
- Rapid Publication: manuscripts are peer-reviewed and a first decision is provided to authors approximately 21.8 days after submission; acceptance to publication is undertaken in 6.3 days (median values for papers published in this journal in the second half of 2024).
- Recognition of Reviewers: reviewers who provide timely, thorough peer-review reports receive vouchers entitling them to a discount on the APC of their next publication in any MDPI journal, in appreciation of the work done.
- Journal Cluster of Neurosciences: Brain Sciences, Neurology International, NeuroSci, Clinical and Translational Neuroscience, Neuroglia, Psychiatry International, Clocks & Sleep and Journal of Dementia and Alzheimer's Disease.
Latest Articles
The Synergistic Roles of Glial Cells and Non-Coding RNAs in the Pathogenesis of Alzheimer’s Disease and Related Dementias (ADRDs)
Neuroglia 2025, 6(2), 22; https://doi.org/10.3390/neuroglia6020022 - 6 May 2025
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This review synthesizes the emerging understanding of the roles of glial cells and non-coding RNAs (ncRNAs) in the pathogenesis and progression of Alzheimer’s disease and related dementias (ADRDs). ADRDs encompass a spectrum of neurodegenerative disorders characterized by cognitive decline, memory impairment, and functional
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This review synthesizes the emerging understanding of the roles of glial cells and non-coding RNAs (ncRNAs) in the pathogenesis and progression of Alzheimer’s disease and related dementias (ADRDs). ADRDs encompass a spectrum of neurodegenerative disorders characterized by cognitive decline, memory impairment, and functional deterioration. The interplay between the most common types of glial cells—astrocytes, microglia, and oligodendrocytes—and ncRNAs is emerging as a critical factor in the development of ADRDs. Glial cells are essential for maintaining homeostasis within the central nervous system (CNS); however, their dysregulation can lead to neuroinflammation and neuronal dysfunction, exacerbating neurodegeneration. Reactive astrocytes and activated microglia can create neurotoxic environments that further impair neuronal health. Concurrently, ncRNAs, particularly long non-coding RNAs (lncRNAs) and microRNAs (miRNAs), have emerged as significant regulators of glial gene expression, influencing inflammatory responses and glial cell function. Understanding the complex interactions between glial cells and ncRNAs is crucial for developing targeted therapeutic strategies. By elucidating the mechanisms underlying their interactions, this review aims to highlight the critical importance of glial cells and ncRNAs in the context of neurodegenerative diseases, paving the way for innovative approaches to prevent and treat ADRDs. Ultimately, enhancing our understanding of these processes may lead to novel therapies and improved outcomes for individuals affected by these debilitating conditions.
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Open AccessArticle
Investigating Glial Fibrillary Acidic Protein Expression and Cell Morphology in a Rat Brain Following Exposure to a Weak Electromagnetic Field and Nitric Oxide Modulation During Development
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Stephanie M. Sissons, Nirosha J. Murugan and Blake T. Dotta
Neuroglia 2025, 6(2), 21; https://doi.org/10.3390/neuroglia6020021 - 3 May 2025
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Background/Objectives: Nitric oxide (NO) and electromagnetic fields (EMFs) have been reported to influence central nervous system (CNS) function and organization. This study explores the effects of NO modulation and EMF exposure on neurodevelopment and glial fibrillary acidic protein (GFAP) expression and cell morphology,
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Background/Objectives: Nitric oxide (NO) and electromagnetic fields (EMFs) have been reported to influence central nervous system (CNS) function and organization. This study explores the effects of NO modulation and EMF exposure on neurodevelopment and glial fibrillary acidic protein (GFAP) expression and cell morphology, extending the prior work on perinatal EMF exposure in Wistar rats. Methods: Rats were perinatally exposed to water, 1 g/L L-arginine (LA), or 0.5 g/L N-methylarginine (NMA), along with a 7 Hz square-wave EMF at intensities of 0 nT, ≤50 nT, or 500 nT, starting three days before birth and continuing for 14 days postnatally. GFAP expression and cell morphology were analyzed via immunohistochemistry in regions including the hypothalamus, amygdala, hippocampus, and cortex. Results: Significant changes in GFAP morphology and expression are observed. A main EMF effect emerged in the right ventromedial hypothalamus, where the branch length of GFAP-expressing cells increased in EMF-exposed groups compared to the controls [t(32) = −2.52, p = 0.017]. In the hippocampus, LA exposure decreased GFAP expression in the right dentate gyrus compared to water controls [t(23) = 2.37, p = 0.027]. A sex-specific EMF effect was detected in the left CA2 hippocampus, where males exposed to EMF showed significant differences from unexposed males [t(15) = −2.90, p = 0.011]. Conclusions: These findings reveal complex interactions between EMF exposure, sex, and NO modulation, with region-specific effects on GFAP expression in the developing rat brain.
