000163488 001__ 163488
000163488 005__ 20240722121853.0
000163488 0247_ $$2doi$$a10.1002/mds.28704
000163488 0247_ $$2pmid$$apmid:34180557
000163488 0247_ $$2ISSN$$a0885-3185
000163488 0247_ $$2ISSN$$a1531-8257
000163488 0247_ $$2altmetric$$aaltmetric:108326461
000163488 037__ $$aDZNE-2022-00248
000163488 041__ $$aEnglish
000163488 082__ $$a610
000163488 1001_ $$0P:(DE-2719)2812186$$aLerche, Stefanie$$b0$$eFirst author$$udzne
000163488 245__ $$aCSF Protein Level of Neurotransmitter Secretion, Synaptic Plasticity, and Autophagy in PD and DLB.
000163488 260__ $$aNew York, NY$$bWiley$$c2021
000163488 3367_ $$2DRIVER$$aarticle
000163488 3367_ $$2DataCite$$aOutput Types/Journal article
000163488 3367_ $$0PUB:(DE-HGF)16$$2PUB:(DE-HGF)$$aJournal Article$$bjournal$$mjournal$$s1721639622_12034
000163488 3367_ $$2BibTeX$$aARTICLE
000163488 3367_ $$2ORCID$$aJOURNAL_ARTICLE
000163488 3367_ $$00$$2EndNote$$aJournal Article
000163488 520__ $$aMolecular pathways associated with α-synuclein proteostasis have been detected in genetic studies and in cell models and include autophagy, ubiquitin-proteasome system, mitochondrial homeostasis, and synaptic plasticity. However, we lack biomarkers that are representative for these pathways in human biofluids.The objective of this study was to evaluate CSF protein profiles of pathways related to α-synuclein proteostasis.We assessed CSF protein profiles associated with neurotransmitter secretion, synapse plasticity, and autophagy in 2 monocentric cohorts with α-synucleinopathy (385 PD patients and 67 DLB patients). We included 80 PD patients and 17 DLB patients with variants in the glucocerebrosidase gene to serve as proxy for accelerated α-synuclein pathology with pronounced clinical trajectories.(1) Proteins associated with neurotransmitter secretion, synaptic plasticity, and endolysosomal autophagy were lower in PD and DLB patients compared with healthy controls. (2) These patterns were more pronounced in DLB than in PD patients, accentuated by GBA variant status in both entities. (3) CSF levels of these proteins were positively associated with CSF levels of total α-synuclein, with lower levels of proteostasis proteins related to lower levels of total α-synuclein. (4) These findings could be confirmed longitudinally. PD patients with low CSF profiles of proteostasis proteins showed lower CSF levels of α-synuclein longitudinally compared with PD patients with a normal proteostasis profile.CSF proteins associated with neurotransmitter secretion, synaptic plasticity, and endolysosomal autophagy might serve as biomarkers related to α-synuclein proteostasis in PD and DLB. © 2021 The Authors. Movement Disorders published by Wiley Periodicals LLC on behalf of International Parkinson and Movement Disorder Society.
000163488 536__ $$0G:(DE-HGF)POF4-353$$a353 - Clinical and Health Care Research (POF4-353)$$cPOF4-353$$fPOF IV$$x0
000163488 588__ $$aDataset connected to CrossRef, PubMed, , Journals: pub.dzne.de
000163488 650_7 $$2Other$$aCSF
000163488 650_7 $$2Other$$aGBA
000163488 650_7 $$2Other$$aPD
000163488 650_7 $$2Other$$alysosome
000163488 650_7 $$2Other$$asecretion
000163488 650_7 $$2Other$$asynaptic plasticity
000163488 650_7 $$2NLM Chemicals$$aBiomarkers
000163488 650_7 $$2NLM Chemicals$$aNeurotransmitter Agents
000163488 650_7 $$2NLM Chemicals$$aalpha-Synuclein
000163488 650_7 $$0EC 3.2.1.45$$2NLM Chemicals$$aGlucosylceramidase
000163488 650_2 $$2MeSH$$aAutophagy
000163488 650_2 $$2MeSH$$aBiomarkers
000163488 650_2 $$2MeSH$$aGlucosylceramidase
000163488 650_2 $$2MeSH$$aHumans
000163488 650_2 $$2MeSH$$aLewy Body Disease
000163488 650_2 $$2MeSH$$aNeuronal Plasticity
000163488 650_2 $$2MeSH$$aNeurotransmitter Agents
000163488 650_2 $$2MeSH$$aParkinson Disease: metabolism
000163488 650_2 $$2MeSH$$aalpha-Synuclein: metabolism
000163488 7001_ $$aSjödin, Simon$$b1
000163488 7001_ $$aBrinkmalm, Ann$$b2
000163488 7001_ $$aBlennow, Kaj$$b3
000163488 7001_ $$0P:(DE-2719)2812736$$aWurster, Isabel$$b4$$udzne
000163488 7001_ $$0P:(DE-2719)2811830$$aRoeben, Benjamin$$b5$$udzne
