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@ARTICLE{Theis:1018435,
      author       = {Theis, Hendrik and Prange, Stéphane and Bischof, Gérard
                      N. and Hoenig, Merle C. and Tittgemeyer, Marc and
                      Timmermann, Lars and Fink, Gereon Rudolf and Drzezga,
                      Alexander and Eggers, Carsten and van Eimeren, Thilo},
      title        = {{I}mpulsive-compulsive behaviour in early {P}arkinson’s
                      disease is determined by apathy and dopamine receptor {D}3
                      polymorphism},
      journal      = {npj Parkinson's Disease},
      volume       = {9},
      number       = {1},
      issn         = {2373-8057},
      address      = {London [u.a.]},
      publisher    = {Nature Publ. Group},
      reportid     = {FZJ-2023-04810},
      pages        = {154},
      year         = {2023},
      abstract     = {Impulsive-compulsive behaviour (ICB) is a frequently
                      observed non-motor symptom in early Parkinson’s disease
                      after initiatingdopamine replacement therapy. At the
                      opposite end of the motivated behaviour spectrum, apathy
                      occurs in early Parkinson’sdisease even before dopamine
                      replacement is started. The co-occurrence of these
                      behavioural conditions in Parkinson’s diseaseraises
                      questions about their relationship and underlying
                      pathophysiological determinants. In previous imaging or
                      genetic studies,both conditions have been associated with
                      the limbic dopaminergic system. The risk variant of the
                      Ser9Gly polymorphism of thedopamine receptor D3 (DRD3) is
                      linked to increased dopamine affinity in the limbic
                      striatum. With this in mind, we investigatedhow ICB
                      expression is explained by apathy and DRD3 polymorphisms and
                      their effects on grey matter volume and dopaminesynthesis
                      capacity. Fifty-four patients with early Parkinson’s
                      disease took part in anatomical T1-weighted MRI. Forty of
                      them alsounderwent dynamic PET imaging using [18F]DOPA to
                      measure striatal dopamine synthesis capacity. Further,
                      Ser9Gly (rs6280) genepolymorphism influencing the DRD3
                      dopamine-binding affinity was determined in all patients.
                      The severity of impulsivecompulsivebehaviour and apathy was
                      assessed using the Questionnaire for Impulsive-Compulsive
                      Disorders Rating Scale and theApathy Evaluation Scale. ICB
                      and the severity of apathy were indeed positively
                      correlated. Apathy and the DRD3 polymorphismwere interactive
                      risk factors for ICB severity. Apathy was significantly
                      linked to atrophy of the bilateral putamen. Patients with
                      theDRD3 risk type had reduced dopamine synthesis capacity in
                      the putamen and limbic striatum, apathy was associated with
                      reduceddopamine synthesis capacity in the limbic striatum.
                      The results of [18F]DOPA reached only trend significance.
                      Apathy in drug-naïvePD patients might be a consequence of
                      impaired striatal dopaminergic tone. This may represent a
                      predisposing factor for thedevelopment of ICB after the
                      initiation of dopamine replacement therapy. The risk type of
                      DRD3 could further amplify thispredisposition due to its
                      higher affinity to dopamine.},
      cin          = {INM-3 / INM-2},
      ddc          = {610},
      cid          = {I:(DE-Juel1)INM-3-20090406 / I:(DE-Juel1)INM-2-20090406},
      pnm          = {5251 - Multilevel Brain Organization and Variability
                      (POF4-525) / DFG project 431549029 - SFB 1451:
                      Schlüsselmechanismen normaler und krankheitsbedingt
                      gestörter motorischer Kontrolle (431549029) / DFG project
                      491111487 - Open-Access-Publikationskosten / 2022 - 2024 /
                      Forschungszentrum Jülich (OAPKFZJ) (491111487) / 5252 -
                      Brain Dysfunction and Plasticity (POF4-525) / 5253 -
                      Neuroimaging (POF4-525)},
      pid          = {G:(DE-HGF)POF4-5251 / G:(GEPRIS)431549029 /
                      G:(GEPRIS)491111487 / G:(DE-HGF)POF4-5252 /
                      G:(DE-HGF)POF4-5253},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {37968562},
      UT           = {WOS:001102226800001},
      doi          = {10.1038/s41531-023-00596-9},
      url          = {https://juser.fz-juelich.de/record/1018435},
}