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Peer-reviewedCC BY 4.0NPJ Parkinson's Disease

Dopamine replacement therapy modulates DDC, prolactin and AOC3 levels in Parkinson’s disease

  • Ludo van Hillegondsberg1,2
  • Shahzad Ahmad2
  • Tanja Zerenner3
  • Michael Lawton3
  • Karolien Groenewald1,2
  • Micah Fletcher2
  • Ayan Ianniello2
  • Yoav Ben-Shlomo3
  • Richard Wade-Martins2,4
  • Paolo Piazza2,5
  • Avigail Taylor2
  • Alexander G. Thompson1,2
1 more authors
  • Michele T. Hu1,2
5 affiliations
  1. 1Nuffield Department of Clinical Neurosciences, University of Oxford, Oxford, UK
  2. 2Oxford-GSK Institute of Molecular and Computational Medicine, University of Oxford, Oxford, UK
  3. 3Population Health Sciences, University of Bristol, Bristol, UK
  4. 4Department of Physiology, Anatomy & Genetics, University of Oxford, Oxford, UK
  5. 5Centre for Human Genetics, University of Oxford, Oxford, UK
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Abstract

Dopa decarboxylase (DDC) is a candidate biomarker in Parkinson’s disease (PD), but its levels are influenced by dopamine replacement therapy (DRT), complicating interpretation. We used high-throughput proteomics to analyze serum and CSF samples from PD patients, individuals with idiopathic REM-sleep behaviour disorder, and controls to assess DRT effects. In serum, DDC increased and prolactin and AOC3 decreased with higher levodopa equivalent daily doses, showing drug class-specific associations. Longitudinally, serum DDC and prolactin levels changed with DRT, while AOC3 remained stable. In CSF, DDC was elevated regardless of treatment, while prolactin was reduced only in treated PD. These results indicate that serum changes in DDC, prolactin, and AOC3 primarily reflect treatment exposure rather than disease biology. Our findings highlight the need to account for medication effects in proteomic studies, identify AOC3 as a novel DRT-sensitive protein, and support the potential of treatment-responsive proteins as pharmacodynamic markers in PD.

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Cite

BibTeXRIS
BibTeX
@article{hillegondsberg2026dopamine,
  title = {{Dopamine replacement therapy modulates DDC, prolactin and AOC3 levels in Parkinson’s disease}},
  author = {Ludo van Hillegondsberg and Shahzad Ahmad and Tanja Zerenner and Michael Lawton and Karolien Groenewald and Micah Fletcher and Ayan Ianniello and Yoav Ben-Shlomo and Richard Wade-Martins and Paolo Piazza and Avigail Taylor and Alexander G. Thompson and Michele T. Hu},
  journal = {NPJ Parkinson's Disease},
  year = {2026},
  month = jul,
  doi = {10.1038/s41531-026-01435-3},
  url = {https://doi.org/10.1038/s41531-026-01435-3},
  note = {CC BY 4.0},
}
RIS
TY  - JOUR
TI  - Dopamine replacement therapy modulates DDC, prolactin and AOC3 levels in Parkinson’s disease
AU  - Ludo van Hillegondsberg
AU  - Shahzad Ahmad
AU  - Tanja Zerenner
AU  - Michael Lawton
AU  - Karolien Groenewald
AU  - Micah Fletcher
AU  - Ayan Ianniello
AU  - Yoav Ben-Shlomo
AU  - Richard Wade-Martins
AU  - Paolo Piazza
AU  - Avigail Taylor
AU  - Alexander G. Thompson
AU  - Michele T. Hu
PY  - 2026
DA  - 2026/07/04
JO  - NPJ Parkinson's Disease
DO  - 10.1038/s41531-026-01435-3
UR  - https://doi.org/10.1038/s41531-026-01435-3
AB  - Dopa decarboxylase (DDC) is a candidate biomarker in Parkinson’s disease (PD), but its levels are influenced by dopamine replacement therapy (DRT), complicating interpretation. We used high-throughput proteomics to analyze serum and CSF samples from PD patients, individuals with idiopathic REM-sleep behaviour disorder, and controls to assess DRT effects. In serum, DDC increased and prolactin and AOC3 decreased with higher levodopa equivalent daily doses, showing drug class-specific associations. Longitudinally, serum DDC and prolactin levels changed with DRT, while AOC3 remained stable. In CSF, DDC was elevated regardless of treatment, while prolactin was reduced only in treated PD. These results indicate that serum changes in DDC, prolactin, and AOC3 primarily reflect treatment exposure rather than disease biology. Our findings highlight the need to account for medication effects in proteomic studies, identify AOC3 as a novel DRT-sensitive protein, and support the potential of treatment-responsive proteins as pharmacodynamic markers in PD.
SN  - 2373-8057
ER  -