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@ARTICLE{Schneeberger:299828,
      author       = {S. Schneeberger and S. J. Kim and M. N. Geesdorf and E.
                      Friebel and P. Eede and M. Jendrach and A. Boltengagen and
                      C. Braeuning and T. Ruhwedel and A. J. Hülsmeier and N.
                      Gimber and M. Foerster and J. Obst and M. Andreadou and S.
                      Mundt and J. Schmoranzer and S. Prokop and W. Kessler and T.
                      Kuhlmann and W. Möbius and K.-A. Nave and T. Hornemann and
                      B. Becher and J. M. Edgar and N. Karaiskos and C. Kocks and
                      N. Rajewsky$^*$ and F. L. Heppner},
      title        = {{I}nterleukin-12 signaling drives {A}lzheimer's disease
                      pathology through disrupting neuronal and oligodendrocyte
                      homeostasis.},
      journal      = {Nature aging},
      volume       = {5},
      number       = {4},
      issn         = {2662-8465},
      address      = {London},
      publisher    = {Nature Research},
      reportid     = {DKFZ-2025-00565},
      pages        = {622-641},
      year         = {2025},
      note         = {2025 Apr;5(4):622-641},
      abstract     = {Neuroinflammation including interleukin
                      (IL)-12/IL-23-signaling is central to Alzheimer's disease
                      (AD) pathology. Inhibition of p40, a subunit of IL-12/IL-23,
                      attenuates pathology in AD-like mice; however, its signaling
                      mechanism and expression pattern remained elusive. Here we
                      show that IL-12 receptors are predominantly expressed in
                      neurons and oligodendrocytes in AD-like APPPS1 mice and in
                      patients with AD, whereas IL-23 receptor transcripts are
                      barely detectable. Consistently, deletion of the IL-12
                      receptor in neuroectodermal cells ameliorated AD pathology
                      in APPPS1 mice, whereas removal of IL-23 receptors had no
                      effect. Genetic ablation of IL-12 signaling alone reverted
                      the loss of mature oligodendrocytes, restored myelin
                      homeostasis, rescued the amyloid-β-dependent reduction of
                      parvalbumin-positive interneurons and restored
                      phagocytosis-related changes in microglia of APPPS1 mice.
                      Furthermore, IL-12 protein expression was increased in human
                      AD brains compared to healthy age-matched controls, and
                      human oligodendrocyte-like cells responded profoundly to
                      IL-12 stimulation. We conclude that oligodendroglial and
                      neuronal IL-12 signaling, but not IL-23 signaling, are key
                      in orchestrating AD-related neuroimmune crosstalk and that
                      IL-12 represents an attractive therapeutic target in AD.},
      cin          = {BE01},
      ddc          = {610},
      cid          = {I:(DE-He78)BE01-20160331},
      pnm          = {899 - ohne Topic (POF4-899)},
      pid          = {G:(DE-HGF)POF4-899},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:40082619},
      doi          = {10.1038/s43587-025-00816-2},
      url          = {https://inrepo02.dkfz.de/record/299828},
}