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@ARTICLE{Tayran:272136,
      author       = {Tayran, Hüseyin and Yilmaz, Elanur and Bhattarai, Prabesh
                      and Min, Yuhao and Wang, Xue and Ma, Yiyi and Wang, Ni and
                      Jeong, Inyoung and Nelson, Nastasia and Kassara, Nada and
                      Cosacak, Mehmet Ilyas and Dogru, Ruya Merve and
                      Reyes-Dumeyer, Dolly and Stenersen, Jakob Mørkved and
                      Reddy, Joseph S and Qiao, Min and Flaherty, Delaney and
                      Gunasekaran, Tamil Iniyan and Yang, Zikun and Jurisch-Yaksi,
                      Nathalie and Teich, Andrew F and Kanekiyo, Takahisa and
                      Tosto, Giuseppe and Vardarajan, Badri N and İş, Özkan and
                      Ertekin-Taner, Nilüfer and Mayeux, Richard and Kizil,
                      Caghan},
      title        = {{ABCA}7-dependent induction of neuropeptide {Y} is required
                      for synaptic resilience in {A}lzheimer's disease through
                      {BDNF}/{NGFR} signaling.},
      journal      = {Cell genomics},
      volume       = {4},
      number       = {9},
      issn         = {2666-979X},
      address      = {Amsterdam},
      publisher    = {Elsevier},
      reportid     = {DZNE-2024-01131},
      pages        = {100642},
      year         = {2024},
      abstract     = {Genetic variants in ABCA7, an Alzheimer's disease
                      (AD)-associated gene, elevate AD risk, yet its functional
                      relevance to the etiology is unclear. We generated a
                      CRISPR-Cas9-mediated abca7 knockout zebrafish to explore
                      ABCA7's role in AD. Single-cell transcriptomics in
                      heterozygous abca7+/- knockout combined with Aβ42 toxicity
                      revealed that ABCA7 is crucial for neuropeptide Y (NPY),
                      brain-derived neurotrophic factor (BDNF), and nerve growth
                      factor receptor (NGFR) expressions, which are crucial for
                      synaptic integrity, astroglial proliferation, and microglial
                      prevalence. Impaired NPY induction decreased BDNF and
                      synaptic density, which are rescuable with ectopic NPY. In
                      induced pluripotent stem cell-derived human neurons exposed
                      to Aβ42, ABCA7-/- suppresses NPY. Clinical data showed
                      reduced NPY in AD correlated with elevated Braak stages,
                      genetic variants in NPY associated with AD, and epigenetic
                      changes in NPY, NGFR, and BDNF promoters linked to ABCA7
                      variants. Therefore, ABCA7-dependent NPY signaling via
                      BDNF-NGFR maintains synaptic integrity, implicating its
                      impairment in increased AD risk through reduced brain
                      resilience.},
      keywords     = {Brain-Derived Neurotrophic Factor: metabolism /
                      Brain-Derived Neurotrophic Factor: genetics / Animals /
                      Alzheimer Disease: metabolism / Alzheimer Disease: genetics
                      / Alzheimer Disease: pathology / Neuropeptide Y: metabolism
                      / Neuropeptide Y: genetics / Humans / Zebrafish / Signal
                      Transduction / Synapses: metabolism / Synapses: pathology /
                      ATP-Binding Cassette Transporters: genetics / ATP-Binding
                      Cassette Transporters: metabolism / Receptors, Nerve Growth
                      Factor: genetics / Receptors, Nerve Growth Factor:
                      metabolism / Zebrafish Proteins: genetics / Zebrafish
                      Proteins: metabolism / Neurons: metabolism / Neurons:
                      pathology / Amyloid beta-Peptides: metabolism / Amyloid
                      beta-Peptides: genetics / Brain-Derived Neurotrophic Factor
                      (NLM Chemicals) / Neuropeptide Y (NLM Chemicals) /
                      ATP-Binding Cassette Transporters (NLM Chemicals) /
                      Receptors, Nerve Growth Factor (NLM Chemicals) / Zebrafish
                      Proteins (NLM Chemicals) / Amyloid beta-Peptides (NLM
                      Chemicals)},
      cin          = {AG Kizil},
      ddc          = {610},
      cid          = {I:(DE-2719)1710007},
      pnm          = {352 - Disease Mechanisms (POF4-352)},
      pid          = {G:(DE-HGF)POF4-352},
      typ          = {PUB:(DE-HGF)16},
      pmc          = {pmc:PMC11480862},
      pubmed       = {pmid:39216475},
      doi          = {10.1016/j.xgen.2024.100642},
      url          = {https://pub.dzne.de/record/272136},
}