Evidence map›Paper›PMID 39198455›Full record

ArticleNPJ Parkinson's disease2024

Exploring causal effects of sarcopenia on risk and progression of Parkinson disease by Mendelian randomization.

Tao Wang, Jiaquan Geng, Xi Zeng, Ruijiang Han, Young Eun Huh, Jiajie Peng

Abstract read
In one paragraph

Article in NPJ Parkinson's disease, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
–field-weighted citation impact
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

13 citing papers in PubMed.

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  6. A survey on deep learning for polygenic risk scores.Briefings in bioinformatics · 2025
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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.

Tao Wang *AI for Science Interdisciplinary Research Center, School of Computer Science, Northwestern Polytechnical University, Xi'an, China.
Jiaquan Geng *AI for Science Interdisciplinary Research Center, School of Computer Science, Northwestern Polytechnical University, Xi'an, China.
Xi ZengAI for Science Interdisciplinary Research Center, School of Computer Science, Northwestern Polytechnical University, Xi'an, China.
Ruijiang HanAI for Science Interdisciplinary Research Center, School of Computer Science, Northwestern Polytechnical University, Xi'an, China.
Young Eun HuhDepartment of Neurology, CHA Bundang Medical Center, CHA University, Seongnam-si, Gyeonggi-do, South Korea. nana1880@hanmail.net.
Jiajie PengAI for Science Interdisciplinary Research Center, School of Computer Science, Northwestern Polytechnical University, Xi'an, China. jiajiepeng@nwpu.edu.cn.ORCID http://orcid.org/0000-0002-3857-7927

Funding

National Natural Science Foundation of China (National Science Foundation of China) 62072376National Research Foundation of Korea (NRF) 2021R1C1C1010753
6 · The paper itself

Abstract

Previous observational studies suggested that sarcopenia is associated with Parkinson disease (PD), but it is unclear whether this association is causal. The objective of this study was to examine causal associations between sarcopenia-related traits and the risk or progression of PD using a Mendelian randomization (MR) approach. Two-sample bidirectional MR analyses were conducted to evaluate causal relationships. Genome-wide association study (GWAS) summary statistics for sarcopenia-related traits, including right handgrip strength (n = 461,089), left handgrip strength (n = 461,026), and appendicular lean mass (n = 450,243), were retrieved from the IEU OpenGWAS database. GWAS data for the risk of PD were derived from the FinnGen database (4235 cases; 373,042 controls). Summary-level data for progression of PD, including progression to Hoehn and Yahr stage 3, progression to dementia, and development of levodopa-induced dyskinesia, were obtained from a recent GWAS publication on progression of PD in 4093 patients from 12 longitudinal cohorts. Significant causal associations identified in MR analysis were verified through a polygenic score (PGS)-based approach and pathway enrichment analysis using genotype data from the Parkinson's Progression Markers Initiative. MR results supported a significant causal influence of right handgrip strength (odds ratio [OR] = 0.152, 95% confidence interval [CI] = 0.055-0.423, adjusted P = 0.0036) and appendicular lean mass (OR = 0.597, 95% CI = 0.440-0.810, adjusted P = 0.0111) on development of levodopa-induced dyskinesia. In Cox proportional hazard analysis, higher PGSs for right handgrip strength (hazard ratio [HR] = 0.225, 95% CI = 0.095-0.530, adjusted P = 0.0019) and left handgrip strength (HR = 0.303, 95% CI = 0.121-0.59, adjusted P = 0.0323) were significantly associated with a lower risk of developing levodopa-induced dyskinesia, after adjusting for covariates. Pathway enrichment analysis revealed that genome-wide significant single-nucleotide polymorphisms for right handgrip strength were substantially enriched in biological pathways involved in the control of synaptic plasticity. This study provides genetic evidence of the protective role of handgrip strength or appendicular lean mass on the development of levodopa-induced dyskinesia in PD. Sarcopenia-related traits can be promising prognostic markers for levodopa-induced dyskinesia and potential therapeutic targets for preventing levodopa-induced dyskinesia in patients with PD.

Identifiers

PMID39198455
PMCPMC11358304

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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.