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@ARTICLE{:270417,
      author       = {İş, Özkan and Wang, Xue and Reddy, Joseph S and Min,
                      Yuhao and Yilmaz, Elanur and Bhattarai, Prabesh and Patel,
                      Tulsi and Bergman, Jeremiah and Quicksall, Zachary and
                      Heckman, Michael G and Tutor-New, Frederick Q and Can
                      Demirdogen, Birsen and White, Launia and Koga, Shunsuke and
                      Krause, Vincent and Inoue, Yasuteru and Kanekiyo, Takahisa
                      and Cosacak, Mehmet Ilyas and Nelson, Nastasia and Lee,
                      Annie J and Vardarajan, Badri and Mayeux, Richard and Kouri,
                      Naomi and Deniz, Kaancan and Carnwath, Troy and Oatman,
                      Stephanie R and Lewis-Tuffin, Laura J and Nguyen, Thuy and
                      Carrasquillo, Minerva M and Graff-Radford, Jonathan and
                      Petersen, Ronald C and Jr Jack, Clifford R and Kantarci,
                      Kejal and Murray, Melissa E and Nho, Kwangsik and Saykin,
                      Andrew J and Dickson, Dennis W and Kizil, Caghan and Allen,
                      Mariet and Ertekin-Taner, Nilüfer},
      collaboration = {Initiative, Alzheimer’s Disease Neuroimaging},
      title        = {{G}liovascular transcriptional perturbations in
                      {A}lzheimer's disease reveal molecular mechanisms of blood
                      brain barrier dysfunction.},
      journal      = {Nature Communications},
      volume       = {15},
      number       = {1},
      issn         = {2041-1723},
      address      = {[London]},
      publisher    = {Nature Publishing Group UK},
      reportid     = {DZNE-2024-00797},
      pages        = {4758},
      year         = {2024},
      abstract     = {To uncover molecular changes underlying blood-brain-barrier
                      dysfunction in Alzheimer's disease, we performed single
                      nucleus RNA sequencing in 24 Alzheimer's disease and control
                      brains and focused on vascular and astrocyte clusters as
                      main cell types of blood-brain-barrier gliovascular-unit.
                      The majority of the vascular transcriptional changes were in
                      pericytes. Of the vascular molecular targets predicted to
                      interact with astrocytic ligands, SMAD3, upregulated in
                      Alzheimer's disease pericytes, has the highest number of
                      ligands including VEGFA, downregulated in Alzheimer's
                      disease astrocytes. We validated these findings with
                      external datasets comprising 4,730 pericyte and 150,664
                      astrocyte nuclei. Blood SMAD3 levels are associated with
                      Alzheimer's disease-related neuroimaging outcomes. We
                      determined inverse relationships between pericytic SMAD3 and
                      astrocytic VEGFA in human iPSC and zebrafish models. Here,
                      we detect vast transcriptome changes in Alzheimer's disease
                      at the gliovascular-unit, prioritize perturbed pericytic
                      SMAD3-astrocytic VEGFA interactions, and validate these in
                      cross-species models to provide a molecular mechanism of
                      blood-brain-barrier disintegrity in Alzheimer's disease.},
      keywords     = {Alzheimer Disease: genetics / Alzheimer Disease: metabolism
                      / Alzheimer Disease: pathology / Humans / Blood-Brain
                      Barrier: metabolism / Blood-Brain Barrier: pathology / Smad3
                      Protein: metabolism / Smad3 Protein: genetics / Zebrafish /
                      Astrocytes: metabolism / Vascular Endothelial Growth Factor
                      A: metabolism / Vascular Endothelial Growth Factor A:
                      genetics / Animals / Pericytes: metabolism / Pericytes:
                      pathology / Male / Induced Pluripotent Stem Cells:
                      metabolism / Female / Aged / Transcriptome / Brain:
                      metabolism / Brain: pathology / Brain: blood supply / Aged,
                      80 and over / Disease Models, Animal / Smad3 Protein (NLM
                      Chemicals) / Vascular Endothelial Growth Factor A (NLM
                      Chemicals) / SMAD3 protein, human (NLM Chemicals) / VEGFA
                      protein, human (NLM Chemicals)},
      cin          = {AG Kizil},
      ddc          = {500},
      cid          = {I:(DE-2719)1710007},
      pnm          = {352 - Disease Mechanisms (POF4-352)},
      pid          = {G:(DE-HGF)POF4-352},
      typ          = {PUB:(DE-HGF)16},
      pmc          = {pmc:PMC11190273},
      pubmed       = {pmid:38902234},
      doi          = {10.1038/s41467-024-48926-6},
      url          = {https://pub.dzne.de/record/270417},
}