prikaz prve stranice dokumenta Glial Cells in Spinal Muscular Atrophy: Speculations on Non-Cell-Autonomous Mechanisms and Therapeutic Implications
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Scientific paper - Review paper
Glial Cells in Spinal Muscular Atrophy: Speculations on Non-Cell-Autonomous Mechanisms and Therapeutic Implications
Neurology International, 17 (2025), 3; 41. https://doi.org/10.3390/neurolint17030041
Belančić, Andrej; Janković, Tamara; Gkrinia, Elvira Meni Maria; Kristić, Iva; Rajič Bumber, Jelena; Rački, Valentino; Pilipović, Kristina; Vitezić, Dinko; Mršić-Pelčić, Jasenka

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Belančić, A., Janković, T., Gkrinia, E. M. M., Kristić, I., Rajič Bumber, J., Rački, V. ... Mršić Pelčić, J. (2025). Glial Cells in Spinal Muscular Atrophy: Speculations on Non-Cell-Autonomous Mechanisms and Therapeutic Implications. Neurology International, 17. (3). doi: 10.3390/neurolint17030041

Belančić, Andrej, et al. "Glial Cells in Spinal Muscular Atrophy: Speculations on Non-Cell-Autonomous Mechanisms and Therapeutic Implications." Neurology International, vol. 17, no. 3, 2025. https://doi.org/10.3390/neurolint17030041

Belančić, Andrej, Tamara Janković, Elvira Meni Maria Gkrinia, Iva Kristić, Jelena Rajič Bumber, Valentino Rački, Kristina Pilipović, Dinko Vitezić and Jasenka Mršić Pelčić. "Glial Cells in Spinal Muscular Atrophy: Speculations on Non-Cell-Autonomous Mechanisms and Therapeutic Implications." Neurology International 17, no. 3 (2025). https://doi.org/10.3390/neurolint17030041

Belančić, A., et al. (2025) 'Glial Cells in Spinal Muscular Atrophy: Speculations on Non-Cell-Autonomous Mechanisms and Therapeutic Implications', Neurology International, 17(3). doi: 10.3390/neurolint17030041

Belančić A, Janković T, Gkrinia EMM, Kristić I, Rajič Bumber J, Rački V, and sur.. Glial Cells in Spinal Muscular Atrophy: Speculations on Non-Cell-Autonomous Mechanisms and Therapeutic Implications. Neurology International [Internet]. 2025 March 13 [cited 2025 March 19];17(3). doi: 10.3390/neurolint17030041

A. Belančić, et al., "Glial Cells in Spinal Muscular Atrophy: Speculations on Non-Cell-Autonomous Mechanisms and Therapeutic Implications", Neurology International, vol. 17, no. 3, March 2025. [Online]. Available at: https://urn.nsk.hr/urn:nbn:hr:184:230961. [Accessed: 19 March 2025]

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Metadata
Title (english)Glial Cells in Spinal Muscular Atrophy: Speculations on Non-Cell-Autonomous Mechanisms and Therapeutic Implications
AuthorAndrej Belančić
AuthorTamara Janković
AuthorElvira Meni Maria Gkrinia
AuthorIva Kristić
AuthorJelena Rajič Bumber
AuthorValentino Rački
AuthorKristina Pilipović
AuthorDinko Vitezić
AuthorJasenka Mršić-Pelčić
Author's institutionUniversity of Rijeka
Faculty of Medicine
(Department of Pharmacology)
Author's institutionUniversity of Rijeka
Faculty of Medicine
(Department of Neurology)
Scientific / art field,
discipline and subdiscipline		BIOMEDICINE AND HEALTHCARE
Clinical Medical Sciences
Neurology
Abstract (english)
Spinal muscular atrophy (SMA) is a neuromuscular disorder caused by homozygous deletions or mutations in the SMN1 gene, leading to progressive motor neuron degeneration. While SMA has been classically viewed as a motor neuron-autonomous disease, increasing evidence indicates a significant role of glial cells—astrocytes, microglia, oligodendrocytes, and Schwann cells—in the disease pathophysiology. Astrocytic dysfunction contributes to motor neuron vulnerability through impaired calcium homeostasis, disrupted synaptic integrity, and neurotrophic factor deficits. Microglia, through reactive gliosis and complement-mediated synaptic stripping, exacerbate neurodegeneration and neuroinflammation. Oligodendrocytes exhibit impaired differentiation and metabolic support, while Schwann cells display abnormalities in myelination, extracellular matrix composition, and neuromuscular junction maintenance, further compromising motor function. Dysregulation of pathways such as NF-κB, Notch, and JAK/STAT, alongside the upregulation of complement proteins and microRNAs, reinforces the non-cell-autonomous nature of SMA. Despite the advances in SMN-restorative therapies, they do not fully mitigate glial dysfunction. Targeting glial pathology, including modulation of reactive astrogliosis, microglial polarization, and myelination deficits, represents a critical avenue for therapeutic intervention. This review comprehensively examines the multifaceted roles of glial cells in SMA and highlights emerging glia-targeted strategies to enhance treatment efficacy and improve patient outcomes.
Keywords (english)
Languageenglish
Publication typeScientific paper - Review paper
Publication statusPublished
Peer reviewPeer review - international
Publication versionPublished version
Journal titleNeurology International
Numberingvol. 17, no. 3, 41
e-ISSN2035-8377
DOIhttps://doi.org/10.3390/neurolint17030041
URN:NBNurn:nbn:hr:184:230961
Publication2025-03-13
Document URLhttps://www.mdpi.com/2035-8377/17/3/41
Type of resourceText
Access conditionsOpen access
Terms of useLicence Attribution 4.0 International (CC BY 4.0) icon
Created on2025-03-14 08:11:24