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Open AccessReview
Advancements in Müller Glia Reprogramming: Pioneering Approaches for Retinal Neuron Regeneration
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Yuyan Zhou, Song Qin and Haixiang Wu
Neuroglia 2025, 6(2), 20; https://doi.org/10.3390/neuroglia6020020 - 2 May 2025
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Müller glia exhibit a remarkable regenerative capacity in zebrafish through spontaneous reprogramming post-injury but remain limited in mammals. This review highlights the key mechanisms underlying Müller glia reprogramming, including gene regulatory networks, cytokine signaling, signal transduction pathways, epigenetic modifications, and transcriptional regulation. Cross-species
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Müller glia exhibit a remarkable regenerative capacity in zebrafish through spontaneous reprogramming post-injury but remain limited in mammals. This review highlights the key mechanisms underlying Müller glia reprogramming, including gene regulatory networks, cytokine signaling, signal transduction pathways, epigenetic modifications, and transcriptional regulation. Cross-species analyses have uncovered conserved gene networks that suppress neurogenesis in mammals, while injury-induced transcriptional profiles reveal divergent regenerative strategies. Combinatorial approaches may enhance the reprogramming of mammalian Müller glia into functional neurons. Nevertheless, significant challenges remain, such as variability in the efficacy of direct reprogramming methods and the limited regeneration of cone photoreceptors, even in regenerative species. We conclude that targeting epigenetic barriers and species-specific regulatory pathways offers promising avenues for clinical translation in retinal disorders such as glaucoma and retinitis pigmentosa. Moving forward, research efforts should prioritize the functional integration of regenerated neurons and the development of standardized methodologies to accelerate therapeutic advancements.
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Open AccessArticle
Electroretinographic and Morphological Characterization of the Retina of Annexin A1 Knockout Mice
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Rafael André da Silva, André Maurício Passos Liber, Luiz Philipe de Souza Ferreira, Francisco Manuel Moreno-Carmona, Diego Dias dos Santos, Monielle Sant’Ana, Marcelo Fernandes Costa, Dora Fix Ventura and Cristiane Damas Gil
Neuroglia 2025, 6(2), 19; https://doi.org/10.3390/neuroglia6020019 - 2 May 2025
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Background/Objectives: The annexin A1 (AnxA1) protein has proven important in ocular disease homeostasis and holds great therapeutic promise. However, its role in the context of the healthy retina remains unknown. Therefore, this study used electroretinography (ERG) to investigate the role of endogenous AnxA1
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Background/Objectives: The annexin A1 (AnxA1) protein has proven important in ocular disease homeostasis and holds great therapeutic promise. However, its role in the context of the healthy retina remains unknown. Therefore, this study used electroretinography (ERG) to investigate the role of endogenous AnxA1 in the retinal function of wild-type (WT) and AnxA1 knockout mice (AnxA1−/−). Methods: An extensive repertoire of full-field ERG was applied to AnxA1−/− and WT mice to examine retinal physiology. Morphometric analyses of the retina were conducted. Results: Our results revealed significant differences in the implicit time of a-wave and b-wave between the WT and AnxA1−/− groups under scotopic conditions. The negative and positive amplitude components of mesopic ON responses were higher in the AnxA1-/- group than in the WT group. In contrast, the implicit time of mesopic ON responses were significantly higher in the WT group than in the AnxA1-/- WT group. However, in photopic OFF responses, only the implicit time was significantly longer in the WT group than in the AnxA1−/− group. In the histomorphometric analysis, the retina of AnxA1−/− mice shows increased thickness. Conclusions: The absence of AnxA1 alters retinal morphology and physiology.
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Open AccessReview
Environmental Enrichment as a Possible Adjunct Therapy in Autism Spectrum Disorder: Insights from Animal and Human Studies on the Implications of Glial Cells
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Enrique Hernández-Arteaga, Josué Antonio Camacho-Candia, Roxana Pluma-Romo, María Isabel Solís-Meza, Myriam Nayeli Villafuerte-Vega and Francisco Aguilar-Guevara
Neuroglia 2025, 6(2), 18; https://doi.org/10.3390/neuroglia6020018 - 25 Apr 2025
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Background/Objectives: Autism Spectrum Disorder (ASD) is a complex neurodevelopmental condition influenced by genetic, environmental, and epigenetic factors, leading to cognitive, emotional, and social impairments. Due to the heterogeneity of ASD, conventional therapies often have limited effectiveness, highlighting the need for complementary interventions. Enriched
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Background/Objectives: Autism Spectrum Disorder (ASD) is a complex neurodevelopmental condition influenced by genetic, environmental, and epigenetic factors, leading to cognitive, emotional, and social impairments. Due to the heterogeneity of ASD, conventional therapies often have limited effectiveness, highlighting the need for complementary interventions. Enriched environments (EEs), characterized by enhanced sensory, cognitive, and motor stimulation, have shown promise in alleviating ASD symptoms. This review examines the role of glial cells in mediating the effects of EE. Methods: A literature review was conducted, analyzing studies on EE interventions in animal models and humans, with a focus on glial involvement in neuroplasticity and synaptic remodeling. Results: Evidence from animal models suggests that EE induces significant glial modifications, including increased synaptogenesis and enhanced neuronal connectivity. Studies in rodent models of ASD have demonstrated that EE reduces stereotypical behaviors, improves social interactions, and enhances cognitive function, effects that are closely associated with astrocyte and microglia activity. Similarly, human studies indicate that EE interventions lead to reduced autism symptom severity and improved cognitive outcomes, further supporting the hypothesis that glial cells play a central role in mediating the beneficial effects of EE. Conclusions: This review highlights the potential of EE as a modulator of the brain’s microenvironment, emphasizing the critical role of glial processes in ASD intervention. These findings suggest that future therapeutic strategies for ASD should integrate approaches that specifically target a glial function to optimize intervention outcomes. However, further research is needed to optimize EE protocols and address ASD heterogeneity.
