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@ARTICLE{Feringa:281814,
      author       = {Feringa, Femke M and Koppes-den Hertog, Sascha J and Wang,
                      Lian Y and Derks, Rico J E and Kruijff, Iris and Erlebach,
                      Lena and Heijneman, Jorin and Miramontes, Ricardo and
                      Pömpner, Nadine and Blomberg, Niek and Olivier-Jimenez,
                      Damien and Johansen, Lill Eva and Cammack, Alexander J and
                      Giblin, Ashling and Toomey, Christina E and Rose, Indigo V L
                      and Yuan, Hebao and Ward, Michael E and Isaacs, Adrian M and
                      Kampmann, Martin and Kronenberg-Versteeg, Deborah and
                      Lashley, Tammaryn and Thompson, Leslie M and Ori, Alessandro
                      and Mohammed, Yassene and Giera, Martin and van der Kant,
                      Rik},
      title        = {{T}he {N}eurolipid {A}tlas: a lipidomics resource for
                      neurodegenerative diseases.},
      journal      = {Nature metabolism},
      volume       = {7},
      number       = {10},
      issn         = {2522-5812},
      address      = {[London]},
      publisher    = {Springer Nature},
      reportid     = {DZNE-2025-01196},
      pages        = {2142 - 2164},
      year         = {2025},
      abstract     = {Lipid alterations in the brain have been implicated in many
                      neurodegenerative diseases. To facilitate comparative
                      lipidomic research across brain diseases, we establish a
                      data common named the Neurolipid Atlas that we prepopulated
                      with isogenic induced pluripotent stem cell (iPS
                      cell)-derived lipidomics data for different brain diseases.
                      Additionally, the resource contains lipidomics data of human
                      and mouse brain tissue. Leveraging multiple datasets, we
                      demonstrate that iPS cell-derived neurons, microglia and
                      astrocytes exhibit distinct lipid profiles that recapitulate
                      in vivo lipotypes. Notably, the Alzheimer disease (AD) risk
                      gene ApoE4 drives cholesterol ester (CE) accumulation
                      specifically in human astrocytes and we also observe CE
                      accumulation in whole-brain lipidomics from persons with AD.
                      Multiomics interrogation of iPS cell-derived astrocytes
                      revealed that altered cholesterol metabolism has a major
                      role in astrocyte immune pathways such as the
                      immunoproteasome and major histocompatibility complex class
                      I antigen presentation. Our data commons, available online (
                      https://neurolipidatlas.com/ ), allows for data deposition
                      by the community and provides a user-friendly tool and
                      knowledge base for a better understanding of lipid
                      dyshomeostasis in neurodegenerative diseases.},
      keywords     = {Humans / Lipidomics: methods / Neurodegenerative Diseases:
                      metabolism / Animals / Mice / Astrocytes: metabolism / Lipid
                      Metabolism / Induced Pluripotent Stem Cells: metabolism /
                      Brain: metabolism / Neurons: metabolism / Alzheimer Disease:
                      metabolism / Microglia: metabolism},
      cin          = {AG Kronenberg-Versteeg / AG Jucker},
      ddc          = {610},
      cid          = {I:(DE-2719)1210015 / I:(DE-2719)1210001},
      pnm          = {351 - Brain Function (POF4-351) / 352 - Disease Mechanisms
                      (POF4-352)},
      pid          = {G:(DE-HGF)POF4-351 / G:(DE-HGF)POF4-352},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:40983680},
      pmc          = {pmc:PMC12552125},
      doi          = {10.1038/s42255-025-01365-z},
      url          = {https://pub.dzne.de/record/281814},
}