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@ARTICLE{Degenhardt:154362,
      author       = {Degenhardt, Karoline and Wagner, Jessica and Skodras,
                      Angelos and Candlish, Michael and Koppelmann, Anna Julia and
                      Wild, Katleen and Maxwell, Rusheka and Rotermund, Carola and
                      von Zweydorf, Felix and Gloeckner, Christian Johannes and
                      Davies, Hannah A and Madine, Jillian and Del Turco, Domenico
                      and Feederle, Regina and Lashley, Tammaryn and Deller,
                      Thomas and Kahle, Philipp and Hefendehl, Jasmin K and
                      Jucker, Mathias and Neher, Jonas},
      title        = {{M}edin aggregation causes cerebrovascular dysfunction in
                      aging wild-type mice.},
      journal      = {Proceedings of the National Academy of Sciences of the
                      United States of America},
      volume       = {117},
      number       = {38},
      issn         = {1091-6490},
      address      = {Washington, DC},
      publisher    = {National Acad. of Sciences},
      reportid     = {DZNE-2021-00215},
      pages        = {23925 - 23931},
      year         = {2020},
      note         = {ISSN 1091-6490 not unique: **3 hits**.},
      abstract     = {Medin is the most common amyloid known in humans, as it can
                      be found in blood vessels of the upper body in virtually
                      everybody over 50 years of age. However, it remains unknown
                      whether deposition of Medin plays a causal role in
                      age-related vascular dysfunction. We now report that
                      aggregates of Medin also develop in the aorta and brain
                      vasculature of wild-type mice in an age-dependent manner.
                      Strikingly, genetic deficiency of the Medin precursor
                      protein, MFG-E8, eliminates not only vascular aggregates but
                      also prevents age-associated decline of cerebrovascular
                      function in mice. Given the prevalence of Medin aggregates
                      in the general population and its role in vascular
                      dysfunction with aging, targeting Medin may become a novel
                      approach to sustain healthy aging.},
      keywords     = {Aged, 80 and over / Aging: metabolism / Amyloid: genetics /
                      Amyloid: metabolism / Animals / Antigens, Surface: genetics
                      / Antigens, Surface: metabolism / Aorta: metabolism / Aorta:
                      pathology / Brain Chemistry: physiology / Cerebrovascular
                      Circulation: physiology / Female / Humans / Male / Mice /
                      Mice, Inbred C57BL / Milk Proteins: genetics / Milk
                      Proteins: metabolism / Vascular Diseases: metabolism /
                      Vascular Diseases: pathology / MFG-E8 (Other) / Medin
                      (Other) / aging (Other) / amyloid (Other) / cerebrovascular
                      dysfunction (Other) / Amyloid (NLM Chemicals) / Antigens,
                      Surface (NLM Chemicals) / MFGE8 protein, human (NLM
                      Chemicals) / Mfge8 protein, mouse (NLM Chemicals) / Milk
                      Proteins (NLM Chemicals)},
      cin          = {AG Jucker / AG Neher (Tübingen) / AG Gasser / AG Gloeckner
                      / AG Feederle / AG Kahle},
      ddc          = {500},
      cid          = {I:(DE-2719)1210001 / I:(DE-2719)1210012 /
                      I:(DE-2719)1210000 / I:(DE-2719)1210007 / I:(DE-2719)1140004
                      / I:(DE-2719)1210000-4},
      pnm          = {352 - Disease Mechanisms (POF4-352) / 353 - Clinical and
                      Health Care Research (POF4-353)},
      pid          = {G:(DE-HGF)POF4-352 / G:(DE-HGF)POF4-353},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:32900929},
      pmc          = {pmc:PMC7519322},
      doi          = {10.1073/pnas.2011133117},
      url          = {https://pub.dzne.de/record/154362},
}