Evidence map›Paper›PMID 11509953›Full record

ArticleGene therapy2001

Fibroblast growth factor-II gene therapy reverts the clinical course and the pathological signs of chronic experimental autoimmune encephalomyelitis in C57BL/6 mice.

F Ruffini, R Furlan, P L Poliani, E Brambilla, P C Marconi, A Bergami, G Desina, J C Glorioso, G Comi, G Martino

Abstract read
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In one paragraph

Article in Gene therapy, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.

0numbers the graph read from it
0cells of the map it votes in
38citing papers in PubMed
3.3field-weighted citation impact, top 6% 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

38 citing papers in PubMed, 112 citations in OpenAlex.

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  6. Oligodendrocyte-specific deletion of FGFR2 ameliorates MOGBrain pathology (Zurich, Switzerland) · 2021
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  19. Fibroblast growth factor-2 signaling in neurogenesis and neurodegeneration.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2014
    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

10 authors at 4 institutions in 2 countries.

F RuffiniNeuroimmunology Unit, Department of Neuroscience, DIBIT-San Raffaele Scientific Institute, Milano, Italy.
R Furlan
P L Poliani
E Brambilla
P C Marconi
A Bergami
G Desina
J C Glorioso
G Comi
G Martino
San Raffaele University of Rome · ITCasa Sollievo della Sofferenza · ITUniversity of Ferrara · ITUniversity of Pittsburgh · US

Funding

Telethon A.136
6 · The paper itself

Abstract

The development of therapies aimed to promote remyelination is a major issue in chronic inflammatory demyelinating disorders of the central nervous system (CNS) such as multiple sclerosis (MS), where the permanent neurological impairment is due to the axonal loss resulting from recurrent episodes of immune-mediated demyelination. Here, we show that the intrathecal injection of a herpes simplex virus (HSV) type-1 replication-defective multigene vector, engineered with the human fibroblast growth factor (FGF)-II gene (TH:bFGF vector), was able to significantly revert in C57BL/6 mice the clinicopathological signs of chronic experimental autoimmune encephalomyelitis (EAE), the animal model of MS. The treatment with the TH:bFGF vector was initiated within 1 week after the clinical onset of EAE and was effective throughout the whole follow-up period (ie 60 days). The disease-ameliorating effect in FGF-II-treated mice was associated with: (1) CNS production of FGF-II from vector-infected cells which were exclusively located around the CSF space (ependymal, choroidal and leptomeningeal cells); (2) significant decrease (P < 0.01) of the number of myelinotoxic cells (T cells and macrophages) both in the CNS parenchyma and in the leptomeningeal space; and (3) significant increase (P < 0.01) of the number of oligodendrocyte precursors and of myelin-forming oligodendrocytes in areas of demyelination and axonal loss. Our results indicate that CNS gene therapy using HSV-1-derived vector coding for neurotrophic factors (ie FGF-II) is a safe and non-toxic approach that might represent a potential useful 'alternative' tool for the future treatment of immune-mediated demyelinating diseases.

Indexed as

AnimalsAxonsEncephalomyelitis, Autoimmune, ExperimentalFemaleFibroblast Growth Factor 2Genetic TherapyGenetic VectorsInjections, SpinalLymphocyte CountMacrophagesMiceMice, Inbred C57BLMultiple SclerosisOligodendrogliaSimplexvirusSpinal CordFibroblast Growth Factor 2

Identifiers

PMID11509953
OpenAlexW2332629879

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.