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@ARTICLE{Levites:271706,
      author       = {Levites, Yona and Dammer, Eric B and Ran, Yong and Tsering,
                      Wangchen and Duong, Duc and Abreha, Measho and Gadhavi,
                      Joshna and Lolo, Kiara and Trejo-Lopez, Jorge and Phillips,
                      Jennifer and Iturbe, Andrea and Erquizi, Aya and Moore,
                      Brenda D and Ryu, Danny and Natu, Aditya and Dillon, Kristy
                      and Torrellas, Jose and Moran, Corey and Ladd, Thomas and
                      Afroz, Farhana and Islam, Tariful and Jagirdar, Jaishree and
                      Funk, Cory C and Robinson, Max and Rangaraju, Srikant and
                      Borchelt, David R and Ertekin-Taner, Nilüfer and Kelly,
                      Jeffrey W and Heppner, Frank L and Johnson, Erik C B and
                      McFarland, Karen and Levey, Allan I and Prokop, Stefan and
                      Seyfried, Nicholas T and Golde, Todd E},
      title        = {{I}ntegrative proteomics identifies a conserved {A}β
                      amyloid responsome, novel plaque proteins, and pathology
                      modifiers in {A}lzheimer's disease.},
      journal      = {Cell reports / Medicine},
      volume       = {5},
      number       = {8},
      issn         = {2666-3791},
      address      = {Maryland Heights, MO},
      publisher    = {Elsevier},
      reportid     = {DZNE-2024-01058},
      pages        = {101669},
      year         = {2024},
      abstract     = {Alzheimer's disease (AD) is a complex neurodegenerative
                      disorder that develops over decades. AD brain proteomics
                      reveals vast alterations in protein levels and numerous
                      altered biologic pathways. Here, we compare AD brain
                      proteome and network changes with the brain proteomes of
                      amyloid β (Aβ)-depositing mice to identify conserved and
                      divergent protein networks with the conserved networks
                      identifying an Aβ amyloid responsome. Proteins in the most
                      conserved network (M42) accumulate in plaques,
                      cerebrovascular amyloid (CAA), and/or dystrophic neuronal
                      processes, and overexpression of two M42 proteins, midkine
                      (Mdk) and pleiotrophin (PTN), increases the accumulation of
                      Aβ in plaques and CAA. M42 proteins bind amyloid fibrils in
                      vitro, and MDK and PTN co-accumulate with cardiac
                      transthyretin amyloid. M42 proteins appear intimately linked
                      to amyloid deposition and can regulate amyloid deposition,
                      suggesting that they are pathology modifiers and thus
                      putative therapeutic targets. We posit that
                      amyloid-scaffolded accumulation of numerous M42+ proteins is
                      a central mechanism mediating downstream pathophysiology in
                      AD.},
      keywords     = {Alzheimer Disease: metabolism / Alzheimer Disease:
                      pathology / Alzheimer Disease: genetics / Proteomics:
                      methods / Animals / Amyloid beta-Peptides: metabolism /
                      Humans / Plaque, Amyloid: metabolism / Plaque, Amyloid:
                      pathology / Mice / Brain: metabolism / Brain: pathology /
                      Proteome: metabolism / Mice, Transgenic / Carrier Proteins:
                      metabolism / Carrier Proteins: genetics / Cytokines:
                      metabolism / Male / Alzheimer’s disease (Other) / Midkine
                      (Other) / Pleiotrophin (Other) / aggregation (Other) /
                      amyloid (Other) / animal models (Other) / plaques (Other) /
                      proteomics (Other) / Amyloid beta-Peptides (NLM Chemicals) /
                      Proteome (NLM Chemicals) / pleiotrophin (NLM Chemicals) /
                      Carrier Proteins (NLM Chemicals) / Cytokines (NLM
                      Chemicals)},
      cin          = {AG Heppner},
      ddc          = {610},
      cid          = {I:(DE-2719)1810007},
      pnm          = {353 - Clinical and Health Care Research (POF4-353)},
      pid          = {G:(DE-HGF)POF4-353},
      typ          = {PUB:(DE-HGF)16},
      pmc          = {pmc:PMC11384960},
      pubmed       = {pmid:39127040},
      doi          = {10.1016/j.xcrm.2024.101669},
      url          = {https://pub.dzne.de/record/271706},
}