Evidence map›Paper›PMID 41661329›Full record

ArticleActa neuropathologica2026

Characteristic patterns of complement deposition in NMOSD, MOGAD, and MS.

Yoshiki Takai, Simon Hametner, Christian Riedl, Tatsuro Misu, Toshiyuki Takahashi, Hiroyoshi Suzuki, Norio Chihara, Masashi Watanabe, Hiroaki Miyahara, Mari Yoshida and 12 more

Abstract read
In one paragraph

Article in Acta neuropathologica, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

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.

2 · The registry

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.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

1 citing paper in PubMed.

  1. Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

22 authors.

Yoshiki Takai *Department of Neurology, Tohoku University Graduate School of Medicine, Sendai, Miyagi, Japan. yoshiki.takai.e6@tohoku.ac.jp.
Simon Hametner *Division of Neuropathology and Neurochemistry, Department of Neurology and Comprehensive Center for Clinical Neurosciences and Mental Health, Medical University of Vienna, Vienna, Austria.
Christian RiedlDivision of Neuropathology and Neurochemistry, Department of Neurology and Comprehensive Center for Clinical Neurosciences and Mental Health, Medical University of Vienna, Vienna, Austria.
Tatsuro MisuDepartment of Neurology, Tohoku University Graduate School of Medicine, Sendai, Miyagi, Japan.
Toshiyuki TakahashiDepartment of Neurology, Tohoku University Graduate School of Medicine, Sendai, Miyagi, Japan.
Hiroyoshi SuzukiDepartment of Pathology, South Miyagi Medical Center, Shibata, Miyagi, Japan.
Norio ChiharaDivision of Neurology, Kobe University Graduate School of Medicine, Kobe, Hyogo, Japan.
Masashi WatanabeDepartment of Neurology, Ehime Prefectural Central Hospital, Matsuyama, Ehime, Japan.
Hiroaki MiyaharaDepartment of Neuropathology, Institute for Medical Science of Aging, Aichi Medical University, Nagakute, Aichi, Japan.
Mari YoshidaDepartment of Neuropathology, Institute for Medical Science of Aging, Aichi Medical University, Nagakute, Aichi, Japan.
Yasushi IwasakiDepartment of Neuropathology, Institute for Medical Science of Aging, Aichi Medical University, Nagakute, Aichi, Japan.
Takashi SuzukiDepartment of Pathology, Tohoku University Hospital, Sendai, Miyagi, Japan.
Franziska Di PauliDepartment of Neurology, Medical University of Innsbruck, Innsbruck, Austria.
Stephan BramowDepartment of Neurology, Danish Multiple Sclerosis Center, Copenhagen University Hospital, Rigshospitalet, Glostrup, Denmark.
Guy LaureysDepartment of Neurology, University Hospital Ghent, Ghent, Belgium.
Brenda BanwellDepartment of Pediatrics, Johns Hopkins University, Baltimore, MD, USA.
Sara MariottoNeurology Unit, Department of Neuroscience, Biomedicine and Movement Sciences, University of Verona, Verona, Italy.
Kazuo FujiharaDepartment of Neurology, Tohoku University Graduate School of Medicine, Sendai, Miyagi, Japan.
Masashi AokiDepartment of Neurology, Tohoku University Graduate School of Medicine, Sendai, Miyagi, Japan.
Monika BradlDivision of Neuroimmunology, Center for Brain Research, Medical University of Vienna, Vienna, Austria.
Hans LassmannDivision of Neuroimmunology, Center for Brain Research, Medical University of Vienna, Vienna, Austria.
Romana HöftbergerDivision of Neuropathology and Neurochemistry, Department of Neurology and Comprehensive Center for Clinical Neurosciences and Mental Health, Medical University of Vienna, Vienna, Austria.

Funding

Deep Gray Matter Iron and Disease Progression in Multiple SclerosisR01NS114227 · NINDS · STATE UNIVERSITY OF NEW YORK AT BUFFALO · PI SCHWESER, FERDINAND · 2021 to 2024
$1.5M
Austrian Science Fund 10.55776/PAT6054424Ministry of Education, Culture, Sports, Science and Technology (MEXT), the Grants-in-Aid for Scientific Research from the Ministry of Health, Labour and Welfare of Japan #23K06959Ministry of Education, Culture, Sports, Science and Technology (MEXT), the Grants-in-Aid for Scientific Research from the Ministry of Health, Labour and Welfare of Japan #24K10634National Institute of Neurological Disorders and Stroke of the National Institutes of Health R01NS114227NINDS NIH HHS R01 NS114227
6 · The paper itself

Abstract

The complement system is involved in the pathogenesis of inflammatory demyelinating diseases (IDDs) of the CNS. While complement inhibition significantly reduces the relapse rate in neuromyelitis optica spectrum disorders (NMOSDs), no clear consensus has been reached regarding the role of complement in myelin oligodendrocyte glycoprotein antibody-associated disease (MOGAD) and multiple sclerosis (MS). Therefore, we examined CNS tissues from patients with NMOSD (18 autopsies and one biopsy, median age: 56 years), MOGAD (seven autopsies and 20 biopsies, median age: 34 years) and MS (24 autopsies, median age: 54.5 years) to assess the involvement of the complement system from a histopathological perspective. To investigate complement activity at multiple steps, the tissue deposition of three different complement components (C4d, C3d, and C9neo) was examined using immunohistochemistry. In NMOSD, the typical perivascular rosette/rim pattern of complement deposition was confirmed by the three different complement products within acute astrocyte-lytic lesions. In MOGAD, we observed C4d deposition around perivenous demyelinating lesions in 83% (20/24 tissues). However, C9neo deposition differed between patients, with 73% (11/15 patients with perivenous demyelination-predominant MOGAD) showing limited deposition of C9neo with relatively well-preserved oligodendrocytes (MOGAD type A), while 27% showing strong deposition accompanied by the disappearance of oligodendrocytes (MOGAD type B). The more destructive type B pathology was more frequent among deceased than living patients who, by contrast, had type A pathology in the vast majority. In MS, only C4d showed clear deposits on myelin sheaths in the peri-plaque white matter bordering the edges of the demyelinating lesions. These findings seemed to be characteristic of MS, and the extent and intensity tended to decrease in accordance with lesion activity. Complement deposition in MS lesions was linked to shorter interval between onset and death. These characteristic patterns of complement deposition in the three IDDs likely reflect the distinct pathogeneses of the diseases.

Indexed as

BrainComplement System ProteinsMultiple SclerosisMyelin Oligodendrocyte Glycoprotein Antibody-Associated DiseaseNeuromyelitis OpticaAdultAgedComplement C3dComplement C4bComplement C9FemaleHumansMaleMiddle AgedMyelin-Oligodendrocyte GlycoproteinPeptide FragmentsComplement C3dComplement C4bcomplement C4dComplement C9Complement System ProteinsMyelin-Oligodendrocyte GlycoproteinPeptide FragmentsC4dC9neoComplementMOGADMSNMOSD

Identifiers

PMID41661329
PMCPMC12886220

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.