Evidence map›Paper›PMID 16554462›Full record

ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2006

Oligodendroglial progenitor cell therapy limits central neurological deficits in mice with metachromatic leukodystrophy.

Maria I Givogri, Francesca Galbiati, Stefania Fasano, Stefano Amadio, Laura Perani, Daniela Superchi, Pablo Morana, Ubaldo Del Carro, Sergio Marchesini, Riccardo Brambilla and 2 more

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed
4.8field-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

33 citing papers in PubMed, 66 citations in OpenAlex.

  1. Review
  2. Review
  3. Review
  4. Remyelination in the Central Nervous System.Cold Spring Harbor perspectives in biology · 2024
    Review
  5. Article
  6. Review
  7. Review
  8. [Neuroprotective effects of oligodendrocyte precursor cells on white matter damage in preterm infants].Zhongguo dang dai er ke za zhi = Chinese journal of contemporary pediatrics · 2018
    Review
  9. Article
  10. Progenitor cell-based treatment of glial disease.Progress in brain research · 2017
    Article
  11. Review
  12. Article
  13. Article
  14. Glia Disease and Repair-Remyelination.Cold Spring Harbor perspectives in biology · 2015
    Review
  15. Article
  16. Article
  17. Article
  18. Review
  19. Review
  20. 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

12 authors at 7 institutions in 3 countries.

Maria I GivogriTelethon Institute for Gene Therapy, San Raffaele Scientific Institute, 20132 Milan, Italy. givogri.maria@hsr.it
Francesca Galbiati
Stefania Fasano
Stefano Amadio
Laura Perani
Daniela Superchi
Pablo Morana
Ubaldo Del Carro
Sergio Marchesini
Riccardo Brambilla
Lawrence Wrabetz
Ernesto Bongarzone
Telethon Foundation · ITVita-Salute San Raffaele University · ITGenomics (United Kingdom) · GBInstitute of Cell Biology and Neurobiology · ITSan Raffaele University of Rome · ITThe San Raffaele Telethon Institute for Gene Therapy · ITUniversity of Brescia · IT

Funding

Telethon TGM06S01Telethon TGT03B01
6 · The paper itself

Abstract

This work describes the first successful oligodendrocyte-based cell therapy for presymptomatic arylsulfatase A (ARSA) null neonate mice, a murine model for human metachromatic leukodystrophy (MLD). We found that oligodendrocyte progenitors (OLPs) engrafted and survived into adulthood when transplanted in the neonatal MLD brain. Transplanted cells integrated nondisruptively, did not produce tumors, and survived as proteolipid protein- and MBP-positive postmitotic myelinating oligodendrocytes (OLs) intermingled with endogenous MLD OLs within the adult MLD white matter. Transplanted MLD mice had reduced sulfatide accumulation in the CNS, increased brain ARSA activity, and full prevention of the electrophysiological and motor deficits that characterize untreated MLD mice. Our results provide direct evidence that healthy OLPs can tolerate the neurotoxic accumulation of sulfatides that evolves during the postnatal development of the MLD brain and contribute to OL cell replacement to limit the accumulation of sulfatides and the evolution of CNS defects in this lysosomal storage disease mouse model.

Indexed as

AnimalsAnimals, NewbornBrain Tissue TransplantationCell DifferentiationCell MovementCells, CulturedCerebroside-SulfataseDisease Models, AnimalGraft SurvivalLeukodystrophy, MetachromaticMiceMice, KnockoutMyelin Basic ProteinMyelin Proteolipid ProteinMyelin SheathNerve Fibers, MyelinatedCerebroside-SulfataseMyelin Basic ProteinMyelin Proteolipid ProteinSulfoglycosphingolipids

Identifiers

PMID16554462
PMCPMC6674100
OpenAlexW2132316000

What OpenQuestion holds

Textmetadata
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.