ArticleActa neuropathologica communications2025
Demyelinated lesion associated compartmental inflammation in progressive multiple sclerosis brains.
Article in Acta neuropathologica communications, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
What it found
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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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
5 citing papers in PubMed.
- Reduced Paramagnetic Rim Visibility Signals Lesion Aging and Tissue Degeneration in Progressive Multiple Sclerosis: Impact on Clinical Trials.Neurology(R) neuroimmunology & neuroinflammation · 2026Article
- Treatment Effects on Chronic Active Lesions in Multiple Sclerosis: Current Evidence and Future Perspectives.Neurology and therapy · 2026Review
- Bruton's Tyrosine Kinase Inhibitors in Multiple Sclerosis: Mechanistic Considerations Across Relapsing and Progressive Disease.Molecules (Basel, Switzerland) · 2026Review
- Meningeal and infiltrating T-cells are associated with repetitive head trauma and tau-mediated neurodegeneration in chronic traumatic encephalopathy.Acta neuropathologica communications · 2026Article
- Smoldering neuroinflammation in progressive multiple sclerosis: mechanisms, imaging biomarkers, and therapeutic opportunities.Frontiers in immunology · 2026Review
Corrections and comments
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Authors and funding
6 authors.
Funding
Abstract
The pathogenesis of progressive multiple sclerosis (PMS) involves aggregates of peripheral and innate immune cells that are collectively referred to as compartmental inflammation. Sites include the meninges, perivascular spaces of vessels, choroid plexus, and borders of demyelinated lesions. Iron-laden activated microglia/macrophages that border cerebral white matter (WM) lesions appear as paramagnetic rims (PRLs) on magnetic resonance imaging. PRLs have been associated with lesion expansion and are considered as a target of brain-penetrable therapies in people with MS. Less is known about inflammatory compartments Bordering cortical lesions. The objective of this retrospective study is to describe the location and morphology of MHC Class II-positive cells in 334 demyelinated lesions from 22 PMS brains. Activated microglia bordered Type III subpial lesions (cortical layers I through III demyelinated) and cortical portions of leukocortical lesions. Activated microglia/macrophages lined the border of chronic active WM lesions, WM portions of leukocortical lesions, and Type IV subpial lesions (all six cortical layers demyelinated). Type IV subpial lesions were lined by activated microglia/macrophages that resided in subcortical WM and were always contiguous with Type III subpial lesions. The location in WM or cortex, rather than lesion type, determined the cellular composition of inflammatory compartments. Since the majority of subpial lesions stop at cortical layer IV and Type IV subpial lesions do not invade subcortical WM, compartments bordering subpial lesions are often associated with lesion stability. Iron was enriched in a subpopulation of inflammatory compartments bordering WM and Type IV subpial lesions, as well as at the border of myelinated cortex and subcortical WM. These myelinated borders were not enriched in microglia and iron was diffusely distributed, providing evidence that iron enrichment is not always associated with lesion expansion nor compartmental inflammation. These data will aid in designing imaging outcome measures for clinical trials targeting inflammatory compartments in PMS.
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