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@ARTICLE{Lerche:151064,
      author       = {Lerche, Stefanie and Wurster, Isabel and Röben, Benjamin
                      and Zimmermann, Milan and Machetanz, Gerrit and Wiethoff,
                      Sarah and Dehnert, Monique and Rietschel, Lea and
                      Riebenbauer, Benjamin and Deuschle, Christian and Stransky,
                      Elke and Liepelt-Scarfone, Inga and Gasser, Thomas and
                      Brockmann, Kathrin},
      title        = {{CSF} {NFL} in a {L}ongitudinally {A}ssessed {PD} {C}ohort:
                      {A}ge {E}ffects and {C}ognitive {T}rajectories},
      journal      = {Movement disorders},
      volume       = {35},
      number       = {7},
      issn         = {0885-3185},
      address      = {New York, NY},
      publisher    = {Wiley},
      reportid     = {DZNE-2020-01049},
      pages        = {1138-1144},
      year         = {2020},
      abstract     = {BackgroundNeurofilament light protein is an unspecific
                      biofluid marker that reflects the extent of neuronal/axonal
                      damage and thereby offers the chance monitor disease
                      severity and progression. The objective of this study was to
                      investigate cerebrospinal fluid (CSF) levels of
                      neurofilament light protein in Parkinson’s disease (PD)
                      patients with clinical trajectories of motor and cognitive
                      function longitudinally.MethodsCSF neurofilament light
                      protein levels were assessed in 371 PDsporadic, 126 genetic
                      PD patients (91 PDGBA, 8 PDLRRK2, 21
                      $PDPRKN/PINK1/DJ1_heterozygous,$ 6
                      $PDPRKN/PINK1/DJ1_homozygous),$ and 71 healthy controls.
                      Participants were followed up longitudinally for up to
                      8 years.ResultsAt baseline, mean CSF neurofilament light
                      protein levels were highest in PD patients with cognitive
                      impairment (Montreal Cognitive Assessment score ≤ 25;
                      1207 pg/mL) but also higher in PD patients with normal
                      cognitive function (757 pg/mL) compared with healthy
                      controls (593 pg/mL; P ≤ 0.001). In healthy controls
                      and in PD patients older age was associated with higher CSF
                      levels of neurofilament light protein (P ≤ 0.001). In
                      PD patients, male gender, older age at onset, longer disease
                      duration, higher Hoehn and Yahr stages, higher UPDRS‐III
                      scores, and lower Montreal Cognitive Assessment scores were
                      associated with higher CSF levels of neurofilament light
                      protein (P < 0.01). In patients who developed cognitive
                      impairment during study, CSF neurofilament light protein
                      levels prior to conversion to cognitive impairment were not
                      significantly different compared with CSF neurofilament
                      light protein levels of patients who remained cognitively
                      normal.ConclusionsIncreased CSF levels of neurofilament
                      light protein are associated with cognitive decline and
                      motor impairment in PD. However, this increase seems not a
                      very early event and does not mark the conversion to
                      cognitive impairment beforehand. Therefore, the predictive
                      value needs to be discussed critically. © 2020
                      International Parkinson and Movement Disorder Society.},
      keywords     = {Age Factors / Aged / Biomarkers / Cognition / Cognitive
                      Dysfunction: etiology / Disease Progression / Humans / Male
                      / Neurofilament Proteins: cerebrospinal fluid / Parkinson
                      Disease: cerebrospinal fluid / Parkinson Disease:
                      complications},
      cin          = {Tübingen common / Biobanking Facility (Tübingen) / AG
                      Gasser},
      ddc          = {610},
      cid          = {I:(DE-2719)6000018 / I:(DE-2719)1240004 /
                      I:(DE-2719)1210000},
      pnm          = {345 - Population Studies and Genetics (POF3-345)},
      pid          = {G:(DE-HGF)POF3-345},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:32445500},
      doi          = {10.1002/mds.28056},
      url          = {https://pub.dzne.de/record/151064},
}