Evidence map›Paper›PMID 29479569›Full record

ArticleeNeurologicalSci2015

Interaction between SNCA, LRRK2 and GAK increases susceptibility to Parkinson's disease in a Chinese population.

Wen-Juan Yu, Lan Cheng, Nan-Nan Li, Ling Wang, Eng-King Tan, Rong Peng

Open access · goldAbstract read
In one paragraph

Article in eNeurologicalSci, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed, 1 pooled it
–field-weighted citation impact, top 96% 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

8 citing papers in PubMed, 1 synthesis or guideline pooled it, 13 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Association betweenFrontiers in genetics · 2025
    Article
  4. LRRK2 and Parkinson's disease: from genetics to targeted therapy.Annals of clinical and translational neurology · 2023
    Review
  5. Article
  6. Association ofFrontiers in genetics · 2021
    Article
  7. Review
  8. 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

6 authors at 2 institutions in 2 countries.

Wen-Juan YuDepartment of Neurology, West China Hospital, Sichuan University, Chengdu, Sichuan Province, PR China.
Lan ChengDepartment of Neurology, West China Hospital, Sichuan University, Chengdu, Sichuan Province, PR China.
Nan-Nan LiDepartment of Neurology, West China Hospital, Sichuan University, Chengdu, Sichuan Province, PR China.
Ling WangDepartment of Neurology, West China Hospital, Sichuan University, Chengdu, Sichuan Province, PR China.
Eng-King TanDuke-NUS Graduate Medical School, Singapore, Singapore.
Rong PengDepartment of Neurology, West China Hospital, Sichuan University, Chengdu, Sichuan Province, PR China.
Sichuan University · CNSingapore General Hospital · SG

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

PD is a complex disease, and may result from gene-gene and gene-environment interactions. There are limited studies on gene-gene interactions in PD. We and others have previously shown that SNCA rs356219, LRRK2 (rs2046932 and rs7304279) and GAK (rs1564282) are risk factors in sporadic PD. Since the expression of SNCA and neurotoxicity of alpha-synuclein are affected by LRRK2 and GAK, we hypothesize that their genetic risk variants may interact with each other. Here we investigated the interaction of SNCA rs356219, LRRK2rs7304279 and rs2046932 and GAK rs1564282 using the Multifactor Dimensionality Reduction (MDR) in a Chinese PD patient-control series (534 patients and 435 controls) and the cumulative risk effect of SNCA, LRRK2 and GAK. The MDR analysis showed a significant gene-gene interaction between the rs356219 of SNCA, rs2046932 of LRRK2 and rs1564282 of GAK. Moreover, individuals with increasing numbers of variants had an increasing likelihood of having PD, compared with those carrying none of the variants. The estimated OR for developing PD in individuals carrying 3 variants was 5.89. We demonstrated for the first time that SNPs in SNCA, LRRK2 and GAK interacted with each other to confer an increased risk of PD. In addition, PD risk increased cumulatively with the increasing number of variants.

Indexed as

GAKGene–gene interactionLRRK2MDRParkinson's diseaseSNCA

Identifiers

PMID29479569
PMCPMC5852682
OpenAlexW1674940342

What OpenQuestion holds

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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.