Evidence map›Paper›PMID 24345222›Full record

ReviewBrain pathology (Zurich, Switzerland)2014

The pathology of an autoimmune astrocytopathy: lessons learned from neuromyelitis optica.

Claudia F Lucchinetti, Yong Guo, Bogdan F Gh Popescu, Kazuo Fujihara, Yasuto Itoyama, Tatsuro Misu

Open access · greenAbstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in Brain pathology (Zurich, Switzerland), 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 194 papers, 6 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
194citing papers in PubMed, 6 pooled it
14.9field-weighted citation impact, top 1% of its field
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

194 citing papers in PubMed, 6 syntheses or guidelines pooled it, 401 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. A meta-analysis comparing first-line immunosuppressants in neuromyelitis optica.Annals of clinical and translational neurology · 2021
    Pooled it
  4. Pooled it
  5. Pooled it
  6. Guideline
  7. Trial
  8. Trial
  9. Trial
  10. Review
  11. Review
  12. Article
  13. Article
  14. Review
  15. Article
  16. Observational
  17. Article
  18. Article
  19. Article
  20. Observational

134 more citing papers are in PubMed but not listed here.

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

6 authors at 4 institutions in 3 countries.

Claudia F LucchinettiDepartment of Neurology, Mayo Clinic, Rochester, MN.
Yong Guo
Bogdan F Gh Popescu
Kazuo Fujihara
Yasuto Itoyama
Tatsuro Misu
Mayo Clinic in Arizona · USTohoku University · JPNational Center of Neurology and Psychiatry · JPUniversity of Saskatchewan · CA

Funding

Mechanisms of Multiple Sclerosis Tissue PathologyR01NS049577 · NINDS · MAYO CLINIC ROCHESTER · PI LUCCHINETTI, CLAUDIA F. · 2006 to 2012
$2.3M
NINDS NIH HHS NS49577-R01NINDS NIH HHS R01 NS049577
6 · The paper itself

Abstract

Neuromyelitis optica (NMO) is a disabling autoimmune astrocytopathy characterized by typically severe and recurrent attacks of optic neuritis and longitudinally extensive myelitis. Until recently, NMO was considered an acute aggressive variant of multiple sclerosis (MS), despite the fact that early studies postulated that NMO and MS may be two distinct diseases with a common clinical picture. With the discovery of a highly specific serum autoantibody (NMO-IgG), Lennon and colleagues provided the first unequivocal evidence distinguishing NMO from MS and other central nervous system (CNS) inflammatory demyelinating disorders. The target antigen of NMO-IgG was confirmed to be aquaporin-4 (AQP4), the most abundant water channel protein in the CNS, mainly expressed on astrocytic foot processes at the blood-brain barrier, subpial and subependymal regions. Pathological studies demonstrated that astrocytes were selectively targeted in NMO as evidenced by the extensive loss of immunoreactivities for the astrocytic proteins, AQP4 and glial fibrillary acidic protein (GFAP), as well as perivascular deposition of immunoglobulins and activation of complement even within lesions with a relative preservation of myelin. In support of these pathological findings, GFAP levels in the cerebrospinal fluid (CSF) during acute NMO exacerbations were found to be remarkably elevated in contrast to MS where CSF-GFAP levels did not substantially differ from controls. Additionally, recent experimental studies showed that AQP4 antibody is pathogenic, resulting in selective astrocyte destruction and dysfunction in vitro, ex vivo and in vivo. These findings strongly suggest that NMO is an autoimmune astrocytopathy where damage to astrocytes exceeds both myelin and neuronal damage. This chapter will review recent neuropathological studies that have provided novel insights into the pathogenic mechanisms, cellular targets, as well as the spectrum of tissue damage in NMO.

Indexed as

AnimalsAquaporin 4AstrocytesBlood-Brain BarrierHumansImmunoglobulin GNeuromyelitis OpticaAquaporin 4Immunoglobulin Gaquaporin-4 (AQP4)astrocytopathyneuromyelitis optica (NMO)

Identifiers

PMID24345222
PMCPMC3905574
OpenAlexW2119987649

What OpenQuestion holds

Textmetadata
LicenceTDM
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 OpenQuestion graph.