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(This article belongs to the Special Issue The Multifaceted Roles of Glia: From Cellular Functions to Neurological Implications)
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Open AccessReview
Central and Peripheral Immunity Responses in Parkinson’s Disease: An Overview and Update
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Ghaidaa Ebrahim, Hunter Hutchinson, Melanie Gonzalez and Abeer Dagra
Neuroglia 2025, 6(2), 17; https://doi.org/10.3390/neuroglia6020017 - 4 Apr 2025
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Parkinson’s disease (PD) is a progressive neurodegenerative disorder characterized by motor and non-motor symptoms, with increasing evidence supporting the role of immune dysregulation in its pathophysiology. Neuroinflammation, mediated by microglial activation, pro-inflammatory cytokine production, and blood–brain barrier dysfunction, plays a crucial role in
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Parkinson’s disease (PD) is a progressive neurodegenerative disorder characterized by motor and non-motor symptoms, with increasing evidence supporting the role of immune dysregulation in its pathophysiology. Neuroinflammation, mediated by microglial activation, pro-inflammatory cytokine production, and blood–brain barrier dysfunction, plays a crucial role in dopaminergic neuronal degeneration. Furthermore, peripheral immune changes, including T cell infiltration, gut microbiota dysbiosis, and systemic inflammation, contribute to disease progression. The bidirectional interaction between the central and peripheral immune systems suggests that immune-based interventions may hold therapeutic potential. While dopaminergic treatments remain the standard of care, immunomodulatory therapies, monoclonal antibodies targeting α-synuclein, and deep brain stimulation (DBS) have demonstrated immunological effects, though clinical efficacy remains uncertain. Advances in immune phenotyping offer new avenues for personalized treatment approaches, optimizing therapeutic responses by stratifying patients based on inflammatory biomarkers. This review highlights the complexities of immune involvement in PD and discusses emerging strategies targeting immune pathways to develop disease-modifying treatments.
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(This article belongs to the Special Issue The Multifaceted Roles of Glia: From Cellular Functions to Neurological Implications)
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Rosenfeld’s Staining: A Valuable Tool for In Vitro Assessment of Astrocyte and Microglia Morphology
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Alana Alves Farias, Ana Carla dos Santos Costa, Jéssica Teles Souza, Érica Novaes Soares, Cinthia Cristina de Oliveira Santos Costa, Ravena Pereira do Nascimento, Silvia Lima Costa, Victor Diogenes Amaral da Silva and Maria de Fátima Dias Costa
Neuroglia 2025, 6(2), 16; https://doi.org/10.3390/neuroglia6020016 - 3 Apr 2025
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In homeostasis, the glial cells support pivotal functions, such as neuronal differentiation, neuroprotection, nutrition, drug metabolism, and immune response in the central nervous system (CNS). Among these cells, astrocytes and microglia have been highlighted due to their role in the pathogenesis of several
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In homeostasis, the glial cells support pivotal functions, such as neuronal differentiation, neuroprotection, nutrition, drug metabolism, and immune response in the central nervous system (CNS). Among these cells, astrocytes and microglia have been highlighted due to their role in the pathogenesis of several diseases or due to their role in the defense against several insults (ex., chemicals, and pathogens). In Vitro cytological analysis of astrocytes and microglia has contributed to the understanding of the role of morphological changes in glial cells associated with a neuroprotective or neurotoxic phenotype. Currently, the main tools used for the investigation of glial cell morphology in culture are phase contrast microscopy or immunolabeling/fluorescence microscopy. However, generally, phase contrast microscopy does not generate images with high resolution and therefore does not contribute to visualizing a single cell morphology in confluent cell cultures. On the other hand, immunolabeling requires high-cost consumable antibodies, epifluorescence microscope or confocal microscope, and presents critical steps during the procedure. Therefore, identifying a fast, reproducible, low-cost alternative method that allows the evaluation of glial morphology is essential, especially for neuroscientists from low-income countries. This article aims to revise the use of Rosenfeld’s staining, as an alternative low-cost and easy-to-reproduce method to analyze astrocytic and microglial morphology in culture. Additionally, it shows Rosenfeld’s staining as a valuable tool to analyze changes in neural cell morphology in toxicological studies.
