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000165626 041__ $$aEnglish
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000165626 1001_ $$0P:(DE-2719)9000358$$aZafar, Saima$$b0$$eFirst author$$udzne
000165626 245__ $$aSWATH Mass Spectrometry-Based CSF Proteome Profile of GBA-Linked Parkinson's Disease Patients.
000165626 260__ $$aBasel$$bMolecular Diversity Preservation International$$c2022
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000165626 520__ $$aβ-glucocerebrosidase (GBA)-associated mutations are a significant risk factor for Parkinson's disease (PD) that aggravate the disease pathology by upregulating the deposition of α-Synuclein (α-Syn). The resultant clinical profile varies for PD patients without GBA mutations. The current study aimed to identify the proteomic targets involved in the pathogenic pathways leading to the differential clinical presentation of GBA-associated PD. CSF samples (n = 32) were obtained from PD patients with GBA mutations (n = 22), PD patients without GBA mutations (n = 7), and healthy controls that were carriers of GBA mutations (n = 3). All samples were subjected to in-gel tryptic digestion followed by the construction of the spectral library and quantitative SWATH-based analysis. CSF α-Syn levels were reduced in both PDIdiopathic and PDGBA cases. Our SWATH-based mass spectrometric analysis detected 363 proteins involved in immune response, stress response, and cell signaling in various groups. Intergroup analysis showed that 52 proteins were significantly up- or downregulated in various groups. Of these 52 targets, 20 proteins were significantly altered in PDGBA cases only while 2 showed different levels in PDIdiopathic patients. Our results show that the levels of several pathologically relevant proteins, including Contactin-1, Selenium-binding protein 1, Adhesion G Protein-Coupled Receptor, and Apolipoprotein E are significantly different among the sporadic and genetic variants of PD and hint at aggravated synaptic damage, oxidative stress, neuronal loss, and aggregation of α-Syn in PDGBA cases.
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000165626 650_7 $$2Other$$aα-synuclein
000165626 650_7 $$2Other$$aCSF
000165626 650_7 $$2Other$$aSWATH
000165626 650_7 $$2Other$$aproteomics
000165626 650_7 $$2Other$$aα-synuclein
000165626 650_7 $$2Other$$aβ-glucocerebrosidase
000165626 650_7 $$0EC 3.2.1.45$$2NLM Chemicals$$aGlucosylceramidase
000165626 650_7 $$2NLM Chemicals$$aProteome
000165626 650_7 $$2Other$$aβ-glucocerebrosidase
000165626 650_2 $$2MeSH$$aGlucosylceramidase: metabolism
000165626 650_2 $$2MeSH$$aHumans
000165626 650_2 $$2MeSH$$aGlucosylceramidase: genetics
000165626 650_2 $$2MeSH$$aProteome
000165626 650_2 $$2MeSH$$aParkinson Disease: genetics
000165626 650_2 $$2MeSH$$aProteomics
000165626 650_2 $$2MeSH$$aMass Spectrometry
000165626 650_2 $$2MeSH$$aParkinson Disease: metabolism
000165626 650_2 $$2MeSH$$aCerebrospinal Fluid: chemistry
000165626 650_2 $$2MeSH$$aCerebrospinal Fluid: metabolism
000165626 7001_ $$0P:(DE-2719)9001208$$aNoor, Aneeqa$$b1$$udzne
000165626 7001_ $$0P:(DE-2719)9001558$$aYounas, Neelam$$b2$$udzne
000165626 7001_ $$aShafiq, Mohsin$$b3
000165626 7001_ $$0P:(DE-2719)9000287$$aSchmitz, Matthias$$b4$$udzne
000165626 7001_ $$0P:(DE-2719)2812736$$aWurster, Isabel$$b5$$udzne
000165626 7001_ $$0P:(DE-2719)2811916$$aBrockmann, Kathrin$$b6$$udzne
000165626 7001_ $$0P:(DE-2719)2320009$$aGasser, Thomas$$b7$$udzne
000165626 7001_ $$0P:(DE-2719)2000058$$aZerr, Inga$$b8$$eLast author$$udzne
000165626 770__ $$aMechanisms and Interventions for Neurological and Psychological Disorders 2.0
000165626 773__ $$0PERI:(DE-600)2019364-6$$a10.3390/ijms232214166$$gVol. 23, no. 22, p. 14166 -$$n22$$p14166$$tInternational journal of molecular sciences$$v23$$x1422-0067$$y2022
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