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Opioid K receptor variant is associated with a delayed onset of dyskinesias in Parkinson’s disease
  1. Roberto Cilia1,
  2. Rosanna Asselta2,3,
  3. Emanuele Cereda4,
  4. Roberta Benfante5,6,
  5. Giuseppina Barbella7,
  6. Davide Vallauri7,
  7. Laura Marabini8,
  8. Diego Fornasari5,6,
  9. Stefano Goldwurm1,
  10. Gianni Pezzoli1
  1. 1 Parkinson Institute, ASST Gaetano Pini-CTO, Milan, Italy
  2. 2 Department of Biomedical Sciences, Humanitas University, Rozzano (Milan), Milan, Italy
  3. 3 Humanitas Clinical and Research Center, Rozzano (Milan), Milan, Italy
  4. 4 Nutrition and Dietetics Service, Fondazione IRCCS Policlinico San Matteo, Pavia, Italy
  5. 5 CNR – Neuroscience Institute, Milan, Italy
  6. 6 Department of Medical Biotechnologies and Translational Medicine, Università degli Studi di Milano, Milan, Italy
  7. 7 Department of Neurosciences, San Gerardo Hospital, University of Milano-Bicocca, Monza, Italy
  8. 8 Department of Pharmacological and Biomolecular Sciences, Università degli Studi di Milano, Milan, Italy
  1. Correspondence to Dr Roberto Cilia, Parkinson Institute, ASST Gaetano Pini-CTO, via Bignami 1, 20126 Milan, Italy; roberto.cilia{at}

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Risk factors for levodopa-induced dyskinesias (LIDs) in Parkinson’s disease (PD) include young age at onset, disease progression and individual dose of levodopa.1 Nevertheless, established risk factors do not fully explain the marked individual variability in the time elapsing between levodopa initiation and the onset of LIDs, and genetic predisposition is likely to play a critical role. To identify the genetic determinants modulating the time at onset of LIDs, we investigated 10 polymorphisms previously associated with LIDs in PD. Among these variants, we selected those additionally associated with addictive disorders, based on the recent hypothesis that pathophysiological mechanisms underlying LIDs share similarities with non-motor hyper-dopaminergic states, such as addictive disorders (including impulse control disorders).2

Clinical records of consecutive outpatients diagnosed with PD, attending our clinic from April 2009 to April 2011 and contributing to the ‘Parkinson Institute Biobank’, were retrospectively reviewed. We included only patients who were free of LIDs at baseline and who developed LIDs during the follow-up (to maximise the accuracy in recording the date of onset of LIDs and to overcome the limitation due to the retrospective study design). Patients were visited at least twice/year by the same neurologist. The onset of LIDs was defined as the first-ever report by the neurologist (off-state dystonia excluded).(e-1) We compared demographic and clinical variables with those of an independent cohort of 1002 PD patients followed during the same period, fulfilling similar inclusion/exclusion criteria but whose genetic data were not available (see online …

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  • RA and EC contributed equally.

  • Contributors All the authors have participated sufficiently in the work to fulfil the criteria for authorship. The contributions were as follows: study concept and design: RC; acquisition of data: RC, RB, DV, LM, MC, SG and GP; analysis and interpretation of data: RC, RA, RB, LM, EC, SG, GP and DF; drafting of the manuscript: RC and GB; critical revision of the manuscript: RC, RA, RB, EC, SG and GP; statistical analysis: RA (genetics) and EC (clinical data); obtained funding: LM, DF, SG and GP; study supervision: SG and GP.

  • Competing interests None declared.

  • Patient consent Obtained.

  • Ethics approval Ethics Committee.

  • Provenance and peer review Not commissioned; externally peer reviewed.