000163488 7001_ $$0P:(DE-2719)9000951$$aZimmermann, Milan$$b6$$udzne
000163488 7001_ $$0P:(DE-2719)2351249$$aHauser, Ann-Kathrin$$b7$$udzne
000163488 7001_ $$0P:(DE-2719)2109499$$aLiepelt-Scarfone, Inga$$b8$$udzne
000163488 7001_ $$aWaniek, Katharina$$b9
000163488 7001_ $$aLachmann, Ingolf$$b10
000163488 7001_ $$0P:(DE-2719)2320009$$aGasser, Thomas$$b11$$udzne
000163488 7001_ $$aZetterberg, Henrik$$b12
000163488 7001_ $$0P:(DE-2719)2811916$$aBrockmann, Kathrin$$b13$$eLast author$$udzne
000163488 773__ $$0PERI:(DE-600)2041249-6$$a10.1002/mds.28704$$gVol. 36, no. 11, p. 2595 - 2604$$n11$$p2595 - 2604$$tMovement disorders$$v36$$x1531-8257$$y2021
000163488 8564_ $$uhttps://pub.dzne.de/record/163488/files/DZNE-2022-00248.pdf$$yOpenAccess
000163488 8564_ $$uhttps://pub.dzne.de/record/163488/files/DZNE-2022-00248.pdf?subformat=pdfa$$xpdfa$$yOpenAccess
000163488 909CO $$ooai:pub.dzne.de:163488$$pdnbdelivery$$pdriver$$pVDB$$popen_access$$popenaire
000163488 9101_ $$0I:(DE-588)1065079516$$6P:(DE-2719)2812186$$aDeutsches Zentrum für Neurodegenerative Erkrankungen$$b0$$kDZNE
000163488 9101_ $$0I:(DE-588)1065079516$$6P:(DE-2719)2812736$$aDeutsches Zentrum für Neurodegenerative Erkrankungen$$b4$$kDZNE
000163488 9101_ $$0I:(DE-588)1065079516$$6P:(DE-2719)2811830$$aDeutsches Zentrum für Neurodegenerative Erkrankungen$$b5$$kDZNE
000163488 9101_ $$0I:(DE-588)1065079516$$6P:(DE-2719)9000951$$aDeutsches Zentrum für Neurodegenerative Erkrankungen$$b6$$kDZNE
000163488 9101_ $$0I:(DE-588)1065079516$$6P:(DE-2719)2351249$$aDeutsches Zentrum für Neurodegenerative Erkrankungen$$b7$$kDZNE
000163488 9101_ $$0I:(DE-588)1065079516$$6P:(DE-2719)2109499$$aDeutsches Zentrum für Neurodegenerative Erkrankungen$$b8$$kDZNE
000163488 9101_ $$0I:(DE-588)1065079516$$6P:(DE-2719)2320009$$aDeutsches Zentrum für Neurodegenerative Erkrankungen$$b11$$kDZNE
000163488 9101_ $$0I:(DE-588)1065079516$$6P:(DE-2719)2811916$$aDeutsches Zentrum für Neurodegenerative Erkrankungen$$b13$$kDZNE
000163488 9131_ $$0G:(DE-HGF)POF4-353$$1G:(DE-HGF)POF4-350$$2G:(DE-HGF)POF4-300$$3G:(DE-HGF)POF4$$4G:(DE-HGF)POF$$aDE-HGF$$bGesundheit$$lNeurodegenerative Diseases$$vClinical and Health Care Research$$x0
000163488 9141_ $$y2021
000163488 915__ $$0StatID:(DE-HGF)0200$$2StatID$$aDBCoverage$$bSCOPUS$$d2022-11-11
000163488 915__ $$0StatID:(DE-HGF)0300$$2StatID$$aDBCoverage$$bMedline$$d2022-11-11
000163488 915__ $$0StatID:(DE-HGF)1030$$2StatID$$aDBCoverage$$bCurrent Contents - Life Sciences$$d2022-11-11
000163488 915__ $$0LIC:(DE-HGF)CCBY4$$2HGFVOC$$aCreative Commons Attribution CC BY 4.0
000163488 915__ $$0StatID:(DE-HGF)0600$$2StatID$$aDBCoverage$$bEbsco Academic Search$$d2022-11-11
000163488 915__ $$0StatID:(DE-HGF)0100$$2StatID$$aJCR$$bMOVEMENT DISORD : 2021$$d2022-11-11
000163488 915__ $$0StatID:(DE-HGF)3001$$2StatID$$aDEAL Wiley$$d2021-01-30$$wger
000163488 915__ $$0StatID:(DE-HGF)0113$$2StatID$$aWoS$$bScience Citation Index Expanded$$d2021-01-30
000163488 915__ $$0StatID:(DE-HGF)0150$$2StatID$$aDBCoverage$$bWeb of Science Core Collection$$d2022-11-11
000163488 915__ $$0StatID:(DE-HGF)0510$$2StatID$$aOpenAccess
000163488 915__ $$0StatID:(DE-HGF)0030$$2StatID$$aPeer Review$$bASC$$d2022-11-11
000163488 915__ $$0StatID:(DE-HGF)9905$$2StatID$$aIF >= 5$$bMOVEMENT DISORD : 2021$$d2022-11-11
000163488 915__ $$0StatID:(DE-HGF)0160$$2StatID$$aDBCoverage$$bEssential Science Indicators$$d2021-01-30
000163488 915__ $$0StatID:(DE-HGF)1110$$2StatID$$aDBCoverage$$bCurrent Contents - Clinical Medicine$$d2022-11-11
000163488 915__ $$0StatID:(DE-HGF)0420$$2StatID$$aNationallizenz$$d2022-11-11$$wger
000163488 915__ $$0StatID:(DE-HGF)0199$$2StatID$$aDBCoverage$$bClarivate Analytics Master Journal List$$d2022-11-11
000163488 9201_ $$0I:(DE-2719)1210000$$kAG Gasser$$lParkinson Genetics$$x0
000163488 9201_ $$0I:(DE-2719)1240005$$kCore ICRU$$lCore ICRU$$x1
000163488 980__ $$ajournal
000163488 980__ $$aVDB
000163488 980__ $$aI:(DE-2719)1210000
000163488 980__ $$aI:(DE-2719)1240005
000163488 980__ $$aUNRESTRICTED
000163488 9801_ $$aFullTexts