Evidence map›Paper›PMID 29995770›Full record

SynthesisMedicine2018

Low expression of aging-related NRXN3 is associated with Alzheimer disease: A systematic review and meta-analysis.

Jun-Juan Zheng, Wen-Xing Li, Jia-Qian Liu, Yi-Cheng Guo, Qian Wang, Gong-Hua Li, Shao-Xing Dai, Jing-Fei Huang

Open access · goldAbstract readMeta-AnalysisSystematic Review
In one paragraph

Synthesis in Medicine, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed
1.6field-weighted citation impact, top 16% 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

33 citing papers in PubMed, 41 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Article
  5. Review
  6. Tau degradation in Alzheimer's disease: Mechanisms and therapeutic opportunities.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025
    Review
  7. Article
  8. Article
  9. DNA Damage and Parkinson's Disease.International journal of molecular sciences · 2024
    Review
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Review
  16. Article
  17. Article
  18. Article
  19. Review
  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

8 authors at 3 institutions in 1 country.

Jun-Juan ZhengState Key Laboratory of Genetic Resources and Evolution, Kunming Institute of Zoology, Chinese Academy of Sciences Kunming College of Life Science, University of Chinese Academy of Sciences KIZ-SU Joint Laboratory of Animal Models and Drug Development, College of Pharmaceutical Sciences, Soochow University Collaborative Innovation Center for Natural Products and Biological Drugs of Yunnan, Kunming, Yunnan, China.
Wen-Xing Li
Jia-Qian Liu
Yi-Cheng Guo
Qian Wang
Gong-Hua Li
Shao-Xing Dai
Jing-Fei Huang
University of Chinese Academy of Sciences · CNKunming Institute of Zoology · CNChinese Academy of Sciences · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundAlzheimer disease (AD) is a common neurodegenerative disorder with distinct pathological features, with aging considered the greatest risk factor. We explored how aging contributes to increased AD risk, and determined concurrent and coordinate changes (including genetic and phenotypic modifications) commonly exhibited in both normal aging and AD.

methodsUsing the Gene Expression Omnibus (GEO) database, we collected 1 healthy aging-related and 3 AD-related datasets of the hippocampal region. The normal aging dataset was divided into 3 age groups: young (20-40 years old), middle-aged (40-60 years old), and elderly (>60 years old). These datasets were used to analyze the differentially expressed genes (DEGs). The Gene Ontology (GO) terms, pathways, and function network analysis of these DEGs were analyzed.

resultsOne thousand two hundred ninety-one DEGs were found to be shared in the natural aging groups and AD patients. Among the shared DEGs, ATP6V1E1, GNG3, NDUFV2, GOT1, USP14, and NAV2 have been previously found in both normal aging individuals and AD patients. Furthermore, using Java Enrichment of Pathways Extended to Topology (JEPETTO) analysis based on Kyoto Encyclopedia of Genes and Genomes (KEGG) database, we determined that changes in aging-related KEGG annotations may contribute to the aging-dependence of AD risk. Interestingly, NRXN3, the second most commonly deregulated gene identified in the present study, is known to carry a mutation in AD patients. According to functional network analysis, NRXN3 plays a critical role in synaptic functions involved in the cognitive decline associated with normal aging and AD.

conclusionOur results indicate that the low expression of aging-related NRXN3 may increase AD risk, though the potential mechanism requires further clarification.

Indexed as

AdultAgedAgingAlzheimer DiseaseDown-RegulationGene ExpressionHumansMiddle AgedNerve Tissue ProteinsPolymorphism, Single NucleotideRisk FactorsYoung AdultNerve Tissue Proteinsneurexin IIIalpha

Identifiers

PMID29995770
PMCPMC6076205
OpenAlexW2816526540

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.