Evidence map›Paper›PMID 35683020›Full record

ReviewInternational journal of molecular sciences2022

The Primary Microglial Leukodystrophies: A Review.

Isidro Ferrer

Open access · goldAbstract readReview
In one paragraph

Review in International journal of molecular sciences, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
3.9field-weighted citation impact, top 5% 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

14 citing papers in PubMed, 39 citations in OpenAlex.

  1. Neurodegenerative Diseases in Children: A Comprehensive Review.International journal of molecular sciences · 2026
    Review
  2. Article
  3. Review
  4. Review
  5. Article
  6. Review
  7. Article
  8. Hematopoietic stem cell gene therapy to halt neurodegeneration.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2024
    Review
  9. Article
  10. Review
  11. Article
  12. Article
  13. Review
  14. 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

1 author at 1 institution in 1 country.

Isidro FerrerNetwork Centre of Biomedical Research of Neurodegenerative Diseases (CIBERNED), Department of Pathology and Experimental Therapeutics, Bellvitge Biomedical Research Institute (IDIBELL), University of Barcelona, 08907 Barcelona, L'Hospitalet de Llobregat, Spain.ORCID 0000-0001-9888-8754
Bellvitge University Hospital · ES

Funding

La Caixa Foundation LCF/PR/HR19/52160007.
6 · The paper itself

Abstract

Primary microglial leukodystrophy or leukoencephalopathy are disorders in which a genetic defect linked to microglia causes cerebral white matter damage. Pigmented orthochromatic leukodystrophy, adult-onset orthochromatic leukodystrophy associated with pigmented macrophages, hereditary diffuse leukoencephalopathy with (axonal) spheroids, and adult-onset leukoencephalopathy with axonal spheroids and pigmented glia (ALSP) are different terms apparently used to designate the same disease. However, ALSP linked to dominantly inherited mutations in

Indexed as

Demyelinating DiseasesLeukoencephalopathiesSubacute Sclerosing PanencephalitisAdultHumansLipodystrophyMicrogliaOsteochondrodysplasiasAARSadult-onset (or dominant) leukodystrophy with axonal spheroids and pigmented gliaadult-onset orthochromatic leukodystrophy associated with pigmented macrophagesCRPCSFR1hereditary diffuse leukoencephalopathy with axonal spheroidsLKENPNasu–Hakola diseasepigmented orthochromatic leukodystrophypolycystic membranous lipomembranous osteodysplasia with sclerosing leukoencephalopathyTREM2TYROBP

Identifiers

PMID35683020
PMCPMC9181167
OpenAlexW4281673314

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.