001     271085
005     20240814121440.0
037 _ _ |a DZNE-2024-00957
100 1 _ |a Dehestani, Mohammad
|0 P:(DE-2719)9002232
|b 0
|u dzne
245 _ _ |a Dataset: Transcriptomic changes in oligodendrocytes and precursor cells predicts clinical outcomes of Parkinson's disease
260 _ _ |c 2024
|b Gene Expression Omnibus
336 7 _ |a MISC
|2 BibTeX
336 7 _ |a Dataset
|b dataset
|m dataset
|0 PUB:(DE-HGF)32
|s 1723625220_28440
|2 PUB:(DE-HGF)
336 7 _ |a Chart or Table
|0 26
|2 EndNote
336 7 _ |a Dataset
|2 DataCite
336 7 _ |a DATA_SET
|2 ORCID
336 7 _ |a ResearchData
|2 DINI
520 _ _ |a Several prior studies have proposed the involvement of various brain regions and cell types in Parkinson's disease (PD) pathology. Here, we performed snRNA-seq on the prefrontal cortex and anterior cingulate regions from post-mortem control and PD brain tissue. We found a significant association of oligodendrocytes (ODCs) and oligodendrocyte precursor cells (OPCs) with PD-linked risk loci and report several dysregulated genes and pathways, including regulation of tau-protein kinase activity, regulation of inclusion body assembly and protein processing involved in protein targeting to mitochondria. In an independent PD cohort with clinical measures (681 cases and 549 controls), polygenic risk scores derived from the dysregulated genes significantly predicted Montreal Cognitive Assessment (MoCA)-, and Beck Depression Inventory-II (BDI-II)-scores but not motor impairment (UPDRS-III). We extended our analysis of clinical outcome prediction by incorporating three separate datasets that were previously published by different laboratories. In the first dataset from the anterior cingulate cortex, we identified a correlation between ODCs and BDI-II. In the second dataset obtained from the substantia nigra (SN), OPCs displayed notable predictive ability for UPDRS-III. In the third dataset from the SN region, a distinct subtype of OPCs, labeled OPC_ADM, exhibited predictive ability for UPDRS-III. Intriguingly, the OPC_ADM cluster also demonstrated a significant increase in PD samples. These results suggest that by expanding our focus to glial cells, we can uncover region-specific molecular pathways associated with PD symptoms.
536 _ _ |a 354 - Disease Prevention and Healthy Aging (POF4-354)
|0 G:(DE-HGF)POF4-354
|c POF4-354
|f POF IV
|x 0
536 _ _ |a 353 - Clinical and Health Care Research (POF4-353)
|0 G:(DE-HGF)POF4-353
|c POF4-353
|f POF IV
|x 1
700 1 _ |a Kozareva, V.
|0 P:(DE-HGF)0
|b 1
700 1 _ |a Blauwendraat, Cornelis
|0 P:(DE-2719)2810837
|b 2
700 1 _ |a Fränkel, E.
|0 P:(DE-HGF)0
|b 3
700 1 _ |a Gasser, Thomas
|0 P:(DE-2719)2320009
|b 4
|u dzne
700 1 _ |a Bansal, Vikas
|0 P:(DE-2719)2812055
|b 5
|u dzne
856 4 _ |u https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE272760
909 C O |o oai:pub.dzne.de:271085
|p VDB
910 1 _ |a Deutsches Zentrum für Neurodegenerative Erkrankungen
|0 I:(DE-588)1065079516
|k DZNE
|b 0
|6 P:(DE-2719)9002232
910 1 _ |a Deutsches Zentrum für Neurodegenerative Erkrankungen
|0 I:(DE-588)1065079516
|k DZNE
|b 4
|6 P:(DE-2719)2320009
910 1 _ |a Deutsches Zentrum für Neurodegenerative Erkrankungen
|0 I:(DE-588)1065079516
|k DZNE
|b 5
|6 P:(DE-2719)2812055
913 1 _ |a DE-HGF
|b Gesundheit
|l Neurodegenerative Diseases
|1 G:(DE-HGF)POF4-350
|0 G:(DE-HGF)POF4-354
|3 G:(DE-HGF)POF4
|2 G:(DE-HGF)POF4-300
|4 G:(DE-HGF)POF
|v Disease Prevention and Healthy Aging
|x 0
913 1 _ |a DE-HGF
|b Gesundheit
|l Neurodegenerative Diseases
|1 G:(DE-HGF)POF4-350
|0 G:(DE-HGF)POF4-353
|3 G:(DE-HGF)POF4
|2 G:(DE-HGF)POF4-300
|4 G:(DE-HGF)POF
|v Clinical and Health Care Research
|x 1
914 1 _ |y 2024
920 1 _ |0 I:(DE-2719)1210013
|k AG Bansal
|l Biomedical Data Science
|x 0
920 1 _ |0 I:(DE-2719)1210000
|k AG Gasser
|l Parkinson Genetics
|x 1
980 _ _ |a dataset
980 _ _ |a VDB
980 _ _ |a I:(DE-2719)1210013
980 _ _ |a I:(DE-2719)1210000
980 _ _ |a UNRESTRICTED


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