Evidence map›Paper›PMID 17955199›Full record

ReviewMolecular neurobiology2007

Neurogenesis and neuroprotection in the CNS--fundamental elements in the effect of Glatiramer acetate on treatment of autoimmune neurological disorders.

Ruth Arnon, Rina Aharoni

Abstract readReview
PubMed Publisher
In one paragraph

Review in Molecular neurobiology, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
1.4field-weighted citation impact, top 21% 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

16 citing papers in PubMed, 41 citations in OpenAlex.

  1. Review
  2. Review
  3. Review
  4. Review
  5. A Comprehensive Review on CopemylNeurology and therapy · 2017
    Review
  6. Article
  7. Review
  8. Article
  9. Review
  10. Review
  11. Glatiramer acetate protects against inflammatory synaptopathy in experimental autoimmune encephalomyelitis.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2013
    Article
  12. Medulloblastoma and gliomatosis cerebri: rare brain tumors in multiple sclerosis patients.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2011
    Article
  13. Article
  14. Review
  15. Promoting oligodendrogenesis and myelin repair using the multiple sclerosis medication glatiramer acetate.Proceedings of the National Academy of Sciences of the United States of America · 2009
    Article
  16. 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

2 authors at 1 institution in 1 country.

Ruth ArnonThe Department of Immunology, The Weizmann Institute of Science, Rehovot, Israel. ruth.arnon@weizmann.ac.il
Rina Aharoni
Weizmann Institute of Science · IL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Multiple sclerosis (MS) is no longer considered to be simply an autoimmune disease. In addition to inflammation and demyelination, axonal injury and neuronal loss underlie the accumulation of disability and the disease progression. Specific treatment strategies should thus aim to act within the central nervous system (CNS) by interfering with both neuroinflammation and neurodegeneration. Specific treatment strategies to autoimmune neurological disorders should aim to act within the CNS by interfering with both neuroinflammation and neurodegeneration. The cumulative effect of Glatiramer acetate (GA; Copaxone(R), Copolymer 1), an approved drug for the treatment of MS, reviewed herewith, draws a direct linkage between anti-inflammatory immunomodulation, neuroprotection, neurogenesis, and therapeutic activity in the CNS. GA treatment augmented the three processes characteristic of neurogenesis, namely, neuronal progenitor cell proliferation, migration, and differentiation. The newborn neurons manifested massive migration through exciting and dormant migratory pathways, into injury sites in brain regions, which do not normally undergo neurogenesis, and differentiated to mature neuronal phenotype, thus, counteracting the neurodegenerative course of disease. The plausible mechanism underlying this multifactorial effect is the induction of GA-reactive T cells in the periphery and their infiltration into the CNS, where they release immunomodulatory cytokines and neurotrophic factors in the injury site.

Indexed as

Adjuvants, ImmunologicAnimalsAutoimmune DiseasesBrainCentral Nervous SystemGlatiramer AcetateHumansImmunosuppressive AgentsInflammationNerve DegenerationNervous System DiseasesPeptidesAdjuvants, ImmunologicGlatiramer AcetateImmunosuppressive AgentsPeptides

Identifiers

PMID17955199
OpenAlexW2025360270

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.