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(This article belongs to the Special Issue The Multifaceted Roles of Glia: From Cellular Functions to Neurological Implications)
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Open AccessReview
Beyond the Neuron: The Integrated Role of Glia in Psychiatric Disorders
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André Demambre Bacchi
Neuroglia 2025, 6(2), 15; https://doi.org/10.3390/neuroglia6020015 - 25 Mar 2025
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In recent decades, substantial evidence has highlighted the integral roles of neuroglia, particularly astrocytes, microglia, oligodendrocytes, and ependymal cells, in the regulation of synaptic transmission, metabolic support, and immune mechanisms within the central nervous system. In addition to their structural role, these cells
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In recent decades, substantial evidence has highlighted the integral roles of neuroglia, particularly astrocytes, microglia, oligodendrocytes, and ependymal cells, in the regulation of synaptic transmission, metabolic support, and immune mechanisms within the central nervous system. In addition to their structural role, these cells actively modulate neurotransmitter homeostasis and influence neuronal plasticity, thereby affecting cognition, mood, and behavior. This review discusses how neuroglial alterations contribute to the pathophysiology of five common psychiatric disorders: major depression, bipolar disorder, anxiety disorders, attention-deficit/hyperactivity disorder (ADHD), and schizophrenia. We synthesized preclinical and clinical findings illustrating that glial dysfunction, including impaired myelination and aberrant neuroinflammatory responses, often parallels disease onset and severity. Moreover, we outline how disruptions in astrocytic glutamate uptake, microglia-mediated synaptic pruning, and blood–brain barrier integrity may underlie the neurobiological heterogeneity observed in these disorders. The therapeutic implications range from anti-inflammatory agents to investigational compounds that aim to stabilize glial function or promote remyelination. However, challenges due to interindividual variability, insufficient biomarkers, and the multifactorial nature of psychiatric illnesses remain. Advances in neuroimaging, liquid biopsy, and more precise molecular techniques may facilitate targeted interventions by stratifying patient subgroups with distinct glial phenotypes. Continued research is essential to translate these insights into clinically efficacious and safe treatments.
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(This article belongs to the Special Issue The Multifaceted Roles of Glia: From Cellular Functions to Neurological Implications)
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Open AccessReview
Tryptophan Metabolism Through the Kynurenine Pathway in Glial Cells
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Deivison Silva Argolo, Lucas Matheus Gonçalves de Oliveira, Gilles J. Guillemin, George E. Barreto, Arthur Morgan Butt, Silvia Lima Costa and Maria de Fátima Dias Costa
Neuroglia 2025, 6(1), 14; https://doi.org/10.3390/neuroglia6010014 - 12 Mar 2025
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The central nervous system (CNS) relies on complex and dynamic interactions between neurons and glial cells. Among glial cells, astrocytes regulate the chemical environment surrounding neurons and supply essential nutrients for brain metabolism whereas microglia, the resident macrophages of the CNS, play critical
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The central nervous system (CNS) relies on complex and dynamic interactions between neurons and glial cells. Among glial cells, astrocytes regulate the chemical environment surrounding neurons and supply essential nutrients for brain metabolism whereas microglia, the resident macrophages of the CNS, play critical roles in homeostasis, defense, and responses to injury. Both microglia and astrocytes contribute to the regulation of excitotoxicity and inflammation mediated by the metabolism of tryptophan (Trp) via the kynurenine pathway. Trp metabolism generates several bioactive metabolites, including quinolinic acid (QUIN) and kynurenic acid (KYNA), which have opposing effects. QUIN, produced by activated microglia, acts as an agonist for NMDA receptors; excessive stimulation of these receptors can lead to excitotoxicity and neuronal death. Conversely, KYNA, primarily produced by astrocytes via kynurenine 2,3-aminotransferases (KAT), acts as an NMDA receptor antagonist, conferring neuroprotection by mitigating excitotoxicity. Dysregulation of the Trp metabolism is implicated in many neurodegenerative diseases such as Alzheimer’s disease, Parkinson’s disease, multiple sclerosis and amyotrophic lateral sclerosis, as well as in various neuropsychiatric disorders. This review examines the cellular and molecular mechanisms underlying Trp metabolism in glial cells, highlighting the unique contributions of each glial phenotype, the implications for CNS pathologies, and the potential biomarkers and therapeutic targets for restoring homeostasis and preventing disease progression.
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Open AccessReview
Current Understanding Regarding the Glioma Microenvironment and Impact of the Immune System
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Enes Demir, Deondra Montgomery, Ammar Saloum, Nasser Yaghi and Michael Karsy
Neuroglia 2025, 6(1), 13; https://doi.org/10.3390/neuroglia6010013 - 7 Mar 2025
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High-grade gliomas are aggressive, primary, central nervous system tumors with low survival rates due to recurrence and resistance to current therapy models. Recent studies have highlighted the importance between the interaction of glioma cancer cells and cells of the tumor microenvironment (TME). Cancer
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High-grade gliomas are aggressive, primary, central nervous system tumors with low survival rates due to recurrence and resistance to current therapy models. Recent studies have highlighted the importance between the interaction of glioma cancer cells and cells of the tumor microenvironment (TME). Cancer stem cells and immune cells play a critical role in the TME of gliomas. TMEs in glioma include the perivascular TME, hypoxic TME, and invasive TME, each of which have evolved as our understanding of the involved cellular players has improved. This review discusses the multidimensional aspects of the current targeted therapies and interactions between glioma cells and the TME with specific focus on targeted immunotherapies. Understanding the complexities of the TME and elucidating the various tumor-cell interactions will be critical for facilitating the development of novel precision strategies, ultimately enabling better patient outcomes.
