% IMPORTANT: The following is UTF-8 encoded.  This means that in the presence
% of non-ASCII characters, it will not work with BibTeX 0.99 or older.
% Instead, you should use an up-to-date BibTeX implementation like “bibtex8” or
% “biber”.

@ARTICLE{Zafar:165626,
      author       = {Zafar, Saima and Noor, Aneeqa and Younas, Neelam and
                      Shafiq, Mohsin and Schmitz, Matthias and Wurster, Isabel and
                      Brockmann, Kathrin and Gasser, Thomas and Zerr, Inga},
      title        = {{SWATH} {M}ass {S}pectrometry-{B}ased {CSF} {P}roteome
                      {P}rofile of {GBA}-{L}inked {P}arkinson's {D}isease
                      {P}atients.},
      journal      = {International journal of molecular sciences},
      volume       = {23},
      number       = {22},
      issn         = {1422-0067},
      address      = {Basel},
      publisher    = {Molecular Diversity Preservation International},
      reportid     = {DZNE-2022-01759},
      pages        = {14166},
      year         = {2022},
      abstract     = {β-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.},
      keywords     = {Glucosylceramidase: metabolism / Humans /
                      Glucosylceramidase: genetics / Proteome / Parkinson Disease:
                      genetics / Proteomics / Mass Spectrometry / Parkinson
                      Disease: metabolism / Cerebrospinal Fluid: chemistry /
                      Cerebrospinal Fluid: metabolism / α-synuclein (Other) / CSF
                      (Other) / SWATH (Other) / proteomics (Other) / α-synuclein
                      (Other) / β-glucocerebrosidase (Other) / Glucosylceramidase
                      (NLM Chemicals) / Proteome (NLM Chemicals) /
                      β-glucocerebrosidase (Other)},
      cin          = {AG Zerr / Ext UMG Zerr / AG Gasser},
      ddc          = {540},
      cid          = {I:(DE-2719)1440011-1 / I:(DE-2719)5000037 /
                      I:(DE-2719)1210000},
      pnm          = {353 - Clinical and Health Care Research (POF4-353)},
      pid          = {G:(DE-HGF)POF4-353},
      typ          = {PUB:(DE-HGF)16},
      pmc          = {pmc:PMC9699576},
      pubmed       = {pmid:36430645},
      doi          = {10.3390/ijms232214166},
      url          = {https://pub.dzne.de/record/165626},
}