Evidence map›Paper›PMID 31071102›Full record

ArticlePloS one2019

Clozapine administration enhanced functional recovery after cuprizone demyelination.

Nikki Templeton, Bronwyn Kivell, Amy McCaughey-Chapman, Bronwen Connor, Anne Camille La Flamme

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
3.5field-weighted citation impact, top 7% 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

19 citing papers in PubMed, 32 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. The Role of Microglial Exosomes in Clozapine Treatment: Effect on Cognition in Schizophrenia.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2025
    Review
  6. Article
  7. Article
  8. Article
  9. Remyelination in Multiple Sclerosis: Findings in the Cuprizone Model.International journal of molecular sciences · 2022
    Review
  10. Article
  11. Review
  12. Review
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. 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

5 authors at 3 institutions in 1 country.

Nikki TempletonCentre for Biodiscovery, School of Biological Sciences and School of Chemical and Physical Sciences, Victoria University of Wellington, Wellington, New Zealand.
Bronwyn KivellCentre for Biodiscovery, School of Biological Sciences and School of Chemical and Physical Sciences, Victoria University of Wellington, Wellington, New Zealand.
Amy McCaughey-ChapmanDepartment of Pharmacology and Clinical Pharmacology, Centre for Brain Research, School of Medical Sciences, FMHS, the University of Auckland, Auckland, New Zealand.
Bronwen ConnorDepartment of Pharmacology and Clinical Pharmacology, Centre for Brain Research, School of Medical Sciences, FMHS, the University of Auckland, Auckland, New Zealand.
Anne Camille La FlammeCentre for Biodiscovery, School of Biological Sciences and School of Chemical and Physical Sciences, Victoria University of Wellington, Wellington, New Zealand.ORCID 0000-0002-2344-7281
University of Auckland · NZVictoria University of Wellington · NZMalaghan Institute of Medical Research · NZ

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The atypical antipsychotic agent, clozapine, is used to treat a variety of neurological disorders including schizophrenia and Parkinson's disease and readily crosses the blood brain barrier to interact with a wide range of neuroreceptors including those for dopamine and serotonin. Recent work has shown that clozapine can reduce neuroinflammation in experimental autoimmune encephalomyelitis, a neuroinflammatory model of multiple sclerosis (MS) and mediates its effects in the central nervous system. To further characterise the protection provided by clozapine, the cuprizone model of demyelination was used to assess the effect of clozapine treatment on the cellular events surrounding demyelination and remyelination. Using this model of non-immune demyelination, we found that clozapine administration was unable to prevent demyelination, but when administered post demyelination, was able to enhance the rate of functional recovery. The more rapid improvement of clozapine-treated mice correlated with a decreased level of astrocyte and microglial activation but only modestly enhanced remyelination. Together, these studies highlight the potential of clozapine to support enhanced functional recovery after demyelination, such as that occurring during MS.

Indexed as

AnimalsAstrocytesCentral Nervous SystemClozapineCuprizoneDemyelinating DiseasesDisease Models, AnimalEncephalomyelitis, Autoimmune, ExperimentalFemaleMiceMice, Inbred C57BLMultiple SclerosisMyelin SheathClozapineCuprizone

Identifiers

PMID31071102
PMCPMC6508663
OpenAlexW2944282970

What OpenQuestion 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 OpenQuestion graph.