Evidence map›Paper›PMID 11245675›Full record

ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2001

Insulin-like growth factor I (IGF-I) protects cells from apoptosis by Alzheimer's V642I mutant amyloid precursor protein through IGF-I receptor in an IGF-binding protein-sensitive manner.

T Niikura, Y Hashimoto, T Okamoto, Y Abe, T Yasukawa, M Kawasumi, T Hiraki, Y Kita, K Terashita, K Kouyama and 1 more

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed, 1 pooled it
5.9field-weighted citation impact, top 3% 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

23 citing papers in PubMed, 1 synthesis or guideline pooled it, 76 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Review
  4. Article
  5. Review
  6. Article
  7. Article
  8. Dysregulation of IGF-1/GLP-1 signaling in the progression of ALS: potential target activators and influences on neurological dysfunctions.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2021
    Review
  9. Article
  10. Humanin: Functional Interfaces with IGF-I.Growth hormone & IGF research : official journal of the Growth Hormone Research Society and the International IGF Research Society · 2016
    Review
  11. Article
  12. Observational
  13. Article
  14. Article
  15. Cardiovascular dementia - a different perspective.The open biochemistry journal · 2010
    Article
  16. Choroid plexus megalin is involved in neuroprotection by serum insulin-like growth factor I.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2005
    Article
  17. Humanin: after the discovery.Molecular neurobiology · 2004
    Review
  18. Article
  19. Article
  20. 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

11 authors at 2 institutions in 1 country.

T NiikuraDepartment of Pharmacology and Neurosciences, Keio University School of Medicine, Shinanomachi, Shinjuku-ku, Tokyo 160-8582, Japan.
Y Hashimoto
T Okamoto
Y Abe
T Yasukawa
M Kawasumi
T Hiraki
Y Kita
K Terashita
K Kouyama
I Nishimoto
Keio University Hospital · JPRIKEN Center for Brain Science · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

It has been found that insulin-like growth factor I (IGF-I) exerts cytoprotection against Abeta amyloid-induced neuronal cell death. Deposits of Abeta amyloid are one of the pathological hallmarks of Alzheimer's disease (AD). Here, we examined whether IGF-I exerts protective activity against cell death induced by a familial AD (FAD)-linked mutant of amyloid precursor protein (APP), and we found that IGF-I protected cells from toxicity of FAD-associated V642I mutant of APP in multiple cell systems. IGFBP-3 blocked this action of IGF-I, but not of des(1-3)IGF-I, which was as active as IGF-I in the presence of IGFBP-3. The data also demonstrated that the IGF-I receptor (IGF-IR) mediates the protective activity of IGF-I. The antagonizing function of the IGF-I/IGF-IR system against V642I-APP, which is further antagonized by IGFBP-3, provides a molecular clue to the understanding of AD pathophysiology and to the establishment of potential therapy for AD.

Indexed as

Amino Acid SubstitutionAmyloid beta-Protein PrecursorAnimalsAntibodiesApoptosisCell LineDose-Response Relationship, DrugHumansInsulin-Like Growth Factor Binding Protein 3Insulin-Like Growth Factor IMiceMutagenesis, Site-DirectedPeptide FragmentsProtein BindingReceptor, IGF Type 1Reverse Transcriptase Polymerase Chain ReactionAmyloid beta-Protein PrecursorAntibodiesinsulin-like growth factor 1, des-(1-3)-Insulin-Like Growth Factor Binding Protein 3Insulin-Like Growth Factor IPeptide FragmentsReceptor, IGF Type 1RNA, Messenger

Identifiers

PMID11245675
PMCPMC6762606
OpenAlexW1576182962

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.