ArticleActa neuropathologica communications2023
Pathological ultrastructural alterations of myelinated axons in normal appearing white matter in progressive multiple sclerosis.
Article in Acta neuropathologica communications, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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21 citing papers in PubMed, 28 citations in OpenAlex.
- Glucocorticoid receptors in oligodendrocyte precursor cells regulate hippocampal network plasticity and stress-induced behavior in mice.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- The hypoxia-inflammation cycle as a key mechanism of smoldering inflammation and progression in multiple sclerosis.Acta neuropathologica · 2026Review
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- Label-free tracking of subcortical white matter degradationBiomedical optics express · 2026Article
- The Associations Between Chronic Active Lesions and White Matter Disease: A 7 Tesla Imaging Study.Annals of clinical and translational neurology · 2025Article
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- Accelerating myelin defect detection in neurodegenerative disorders: a human-in-the-loop deep learning approach with birefringence microscopy.Neurophotonics · 2025Article
- Ultrastructural membrane dynamics of mouse and human cortical synapses.bioRxiv : the preprint server for biology · 2025Article
- Sterol imbalances and cholesterol-24-hydroxylase dysregulation is linked to the underlying progression of multiple sclerosis.Brain pathology (Zurich, Switzerland) · 2025Article
- A focus on the normal-appearing white and gray matter within the multiple sclerosis brain: a link to smoldering progression.Acta neuropathologica · 2025Review
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- Multiple sclerosis: what have we learned and can we still learn from electron microscopy.Cellular and molecular life sciences : CMLS · 2025Review
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- Evaluating ultrastructural preservation quality in banked brain tissue.Free neuropathology · 2025Article
- Understanding the MyelinASN neuro · 2025Article
- Preservation of cellular structure via immersion fixation in brain banking.Free neuropathology · 2025Article
- Dynamic imaging of myelin pathology in physiologically preserved human brain tissue using third harmonic generation microscopy.PloS one · 2025Article
- Article
- Trem2-deficiency aggravates and accelerates age-related myelin degeneration.Acta neuropathologica communications · 2024Article
- Pilot Study of the Total and Phosphorylated Tau Proteins in Early-Stage Multiple Sclerosis.Medicina (Kaunas, Lithuania) · 2024Article
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Multiple sclerosis (MS) pathophysiology includes inflammation, demyelination and neurodegeneration, but the exact mechanisms of disease initiation and progression are unknown. A major feature of lesions is lack of myelin, which increases axonal energy demand and requires adaptation in number and size of mitochondria. Outside lesions, subtle and diffuse alterations are observed in normal appearing white matter (NAWM) and normal appearing grey matter (NAGM), including increased oxidative stress, reduced axon density and changes in myelin composition and morphology. On an ultrastructural level, only limited data is available on alterations in myelinated axons. We generated large scale 2D scanning transmission electron microscopy images ('nanotomy') of non-demyelinated brain tissue of control and progressive MS donors, accessible via an open-access online repository. We observed a reduced density of myelinated axons in NAWM, without a decrease in cross-sectional axon area. Small myelinated axons were less frequently and large myelinated axons were more frequently present in NAWM, while the g-ratio was similar. The correlation between axonal mitochondrial radius and g-ratio was lost in NAWM, but not in NAGM. Myelinated axons in control GM and NAGM had a similar g-ratio and radius distribution. We hypothesize that axonal loss in NAWM is likely compensated by swelling of the remaining myelinated axons and subsequent adjustment of myelin thickness to maintain their g-ratio. Failure of axonal mitochondria to adjust their size and fine-tuning of myelin thickness may render NAWM axons and their myelin more susceptible to injury.
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