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Peer-reviewedCC BYNature communications

Genome-wide cross-trait analysis to compare genetic architecture between Parkinson's disease and kidney-related traits.

  • Le Chang1,2
  • Sadaf Gawhary1,2
  • Lyza Maameri2,3
  • Wiame Belbellaj1,2
  • Frida Lona-Durazo1,2
  • Sarah A Gagliano Taliun4,5,6
6 affiliations
  1. 1Faculty of Medicine, Université de Montréal, Montréal, QC, Canada.
  2. 2Research Centre, Montréal Heart Institute, Montréal, QC, Canada.
  3. 3Faculty of Medicine, Université Laval, Québec, QC, Canada.
  4. 4Research Centre, Montréal Heart Institute, Montréal, QC, Canada. [email protected].
  5. 5Department of Medicine, Faculty of Medicine, Université de Montréal, Montréal, QC, Canada. [email protected].
  6. 6Department of Neurosciences, Faculty of Medicine, Université de Montréal, Montréal, QC, Canada. [email protected].
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Abstract

Epidemiological studies link kidney function to Parkinson's disease risk, but the genetic basis of this relationship remains unclear. Here, we leverage genome-wide association data for Parkinson's disease and five UK Biobank-derived kidney-related traits in individuals of European ancestry, combining genetic correlation, pleiotropy mapping, colocalization and enrichment across sex-combined and sex-stratified analyses. Genome-wide genetic correlations with Parkinson's are modest, with only a significant correlation with urinary potassium-to-creatinine ratio significant, yet we identify shared loci across 9 of 15 trait pairs. Resolving these loci, the two traits are more often driven by different causal variants within a shared region than by the same variant. Four loci carry a shared causal variant, implicating BIN3, MSRA and TNK2 in protein quality control. These findings provide evidence for shared genomic loci between Parkinson's disease and kidney function, offering specific loci and biological pathways for future investigation of the kidney-brain axis in neurodegeneration.

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Cite

BibTeXRIS
BibTeX
@article{chang2026genomewide,
  title = {{Genome-wide cross-trait analysis to compare genetic architecture between Parkinson's disease and kidney-related traits.}},
  author = {Le Chang and Sadaf Gawhary and Lyza Maameri and Wiame Belbellaj and Frida Lona-Durazo and Sarah A Gagliano Taliun},
  journal = {Nature communications},
  year = {2026},
  month = sep,
  doi = {10.1038/s41467-026-77920-3},
  url = {https://europepmc.org/article/MED/42901928},
  note = {CC BY},
}
RIS
TY  - JOUR
TI  - Genome-wide cross-trait analysis to compare genetic architecture between Parkinson's disease and kidney-related traits.
AU  - Le Chang
AU  - Sadaf Gawhary
AU  - Lyza Maameri
AU  - Wiame Belbellaj
AU  - Frida Lona-Durazo
AU  - Sarah A Gagliano Taliun
PY  - 2026
DA  - 2026/09/18
JO  - Nature communications
DO  - 10.1038/s41467-026-77920-3
UR  - https://europepmc.org/article/MED/42901928
AB  - Epidemiological studies link kidney function to Parkinson's disease risk, but the genetic basis of this relationship remains unclear. Here, we leverage genome-wide association data for Parkinson's disease and five UK Biobank-derived kidney-related traits in individuals of European ancestry, combining genetic correlation, pleiotropy mapping, colocalization and enrichment across sex-combined and sex-stratified analyses. Genome-wide genetic correlations with Parkinson's are modest, with only a significant correlation with urinary potassium-to-creatinine ratio significant, yet we identify shared loci across 9 of 15 trait pairs. Resolving these loci, the two traits are more often driven by different causal variants within a shared region than by the same variant. Four loci carry a shared causal variant, implicating BIN3, MSRA and TNK2 in protein quality control. These findings provide evidence for shared genomic loci between Parkinson's disease and kidney function, offering specific loci and biological pathways for future investigation of the kidney-brain axis in neurodegeneration.
SN  - 2041-1723
ER  -