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Open AccessReview
The Potential Roles of Astrocytes and Microglia in the Spinal Cord and Brain After Spinal Cord Injury
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Fernando da Silva Fiorin and Caroline Cunha do Espírito Santo
Neuroglia 2025, 6(1), 12; https://doi.org/10.3390/neuroglia6010012 - 2 Mar 2025
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Background/Objectives: Spinal cord injury (SCI) is a devastating condition that leads to a cascade of cellular and molecular events, resulting in both primary and secondary damage. Among the many cells involved in the post-SCI environment, glial cells in the spinal cord and
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Background/Objectives: Spinal cord injury (SCI) is a devastating condition that leads to a cascade of cellular and molecular events, resulting in both primary and secondary damage. Among the many cells involved in the post-SCI environment, glial cells in the spinal cord and brain are pivotal in determining the trajectory of injury and repair. Methods: While recent SCI studies have shown changes in the genotype of glial cells following injury, exactly how these alterations occur after damage remains unknown. In this sense, the systemic inflammatory molecules could be involved in the connection between the spinal cord and brain, inducing glial activation by different signaling pathways. Preclinical studies have shown that nuclear factor-κB (NF-κB), Janus kinase/signal transducer and activator of transcription (JAK/STAT), and phosphoinositide 3-kinase/Akt (PI3K/Akt) signaling pathways are involved in the change in glial type. Results: These cells, which include astrocytes and microglia, exhibit dynamic responses following spinal injury, contributing to both neuroprotection and neurodegeneration. These different effects indicate that the molecular environment causes changes in the type of astrocytes and microglia, leading to different actions. Conclusions: Understanding the mechanisms of glial cell activation, it is possible to clarify the roles of these glial cells in pathophysiology and their potential repair mechanisms post-injury.
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Open AccessReview
Neuroglial Dysregulation in Autism Spectrum Disorder: Pathogenetic Insights, Genetic Threads, and Therapeutic Horizons
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Nikola Ilic and Adrijan Sarajlija
Neuroglia 2025, 6(1), 11; https://doi.org/10.3390/neuroglia6010011 - 1 Mar 2025
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Background/Objectives: Autism Spectrum Disorder (ASD) is a complex neurodevelopmental condition marked by challenges in social communication, restricted interests, and repetitive behaviors. Recent studies highlight the crucial roles of neuroglial cells—astrocytes, microglia, and oligodendrocytes—in synaptic function, neural connectivity, and neuroinflammation. These findings offer a
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Background/Objectives: Autism Spectrum Disorder (ASD) is a complex neurodevelopmental condition marked by challenges in social communication, restricted interests, and repetitive behaviors. Recent studies highlight the crucial roles of neuroglial cells—astrocytes, microglia, and oligodendrocytes—in synaptic function, neural connectivity, and neuroinflammation. These findings offer a fresh perspective on ASD pathophysiology. This review synthesizes current knowledge on neuroglial dysfunction in ASD, emphasizing its role in pathophysiological mechanisms, genetic influences, and potential therapeutic strategies. Methods: We conducted a comprehensive literature review, integrating insights from neuroscience, molecular biology, and clinical studies. Special focus was given to glial-mediated neuroinflammatory mechanisms, synaptic plasticity regulation, and the impact of genetic mutations on neuroglial signaling and homeostasis. Results: Neuroglial dysfunction in ASD is evident in abnormal synaptic pruning by microglia, impaired astrocytic glutamate regulation, and defective oligodendrocyte-driven myelination, which collectively disrupt neuronal architecture. Emerging therapies targeting these pathways, including anti-inflammatory drugs, microglial modulators, and cell-based approaches, show promise in alleviating key ASD symptoms. Additionally, advanced interventions such as gene editing and glial progenitor therapy present opportunities to correct underlying neuroglial dysfunction. Conclusions: This review establishes a comprehensive framework for understanding neuroglial contributions to ASD. By integrating insights from diverse disciplines, it enhances our understanding of ASD pathophysiology and paves the way for novel therapeutic strategies targeting neuroglial pathways.
