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@MISC{Karmali:285262,
      author       = {Karmali, Nasser},
      title        = {{D}ataset: {S}ingle-cell transcriptomic changes in
                      oligodendroglial lineage cells derived from {P}arkinson’s
                      disease patient-i{PSC}s with {LRRK}2-{G}2019{S} mutation
                      ({S}eries {GSE}277350)},
      publisher    = {Gene Expression Omnibus},
      reportid     = {DZNE-2026-00204},
      year         = {2026},
      abstract     = {Despite extensive research, the contribution of the LRRK2
                      p.G2019S mutation to Parkinson's disease (PD) remains
                      unclear. Recent findings indicate oligodendrocytes (ODCs)
                      and their progenitors are vulnerable in PD pathogenesis.
                      Notably, oligodendrocyte precursor cells (OPCs) exhibit high
                      endogenous expression of LRRK2. We induced PD patient-iPSCs
                      with the LRRK2 p.G2019S mutation into oligodendroglial
                      lineages and performed single-cell RNA sequencing. Cell type
                      composition analysis revealed an increase in OPCs,
                      proliferating OPCs and ciliated ependymal cells in LRRK2
                      lines, all of which are characterized by LRRK2 expression.
                      Differential expression analysis revealed transcriptomic
                      changes in several pathways, including down-regulation of
                      genes related to myelin assembly in ODCs, semaphorin-plexin
                      pathway in OPCs, and cilium movement in proliferating OPCs.
                      Cell-cell communication analysis identified significant
                      alterations in several signaling pathways including a
                      deactivation of PSAP signaling and an activation of MIF
                      signaling in LRRK2 lines. Additionally, we observed an
                      overall increase in SEMA6 signaling communication in LRRK2
                      cell lines; however, OPCs derived from these LRRK2 lines
                      specifically lost SEMA6 signaling due to a down-regulation
                      of SEMA6A and PLXNA2. Pseudotemporal trajectory analysis
                      revealed that SHH had significantly altered expression along
                      the pseudotime, accompanied by higher expression levels in
                      LRRK2 lines. We propose that dysfunctional semaphorin-plexin
                      signaling, along with cilia movement and SHH signaling,
                      might represent early events in PD pathology.},
      cin          = {AG Heutink},
      cid          = {I:(DE-2719)1210002},
      pnm          = {354 - Disease Prevention and Healthy Aging (POF4-354)},
      pid          = {G:(DE-HGF)POF4-354},
      typ          = {PUB:(DE-HGF)32},
      url          = {https://pub.dzne.de/record/285262},
}