Evidence map›Paper›PMID 12777685›Full record

ReviewMolecular neurobiology2003

Brain repair and neuroprotection by serum insulin-like growth factor I.

Eva Carro, Jose Luis Trejo, Angel Núñez, Ignacio Torres-Aleman

Open access · greenAbstract readReview
PubMed Publisher
In one paragraph

Review in Molecular neurobiology, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers.

0numbers the graph read from it
0cells of the map it votes in
43citing papers in PubMed
4.8field-weighted citation impact, top 4% 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

43 citing papers in PubMed, 122 citations in OpenAlex.

  1. Journal of traditional and complementary medicine · 2026
    Article
  2. Article
  3. Review
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  12. Deleting IGF-1 receptor from forebrain neurons confers neuroprotection during stroke and upregulates endocrine somatotropin.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2017
    Article
  13. Insulin-Like Growth Factor-1 and Neuroinflammation.Frontiers in aging neuroscience · 2017
    Review
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. CNS repair requires both effector and regulatory T cells with distinct temporal and spatial profiles.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2014
    Article
  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

4 authors at 3 institutions in 1 country.

Eva CarroLaboratory of Neuroendocrinology, Instituto Cajal, CSIC, Madrid, Universidad Autonoma de Madrid, Spain.
Jose Luis Trejo
Angel Núñez
Ignacio Torres-Aleman
Consejo Superior de Investigaciones Científicas · ESInstituto Cajal · ESUniversidad Autónoma de Madrid · ES

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The existence of protective mechanisms in the adult brain is gradually being recognized as an important aspect of brain function. For many years, self-repair processes in the post-embryonic brain were considered of minor consequence or nonexistent. This notion dominated the study of neurotrophism. Thus, although the possibility that neurotrophic factors participate in brain function in adult life was prudently maintained, the majority of the studies on the role of trophic factors in the brain were focused on developmental aspects. With the recent recognition that the adult brain keeps a capacity for cell renewal, although limited, a new interest in the regenerative properties of brain tissue has emerged. New findings on the role of insulin-like growth factor I (IGF-I), a potent neurotrophic peptide present at high levels in serum, may illustrate this current trend. Circulating IGF-I is an important determinant of proper brain function in the adult. Its pleiotropic effects range from classical trophic actions on neurons such as housekeeping or anti-apoptotic/ pro-survival effects to modulation of brain-barrier permeability, neuronal excitability, or new neuron formation. More recent findings indicate that IGF-I participates in physiologically relevant neuroprotective mechanisms such as those triggered by physical exercise. The increasing number of neurotrophic features displayed by serum IGF-I reinforces the view of a physiological neuroprotective network formed by IGF-I, and possibly other still uncharacterized signals. Future studies with IGF-I, and hopefully other neurotrophic factors, will surely reveal and teach us how to potentiate the self-reparative properties of the adult brain.

Indexed as

AnimalsBrainCell DivisionHumansInsulin-Like Growth Factor INerve DegenerationNerve Growth FactorsNerve RegenerationNeuronsPhysical Conditioning, AnimalInsulin-Like Growth Factor INerve Growth Factors

Identifiers

PMID12777685
OpenAlexW2089302208

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.