Evidence map›Paper›PMID 26856603›Full record

ArticleAging2016

Primate-specific miR-603 is implicated in the risk and pathogenesis of Alzheimer's disease.

Chi Zhang, Jie Lu, Bing Liu, Qinghua Cui, Yun Wang

Open access · hybridAbstract read
In one paragraph

Article in Aging, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed, 1 pooled it
2.5field-weighted citation impact, top 12% 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

21 citing papers in PubMed, 1 synthesis or guideline pooled it, 38 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. PeerJ · 2025
    Article
  4. Article
  5. Review
  6. Frontiers in neuroscience · 2021
    Article
  7. Article
  8. Review
  9. Review
  10. Review
  11. The RND1 Small GTPase: Main Functions and Emerging Role in Oncogenesis.International journal of molecular sciences · 2019
    Review
  12. Species-Specific miRNAs in Human Brain Development and Disease.Frontiers in cellular neuroscience · 2019
    Article
  13. Review
  14. Article
  15. Article
  16. Review
  17. Primate-specific Long Non-coding RNAs and MicroRNAs.Genomics, proteomics & bioinformatics · 2017
    Review
  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

5 authors at 3 institutions in 1 country.

Chi ZhangNeuroscience Research Institute and Department of Neurobiology, Key Laboratory for Neuroscience of Ministry of Education, National Health and Family Planning Commission, School of Basic Medical Sciences, Peking University Health Science Center, Beijing, 100191, China.
Jie LuNeuroscience Research Institute and Department of Neurobiology, Key Laboratory for Neuroscience of Ministry of Education, National Health and Family Planning Commission, School of Basic Medical Sciences, Peking University Health Science Center, Beijing, 100191, China.
Bing LiuBrainnetome Center, National Laboratory of Pattern Recognition, Institute of Automation, Chinese Academy of Sciences, Beijing, 100190, China.
Qinghua CuiDepartment of Biomedical Informatics, School of Basic Medical Sciences, Peking University Health Science Center, Beijing,100191, China.
Yun WangNeuroscience Research Institute and Department of Neurobiology, Key Laboratory for Neuroscience of Ministry of Education, National Health and Family Planning Commission, School of Basic Medical Sciences, Peking University Health Science Center, Beijing, 100191, China.
Peking University · CNInstitute of Automation · CNNational Health and Family Planning Commission · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Alzheimer's disease (AD) is a serious neurodegenerative disease, and microRNAs (miRNAs) have been linked to its pathogenesis. miR-603, a novel primate-specific miRNA and an intronic miRNA of a human brain highly expressed gene KIAA1217, is implicated in the risk and pathogenesis of AD. The rs11014002 single nucleotide polymorphism (SNP) (C/U), which locates in miR-603 precursor (pre-miR-603), exhibits a protective effect towards AD risk. Additionally, the rs11014002 SNP promotes the biogenesis of mature miR-603. miR-603 downregulates LRPAP1 mRNA and protein levels through directly binding the 3' untranslated region (3'UTR) of LRPAP1. Moreover, miR-603 increases LRP1 protein expression. LRPAP1 and LRP1, playing opposite roles, are involved in Aβ clearance and pathogenesis of AD. Strikingly, miR-603 exhibits a relatively higher expression and there is a loss of a negative correlation between miR-603 and LRPAP1/RND1 mRNA levels in the hippocampi of patients with AD. In addition, miR-603 directly downregulates a key neuronal apoptotic component-E2F1, and prevents HeLa cells from undergoing H2O2-induced apoptosis. This work suggests that miR-603 may be a novel AD-relevant miRNA and that its rs11014002 SNP may serve as a protective factor against AD.

Indexed as

AgedAged, 80 and overAlzheimer DiseaseBlotting, WesternFemaleGenetic Predisposition to DiseaseHumansMaleMicroRNAsPolymorphism, Single NucleotideReverse Transcriptase Polymerase Chain ReactionRisk FactorsTransfectionMicroRNAsMIRN603 microRNA, humanAlzheimer's disease riskbiogenesismiR-603pathogenesissingle nucleotide polymorphism (SNP)

Identifiers

PMID26856603
PMCPMC4789582
OpenAlexW2410685394

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.