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000151064 041__ $$aEnglish
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000151064 1001_ $$0P:(DE-2719)2812186$$aLerche, Stefanie$$b0$$eFirst author
000151064 245__ $$aCSF NFL in a Longitudinally Assessed PD Cohort: Age Effects and Cognitive Trajectories
000151064 260__ $$aNew York, NY$$bWiley$$c2020
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000151064 520__ $$aBackgroundNeurofilament 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.
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000151064 542__ $$2Crossref$$i2020-05-23$$uhttp://onlinelibrary.wiley.com/termsAndConditions#vor
000151064 542__ $$2Crossref$$i2020-05-23$$uhttp://doi.wiley.com/10.1002/tdm_license_1.1
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000151064 650_2 $$2MeSH$$aAge Factors
000151064 650_2 $$2MeSH$$aAged
000151064 650_2 $$2MeSH$$aBiomarkers
000151064 650_2 $$2MeSH$$aCognition
000151064 650_2 $$2MeSH$$aCognitive Dysfunction: etiology
000151064 650_2 $$2MeSH$$aDisease Progression
000151064 650_2 $$2MeSH$$aHumans
000151064 650_2 $$2MeSH$$aMale
000151064 650_2 $$2MeSH$$aNeurofilament Proteins: cerebrospinal fluid
000151064 650_2 $$2MeSH$$aParkinson Disease: cerebrospinal fluid
000151064 650_2 $$2MeSH$$aParkinson Disease: complications
000151064 7001_ $$0P:(DE-2719)2812736$$aWurster, Isabel$$b1
000151064 7001_ $$0P:(DE-2719)2811830$$aRöben, Benjamin$$b2
000151064 7001_ $$0P:(DE-2719)9000951$$aZimmermann, Milan$$b3
000151064 7001_ $$0P:(DE-2719)9000193$$aMachetanz, Gerrit$$b4
000151064 7001_ $$0P:(DE-2719)2814026$$aWiethoff, Sarah$$b5
000151064 7001_ $$aDehnert, Monique$$b6
000151064 7001_ $$aRietschel, Lea$$b7
000151064 7001_ $$0P:(DE-2719)9000377$$aRiebenbauer, Benjamin$$b8
000151064 7001_ $$0P:(DE-2719)2812432$$aDeuschle, Christian$$b9
000151064 7001_ $$0P:(DE-2719)9000441$$aStransky, Elke$$b10
000151064 7001_ $$0P:(DE-2719)2109499$$aLiepelt-Scarfone, Inga$$b11
000151064 7001_ $$0P:(DE-2719)2320009$$aGasser, Thomas$$b12
000151064 7001_ $$0P:(DE-2719)2811916$$aBrockmann, Kathrin$$b13$$eLast author
000151064 77318 $$2Crossref$$3journal-article$$a10.1002/mds.28056$$b : Wiley, 2020-05-23$$n7$$p1138-1144$$tMovement Disorders$$v35$$x0885-3185$$y2020
000151064 773__ $$0PERI:(DE-600)2041249-6$$a10.1002/mds.28056$$gVol. 35, no. 7, p. 1138 - 1144$$n7$$p1138-1144$$tMovement disorders$$v35$$x0885-3185$$y2020
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