ReviewAdvances in neurobiology2025
Neuroglial Pathophysiology of Leukodystrophies.
Review in Advances in neurobiology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
1 citing paper in PubMed.
- Oligodendrocytes Are Active Participants in the Pathogenesis of Multiple Sclerosis and Its Animal Models.International journal of molecular sciences · 2026Review
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4 authors.
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Abstract
Leukodystrophies are a diverse group of inherited diseases characterised by white matter degenerative pathology. Leukodystrophies have a highly heterogeneous genetic background linked mainly to mutations in oligodendrocyte and astrocyte genes and, to lesser extent, microglia. The most prevalent leukodystrophies are caused by mutations in oligodendrocyte genes that encode the essential myelin proteins PLP1 and GalC in Pelizaeus-Merzbacher disease and Krabbe disease, respectively. Astrocyte leukodystrophies are led by Alexander disease, caused by mutations in the astrocyte gene GFAP. Vanishing white matter disease, the most prevalent inherited white matter pathology in children, is associated with astrocyte atrophy and cystic degeneration of the cerebral white matter. The pathogenic mechanisms in leukodystrophies depend on the genetic mutations and hence are extremely varied, but the diseases have in common white matter atrophy caused by the loss of oligodendrocytes and myelin, with or without marked reactive astrogliosis and microglia activation. The development of a range of animal models with the disruption of specific genes causing leukodystrophies and the use of pluripotent stem cells from people with different forms of leukodystrophy is advancing the understanding of the functional and cellular pathophysiology of these rare diseases.
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