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Open AccessReview
The Impact of Neuroglia on Vestibular Disorders: Insights and Implications
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Melissa Castillo-Bustamante, Andrés Felipe Herrón-Arango, María José Bedoya, Juan José Figueroa, Valeria Rees and Alejandro García
Neuroglia 2025, 6(1), 10; https://doi.org/10.3390/neuroglia6010010 - 1 Mar 2025
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Vestibular disorders significantly affect individuals by impairing balance, spatial orientation, and quality of life. Despite the focus on neuronal mechanisms, emerging research emphasizes the importance of neuroglia—astrocytes, microglia, oligodendrocytes, and Schwann cells—in the onset, progression, and resolution of these conditions. This narrative review
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Vestibular disorders significantly affect individuals by impairing balance, spatial orientation, and quality of life. Despite the focus on neuronal mechanisms, emerging research emphasizes the importance of neuroglia—astrocytes, microglia, oligodendrocytes, and Schwann cells—in the onset, progression, and resolution of these conditions. This narrative review explores the roles of neuroglia in vestibular disorders, including vestibular migraines and unilateral and bilateral vestibulopathies. It discusses established facts, challenges, and future perspectives, offering insights into their pathophysiological roles and therapeutic implications, and the limitations of current research. By understanding the interplay between neuroglia and vestibular function, this review aims to advance diagnostic and treatment strategies for these disorders
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Open AccessReview
Nanomedicine: Pioneering Advances in Neural Disease, Stroke and Spinal Cord Injury Treatment
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Borish Loushambam, Sangeeta Yanglem, Venkateswaran Krishnaswami, Munish Kumar and Sivakumar Vijayaraghavalu
Neuroglia 2025, 6(1), 9; https://doi.org/10.3390/neuroglia6010009 - 21 Feb 2025
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Background: Neurological disorders such as Alzheimer’s disease (AD), Parkinson’s disease (PD), stroke, and spinal cord injury (SCI) are significant global health challenges due to their complex pathology and limited therapeutic options. Conventional treatments often fail to efficiently cross the blood–brain barrier (BBB), leading
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Background: Neurological disorders such as Alzheimer’s disease (AD), Parkinson’s disease (PD), stroke, and spinal cord injury (SCI) are significant global health challenges due to their complex pathology and limited therapeutic options. Conventional treatments often fail to efficiently cross the blood–brain barrier (BBB), leading to poor bioavailability and systemic toxicity. This narrative review explores the potential of nanomedicine in addressing these limitations and advancing targeted therapies for neural disorders. Methods: This review examines recent studies on the use of engineered nanoparticles (NPs), including liposomes, dendrimers, micelles, and nanogels, for targeted drug delivery and multifunctional theranostics in neural diseases. It evaluates their role in promoting axon regeneration, reducing neuroinflammation, and repairing neural damage. Additionally, innovative applications in gene therapy and RNA-based treatments, such as CRISPR-Cas9 and RNA interference (RNAi), are discussed. Challenges related to toxicity, scalability, affordability, and regulatory barriers are highlighted, along with potential strategies to address these issues. Results: Nanoparticles have shown significant promise in crossing the BBB, delivering therapeutic agents to neural tissues, and minimizing off-target effects. Emerging applications in gene and RNA-based therapies demonstrate their versatility in addressing disease-specific challenges. However, unresolved issues such as long-term safety, manufacturing scalability, and cost continue to pose challenges. Conclusions: Nanomedicine offers a promising approach to overcoming current limitations in the treatment of neural disorders. This review emphasizes the need for continued interdisciplinary efforts to address translational barriers and highlights the potential for nanomedicine to improve the outcomes and quality of life for patients with neural disorders, stroke, and SCI.
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Open AccessArticle
U87 Glioblastoma Cell-Derived Extracellular Vesicle Mediated Dysregulation of Angiogenic Mediators in Endothelial Cells: An In Silico and In Vitro Analysis
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Swagatama Mukherjee and Prakash P. Pillai
Neuroglia 2025, 6(1), 8; https://doi.org/10.3390/neuroglia6010008 - 10 Feb 2025
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Background: Angiogenesis is a key factor necessary for tissue growth but becomes often dysregulated in cancer, driving tumour progression. Glioblastoma multiforme (GBM) induces abnormal vascular remodelling via Hypoxia-activated VEGF, FGF and PDGF. Despite increased vascularization, hypoxia persists, worsening malignancy. Additionally, emerging evidence highlights
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Background: Angiogenesis is a key factor necessary for tissue growth but becomes often dysregulated in cancer, driving tumour progression. Glioblastoma multiforme (GBM) induces abnormal vascular remodelling via Hypoxia-activated VEGF, FGF and PDGF. Despite increased vascularization, hypoxia persists, worsening malignancy. Additionally, emerging evidence highlights extracellular vesicles (EVs) as key mediators of angiogenesis as conduits transferring bioactive cargo modulating cellular signaling. By promoting neovascularization, EVs can facilitate tumour growth, hinder drug delivery, and contribute to therapeutic resistance, making them potential therapeutic targets. Objective: This study explores the role of GBM-derived EVs in promoting aberrant angiogenesis by modulating VEGF and MMP signalling and correlating them with EV biogenesis to better understand tumour vascularisation and therapeutic paucities. Methods: This study investigates the role of GBM-derived EVs in angiogenesis dysregulation, via in silico and in vitro approaches, making use of available databases to study the enrichment profiles of key angiogenic drivers enriched in GBM and EVs followed by validation studies using 2D cell culture of HUVEC and U87MG cells on treatment with EV inhibitor. Results: We observed that GBM-derived EVs can be key collaborators of promoting angiogenesis by upregulating key pro-angiogenic genes (VEGFA, NRP1, MMP9) and EV biogenesis markers (CD9, CD81, TSG101), facilitating endothelial cell migration and vascular remodelling. Functional assays further confirmed that EVs act as vectors for pro-angiogenic signals, while their inhibition with GW4869 significantly reduced angiogenic activity, highlighting their role in tumour vascularization. Conclusions: Targeting EV-mediated angiogenesis presents a promising therapeutic strategy for GBM, warranting further validation in preclinical and clinical models.
