Evidence map›Paper›PMID 42168222›Full record

ArticleNPJ Parkinson's disease2026

Genome-wide association and population-tailored polygenic risk for Parkinson's disease in Taiwan.

Yung-Tsai Chu, Yu-An Su, Chin-Hsien Lin, Chun-Hwei Tai, Yih-Ru Wu, Chien-Tai Hong, Yu-Wei Chen, Mong-Hsun Tsai, John Hardy, Kin-Ying Mok and 3 more

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In one paragraph

Article in NPJ Parkinson's disease, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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0citing papers in PubMed
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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

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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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

13 authors.

Yung-Tsai ChuCenter of Parkinson's Disease and Movement Disorders, Department of Neurology, National Taiwan University Hospital, Taipei, Taiwan.ORCID http://orcid.org/0000-0001-5817-460X
Yu-An SuNational Taiwan University College of Medicine Graduate Institute of Clinical Medicine, Taipei, Taiwan.
Chin-Hsien LinCenter of Parkinson's Disease and Movement Disorders, Department of Neurology, National Taiwan University Hospital, Taipei, Taiwan.
Chun-Hwei TaiCenter of Parkinson's Disease and Movement Disorders, Department of Neurology, National Taiwan University Hospital, Taipei, Taiwan.
Yih-Ru WuDepartment of Neurology, Linkou Chang Gung Memorial Hospital, Taoyuan, Taiwan.
Chien-Tai HongTaipei Medical University-Shuang Ho Hospital, Ministry of Health and Welfare, New Taipei, Taiwan.
Yu-Wei ChenCenter of Parkinson's Disease and Movement Disorders, Department of Neurology, National Taiwan University Hospital, Taipei, Taiwan.
Mong-Hsun TsaiGenome and Systems Biology Degree Program, Academia Sinica and National Taiwan University, Taipei, Taiwan.
John HardyDepartment of Neurodegenerative Disease, Queen Square Institute of Neurology, UCL, London, UK.
Kin-Ying MokDivision of Life Science, The Hong Kong University of Science and Technology, Hong Kong Special Administrative Region, Hong Kong, China. mok@ust.hk.ORCID http://orcid.org/0000-0003-3145-880X
Ruey-Meei WuCenter of Parkinson's Disease and Movement Disorders, Department of Neurology, National Taiwan University Hospital, Taipei, Taiwan. robinwu@ntu.edu.tw.ORCID http://orcid.org/0000-0002-4947-5467
East Asian Parkinson Disease Genomics Consortium
Global Parkinson’s Genetics Program

Funding

Michael J. Fox Foundation for Parkinson's Research 17474
6 · The paper itself

Abstract

Genetic risk factors for Parkinson's disease (PD) remain under-characterized in East Asian populations. We assembled a Taiwanese case-control cohort (2245 PD; 2147 controls), genotyped participants using the Illumina NeuroBooster Array, and imputed 7.6 million variants with the Taiwan Biobank reference panel. Logistic-regression GWAS identified genome-wide significant associations at SNCA and MCCC1, with the lead SNCA signal located in intron 4; conditional and joint analyses suggested an additional 5' SNCA component. We observed suggestive associations at GCH1, PPARGC1A, and GALNT13. Locus-focused haplotype analyses refined the SNCA signal, delineating an East Asian-enriched risk haplotype, and confirmed risk effects of LRRK2 p.G2385R and p.R1628P, including evidence consistent with a gene-dosage effect. A European-derived PRS showed modest discrimination in our cohort (AUC 0.59), while incorporating East Asian and Taiwan-relevant variants improved performance (AUC 0.62). Together, these results define the genetic architecture of PD in Taiwan, highlight shared and population-enriched risk components, and support ancestry-aware PRS construction for improved risk stratification.

Identifiers

PMID42168222
PMCPMC13470500

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