Evidence map›Paper›PMID 40536593›Full record

ArticleActa neuropathologica2025

Role of CSF flow and meningeal barriers in the development of inflammatory lesions at the CNS-PNS transition zone of cranial nerves in autoimmune demyelinating diseases.

Li Xin, Hideaki Nishihara, Adrian Madarasz, Petr Pleskac, Linh Tran, Daniela C Ivan, Fumitaka Shimizu, Simone Aleandri, Giuseppe Locatelli, Paola Luciani and 1 more

Abstract read
In one paragraph

Article in Acta neuropathologica, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing 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

8 citing papers in PubMed.

  1. Review
  2. Article
  3. Article
  4. The cribriform plate: A dynamic central nervous system-immune hub.The Journal of experimental medicine · 2026
    Review
  5. Article
  6. Article
  7. Article
  8. Article
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

11 authors.

Li XinTheodor Kocher Institute, University of Bern, CH-3012, Bern, Switzerland. li.xin@unibe.ch.
Hideaki NishiharaDepartment of Neurology and Clinical Neuroscience, Yamaguchi University, Yamaguchi, Japan.
Adrian MadaraszTheodor Kocher Institute, University of Bern, CH-3012, Bern, Switzerland.
Petr PleskacTheodor Kocher Institute, University of Bern, CH-3012, Bern, Switzerland.
Linh TranTheodor Kocher Institute, University of Bern, CH-3012, Bern, Switzerland.
Daniela C IvanTheodor Kocher Institute, University of Bern, CH-3012, Bern, Switzerland.
Fumitaka ShimizuDepartment of Neurology and Clinical Neuroscience, Yamaguchi University, Yamaguchi, Japan.
Simone AleandriDepartment of Chemistry, Biochemistry and Pharmaceutical Sciences, University of Bern, Bern, Switzerland.
Giuseppe LocatelliTheodor Kocher Institute, University of Bern, CH-3012, Bern, Switzerland.
Paola LucianiDepartment of Chemistry, Biochemistry and Pharmaceutical Sciences, University of Bern, Bern, Switzerland.
Steven T ProulxTheodor Kocher Institute, University of Bern, CH-3012, Bern, Switzerland. steven.proulx@unibe.ch.

Funding

Japan Society for the Promotion of Science JPJSJRP20221507JST FOREST Program JPMJFR2269Schweizerischer Nationalfonds zur Förderung der Wissenschaftlichen Forschung CRSII5_213535University of Bern 310030_189226
6 · The paper itself

Abstract

Patients with autoimmune inflammatory demyelinating diseases have been shown to present with trigeminal and cochlear nerve lesions restricted at the root transition zone, which contrasts with the relatively extensive distribution of lesions in optic neuritis. To better understand the mechanism underlying the different distribution pattern for cranial nerve lesions in these autoimmune neuroinflammatory diseases, we focused on the CNS-PNS transition zone (TZ) of the trigeminal and cochlear nerves in a MOG-driven active EAE model. These nerves were found to exhibit unique arrangements of anatomical barrier layers including the arachnoid and glia limitans, which affected cerebrospinal fluid (CSF) tracer distribution as well as CCR2

Indexed as

Cerebrospinal FluidCranial NervesEncephalomyelitis, Autoimmune, ExperimentalMeningesAnimalsCentral Nervous SystemFemaleMiceMice, Inbred C57BLCCR2+ cellsCerebrospinal fluid (CSF)CNS–PNS transition zoneCranial nerve lesionsNeuroinflammation

Identifiers

PMID40536593
PMCPMC12178981

What Socratic holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

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 Socratic graph.