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Open AccessArticle
Notch-1 Immunopositivity in Brain Lesions Associated with Pharmacoresistant Epilepsy
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Dimitar Metodiev, Petia Dimova, Margarita Ruseva, Dimitar Parvanov, Rumiana Ganeva, Georgi Stamenov, Sevdalin Nachev, Vesela Ivanova, Rumen Marinov and Krassimir Minkin
Neuroglia 2025, 6(1), 7; https://doi.org/10.3390/neuroglia6010007 - 8 Feb 2025
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Background: The Notch signaling pathway is an important regulator of stem cell activity in various tissues, including the central nervous system. It has been implicated in neurodevelopmental processes, including neuronal differentiation and synaptic plasticity. Research suggests that its expression may be associated with
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Background: The Notch signaling pathway is an important regulator of stem cell activity in various tissues, including the central nervous system. It has been implicated in neurodevelopmental processes, including neuronal differentiation and synaptic plasticity. Research suggests that its expression may be associated with certain epileptogenic lesions, particularly those with neurodevelopmental origin. The aim of this study was to investigate the expression of Notch-1 in brain biopsies from various cases of pharmacoresistant epilepsy. Methods: Here, we used immunohistochemistry staining to retrospectively analyze 128 developmental lesions associated with pharmacoresistant epilepsy, including 13 cases with focal cortical dysplasia (FCD) type I, 39 with FCD type II, 37 with hippocampal sclerosis (HS), 23 with FCD IIIc, 9 with mild malformations of cortical development (MCD), 4 cases with mild malformation of cortical development with oligodendroglial hyperplasia and epilepsy (MOGHE), and 3 with tuberous sclerosis (TS). The tissues were stained for Neurofilament protein, Vimentin, S-100 protein, NeuN, and GFAP, as well as the stem cell marker Notch-1. Tissue that stained positively for Notch-1 was further characterized. Results: A positive Notch-1 reaction was found in all cases of FCD type IIb and TS, where it appeared in balloon cells but not in dysmorphic neurons, and in a single case of meningioangiomatosis (FCD IIIc), where it stained spider-like cells. Notch-1-positive cells showed a stem-like, glio-neuronal precursor immunophenotype. No staining was observed in the remaining cases with FCD type I, type III, HS, mild MCD, and MOGHE. Conclusions: Notch-1 displays a distinct pattern of expression in some epileptogenic lesions, potentially highlighting a stem cell-like origin or neurodevelopmental abnormalities contributing to pharmacoresistant epilepsy; however, it is not a general marker of such lesions. Its differential expression may prove useful in distinguishing between different types of FCD or other cortical malformations, which could assist in both their diagnosis and potentially in the development of more targeted therapeutic approaches. Further studies with different stem cell markers are needed in this direction.
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Open AccessReview
Clinical Management in Multiple Sclerosis
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Ana Victoria Arredondo-Robles, Karen Paola Rodríguez-López and Rodolfo Daniel Ávila-Avilés
Neuroglia 2025, 6(1), 6; https://doi.org/10.3390/neuroglia6010006 - 5 Feb 2025
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This review aims to provide a comprehensive overview of the main types, subtypes, clinical manifestations, and current therapeutic strategies for multiple sclerosis, emphasizing recent advancements and clinical challenges. Multiple Sclerosis (MS) is a demyelinating, chronic, autoimmune, and inflammatory disease that affects the Central
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This review aims to provide a comprehensive overview of the main types, subtypes, clinical manifestations, and current therapeutic strategies for multiple sclerosis, emphasizing recent advancements and clinical challenges. Multiple Sclerosis (MS) is a demyelinating, chronic, autoimmune, and inflammatory disease that affects the Central Nervous System (CNS). Its classification has the following subtypes: Relapsing-Remitting (RRMS), Secondary-Progressive (SPMS), and Primary-Progressive (PPMS), including rarer subtypes such as Clinically Isolated Syndrome (CIS), Radiologically Isolated Syndrome (RIS), Balo’s Concentric Sclerosis (BCS), Schilder’s Disease (SD), and Progressive-Relapsing MS (PRMS). This article divides the various treatments for MS into the following three categories: acute relapse management, symptomatic treatments, and Disease-Modifying Treatments (DMTs). The latter represents revolutionary research in MS, since they are the drugs considered as the best treatment alternatives for this disease.
