Evidence map›Paper›PMID 25393479›Full record

ArticleCell death & disease2014

Neuritin can normalize neural deficits of Alzheimer's disease.

K An, J H Jung, A Y Jeong, H G Kim, S Y Jung, K Lee, H J Kim, S-J Kim, T-Y Jeong, Y Son and 2 more

Abstract read
In one paragraph

Article in Cell death & disease, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
–field-weighted citation impact
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

24 citing papers in PubMed.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Exome sequencing identifies genes for socioeconomic status in 350,770 individuals.Proceedings of the National Academy of Sciences of the United States of America · 2025
    Article
  6. Article
  7. Review
  8. Article
  9. Article
  10. International journal of molecular sciences · 2022
    Article
  11. Article
  12. Review
  13. Article
  14. Review
  15. Article
  16. Article
  17. Article
  18. Review
  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

12 authors.

K AnDepartment of Life Sciences, Pohang University of Science and Technology (POSTECH), Pohang, Gyungbuk 790-784, Korea.
J H JungDepartment of Life Sciences, Pohang University of Science and Technology (POSTECH), Pohang, Gyungbuk 790-784, Korea.
A Y JeongDepartment of Life Sciences, Pohang University of Science and Technology (POSTECH), Pohang, Gyungbuk 790-784, Korea.
H G KimDepartment of Life Sciences, Pohang University of Science and Technology (POSTECH), Pohang, Gyungbuk 790-784, Korea.
S Y JungDepartment of Life Sciences, Pohang University of Science and Technology (POSTECH), Pohang, Gyungbuk 790-784, Korea.
K LeeDepartment of Pharmacology, College of Medicine, Seoul National University, Seoul 110-799, Korea.
H J KimDepartment of Life Sciences, Pohang University of Science and Technology (POSTECH), Pohang, Gyungbuk 790-784, Korea.ORCID 000000019108151X
S-J KimDepartment of Life Sciences, Pohang University of Science and Technology (POSTECH), Pohang, Gyungbuk 790-784, Korea.
T-Y JeongDepartment of Life Sciences, Pohang University of Science and Technology (POSTECH), Pohang, Gyungbuk 790-784, Korea.
Y SonDepartment of Life Sciences, Pohang University of Science and Technology (POSTECH), Pohang, Gyungbuk 790-784, Korea.
H-S KimDepartment of Pharmacology, College of Medicine, Seoul National University, Seoul 110-799, Korea.
J-H KimDepartment of Life Sciences, Pohang University of Science and Technology (POSTECH), Pohang, Gyungbuk 790-784, Korea.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Reductions in hippocampal neurite complexity and synaptic plasticity are believed to contribute to the progressive impairment in episodic memory and the mild cognitive decline that occur particularly in the early stages of Alzheimer's disease (AD). Despite the functional and therapeutic importance for patients with AD, intervention to rescue or normalize dendritic elaboration and synaptic plasticity is scarcely provided. Here we show that overexpression of neuritin, an activity-dependent protein, promoted neurite outgrowth and maturation of synapses in parallel with enhanced basal synaptic transmission in cultured hippocampal neurons. Importantly, exogenous application of recombinant neuritin fully restored dendritic complexity as well as spine density in hippocampal neurons prepared from Tg2576 mice, whereas it did not affect neurite branching of neurons from their wild-type littermates. We also showed that soluble recombinant neuritin, when chronically infused into the brains of Tg2576 mice, normalized synaptic plasticity in acute hippocampal slices, leading to intact long-term potentiation. By revealing the protective actions of soluble neuritin against AD-related neural defects, we provide a potential therapeutic approach for patients with AD.

Indexed as

Alzheimer DiseaseAnimalsDendritesDisease Models, AnimalGene ExpressionGPI-Linked ProteinsHippocampusHumansLong-Term PotentiationMaleMiceMicrotomyNerve Tissue ProteinsNeuritesNeuronal PlasticityNeuroprotective AgentsGPI-Linked ProteinsNerve Tissue ProteinsNeuroprotective AgentsNrn1 protein, mouseRecombinant Proteins

Identifiers

PMID25393479
PMCPMC4260736

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.