Evidence map›Paper›PMID 23651603›Full record

ArticleBehavioral and brain functions : BBF2013

P268S in NOD2 associates with susceptibility to Parkinson's disease in Chinese population.

Qilin Ma, Xingkai An, Zhiming Li, Huanjing Zhang, Wenqing Huang, Liangliang Cai, Peng Hu, Qing Lin, Chi-Meng Tzeng

Open access · goldAbstract read
In one paragraph

Article in Behavioral and brain functions : BBF, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing 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

18 citing papers in PubMed, 28 citations in OpenAlex.

  1. Article
  2. Article
  3. Role and molecular mechanism of NOD2 in chronic non-communicable diseases.Journal of molecular medicine (Berlin, Germany) · 2024
    Review
  4. Review
  5. Review
  6. Review
  7. Review
  8. Review
  9. Article
  10. A Comprehensive Analysis of Population Differences inFrontiers in aging neuroscience · 2019
    Article
  11. Article
  12. Article
  13. Functional Variant rs3135500 inFrontiers in aging neuroscience · 2018
    Article
  14. Review
  15. Article
  16. Chronic Inflammation Links Cancer and Parkinson's Disease.Frontiers in aging neuroscience · 2016
    Review
  17. Article
  18. 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

9 authors at 2 institutions in 1 country.

Qilin MaDepartment of Neurology, The First Affiliated Hospital of Xiamen University, Xiamen, Fujian 361003, China.
Xingkai An
Zhiming Li
Huanjing Zhang
Wenqing Huang
Liangliang Cai
Peng Hu
Qing Lin
Chi-Meng Tzeng
Xiamen University · CNFirst Affiliated Hospital of Xiamen University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundThe cause of almost all cases of Parkinson's disease (PD) remains unknown. Recent years have seen an explosion in the rate of discovery of genetic defects linked to PD. Different racial and geographical populations may have different distributions of genetic variants.

methodsIn the current study, we screened the following genetic variants, including some rare mutations and single nucleotide polymorphisms (SNPs), in a pedigree and cases-controls. To best of our knowledge, we first screened these variants known to be associated with neurodegeneration disease, E46K (rs104893875) in SNCA, A1442P in LRRK2, IVS9 in PARK2, A350V in SLC41A1, P268S (rs2066842), R702W (rs2066844), G908R (rs2066845), 1007fs (rs2066847) in NOD2 and G2385R (rs34778348) in LRRK2 from southern China population. Genotyping was performed by jointly using primers overlapping polymerase chain reaction (PCR) site-directed mutagenesis, restriction fragment length polymorphism (RFLP), and capillary electrophoresis (CE).

resultsWe didn't discover above 9 variants in the family members of the pedigree. Furthermore, of 237 patients with sporadic Parkinson's disease and 190 controls, no heterozygosity or homozygosity were found from E46K, A1442P, A350V, R702W, G908R, or 1007fs but heterozygosity onto G2385R, IVS9, and P268S. No significant difference between cases and controls was found in both allele frequency (P = 0.572) and genotype frequency (P = 0.348) of IVS9. However, significant differences in genotype frequency (P = 0.009) of G2385R were consistent with prior observation. Eight patients with Parkinson's disease (2 women and 6 men are over the age of 50 years at onset of PD) carried the P268S heterozygous variation in NOD2. There was no heterozygosity or homozygosity of P268S in the controls. Genotype frequency of P268S (P = 0.0450) had significant differences.

conclusionsOur results suggested that the P268S variant in NOD2 might be a risk factor for susceptibility to sporadic Parkinson's disease in Chinese populations. It also implied that the inflammatory response may play a role in PD.

Indexed as

Genetic Predisposition to DiseasePolymorphism, Single NucleotideAdultAgedAged, 80 and overAllelesAsian PeopleChinaFemaleGene FrequencyGenetic Association StudiesHeterozygoteHomozygoteHumansMaleMiddle AgedNOD2 protein, humanNod2 Signaling Adaptor Protein

Identifiers

PMID23651603
PMCPMC3662627
OpenAlexW2165946584

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Registered trials

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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.