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Open AccessReview
The Antiglioma Potential of Plant Lectins: Molecular Targets, Mechanisms, and Future Directions
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Rodrigo Bainy Leal, Vanir Reis Pinto-Junior, Messias Vital Oliveira, Vinicius Jose Silva Osterne, Nicole Sartori, Ana Carolina dos Santos, Ricardo Castilho Garcez, Kyria Santiago Nascimento and Benildo Sousa Cavada
Neuroglia 2025, 6(1), 5; https://doi.org/10.3390/neuroglia6010005 - 2 Feb 2025
Cited by 1
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Gliomas, ranging from low-grade pilocytic astrocytomas to highly malignant glioblastomas, are primary brain tumors that originate from neural or glial stem cells. Classified by the WHO into grades 1 to 4, these tumors exhibit varying prognoses, with oligodendrogliomas and astrocytomas having better and
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Gliomas, ranging from low-grade pilocytic astrocytomas to highly malignant glioblastomas, are primary brain tumors that originate from neural or glial stem cells. Classified by the WHO into grades 1 to 4, these tumors exhibit varying prognoses, with oligodendrogliomas and astrocytomas having better and intermediate outcomes, respectively, while glioblastomas are associated with a poor prognosis. Despite advancements in molecular and genetic research that have improved diagnosis and the development of targeted therapies, treating high-grade gliomas remains a significant challenge due to their diffuse nature. In this context, lectins, carbohydrate-binding proteins, have shown promise as diagnostic and therapeutic agents for cancer, including gliomas. Plant lectins, particularly those from legumes, exhibit significant antiproliferative effects on glioma cells. These effects include decreased cell viability and migration, alongside the induction of autophagy and apoptosis, suggesting their potential as therapeutic agents. Although the mechanisms underlying these effects are not yet fully understood, molecular targets and pathways involved in the antiglioma activity of lectins have been identified. Key targets include matrix metalloproteinases (MMPs), epidermal growth factor receptor (EGFR), CD98 (xc- system), AMPA receptor, and CD73. This review focuses on the antiglioma potential of legume lectins, their applications, and the main molecular targets based on their functions, structures, and associated molecular mechanisms.
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Open AccessReview
Glial Perturbation in Metal Neurotoxicity: Implications for Brain Disorders
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Olayemi K. Ijomone, Ileje I. Ukwubile, Vivian O. Aneke, Tobiloba S. Olajide, Happiness O. Inyang, Omolabake I. Omotosho, Toheeb O. Oyerinde, Victor E. Anadu, Tolulope J. Gbayisomore, Oritoke M. Okeowo, David A. Oyeniran, Olumide A. T. Ogundahunsi and Omamuyovwi M. Ijomone
Neuroglia 2025, 6(1), 4; https://doi.org/10.3390/neuroglia6010004 - 6 Jan 2025
Cited by 3
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Overexposure of humans to heavy metals and essential metals poses a significant risk for the development of neurological and neurodevelopmental disorders. The mechanisms through which these metals exert their effects include the generation of reactive oxygen species, mitochondrial dysfunction, activation of inflammatory pathways,
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Overexposure of humans to heavy metals and essential metals poses a significant risk for the development of neurological and neurodevelopmental disorders. The mechanisms through which these metals exert their effects include the generation of reactive oxygen species, mitochondrial dysfunction, activation of inflammatory pathways, and disruption of cellular signaling. The function of glial cells in brain development and in the maintenance of homeostasis cannot be overlooked. The glial cells are particularly susceptible to metal-induced neurotoxicity. Accumulation of metals in the brain promotes microglial activation, triggering inflammatory responses that can coincide with other mechanisms of neurotoxicity, inducing alteration in synaptic transmission, cognitive deficit, and neuronal damage. In this review, we highlighted the role of glial dysfunction in some selected neurodegenerative diseases and neurodevelopmental disorders. We further dive into how exposure to metals such as nickel, manganese, methyl mercury, cadmium, iron, arsenic, and lead affect the functions of the microglia, astrocytes, and oligodendrocytes and the mechanisms through which they exert the effects on the brain in relation to some selected neurodegenerative diseases and neurodevelopmental disorders. Potential therapeutic interventions such as the use of new and improved chelating agents and antioxidant therapies might be a significant approach to alleviating these metal-induced glial perturbations.
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Open AccessArticle
Brain-Homing Peptide Expression on the Membrane Enhances the Delivery of Exosomes to Neural Cells and Tissue
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Jonhoi Smith, Melvin Field and Kiminobu Sugaya
Neuroglia 2025, 6(1), 3; https://doi.org/10.3390/neuroglia6010003 - 4 Jan 2025
Cited by 1
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Background/Objectives: Glioblastoma (GBM), a highly aggressive grade IV astrocytoma, poses a major therapeutic challenge due to the resistance of cancer stem cells (CSCs) existing within its cell population to the conventional therapies. Recently, we reported that RNA interference targeting CSC protection mechanism significantly
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Background/Objectives: Glioblastoma (GBM), a highly aggressive grade IV astrocytoma, poses a major therapeutic challenge due to the resistance of cancer stem cells (CSCs) existing within its cell population to the conventional therapies. Recently, we reported that RNA interference targeting CSC protection mechanism significantly improved therapeutic efficacy. However, challenges remain, including limited transfection efficiency in neural cells and the difficulty of crossing the blood–brain barrier (BBB). Methods: In this study, we investigated the potential of exosome-mediated delivery of therapeutic cargo to GBM cells by engineering the exosomes to carry green fluorescent protein (GFP) and expressing brain-homing peptide (BHP) on their surface, which has high affinity to the neural cells. Results: We found that BHP-modified exosomes doubled GFP delivery efficacy from 20% to 40%, outperforming traditional transfection methods like lipofection in vitro. In vivo, BHP-modified exosomes demonstrated an ability to cross the BBB and targeted cargo delivery to brain regions following intranasal and subcutaneous administration. Conclusions: These results underscore the potential of engineered exosomes for efficient cargo delivery to enhance therapeutic efficacy against brain tumors and suggest novel avenues for delivering biomolecules to the brain in the treatment of neurological disorders.
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