%0 Journal Article
%A Degenhardt, Karoline
%A Wagner, Jessica
%A Skodras, Angelos
%A Candlish, Michael
%A Koppelmann, Anna Julia
%A Wild, Katleen
%A Maxwell, Rusheka
%A Rotermund, Carola
%A von Zweydorf, Felix
%A Gloeckner, Christian Johannes
%A Davies, Hannah A
%A Madine, Jillian
%A Del Turco, Domenico
%A Feederle, Regina
%A Lashley, Tammaryn
%A Deller, Thomas
%A Kahle, Philipp
%A Hefendehl, Jasmin K
%A Jucker, Mathias
%A Neher, Jonas
%T Medin aggregation causes cerebrovascular dysfunction in aging wild-type mice.
%J Proceedings of the National Academy of Sciences of the United States of America
%V 117
%N 38
%@ 1091-6490
%C Washington, DC
%I National Acad. of Sciences
%M DZNE-2021-00215
%P 23925 - 23931
%D 2020
%Z ISSN 1091-6490 not unique: **3 hits**.
%X 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.
%K Aged, 80 and over
%K Aging: metabolism
%K Amyloid: genetics
%K Amyloid: metabolism
%K Animals
%K Antigens, Surface: genetics
%K Antigens, Surface: metabolism
%K Aorta: metabolism
%K Aorta: pathology
%K Brain Chemistry: physiology
%K Cerebrovascular Circulation: physiology
%K Female
%K Humans
%K Male
%K Mice
%K Mice, Inbred C57BL
%K Milk Proteins: genetics
%K Milk Proteins: metabolism
%K Vascular Diseases: metabolism
%K Vascular Diseases: pathology
%K MFG-E8 (Other)
%K Medin (Other)
%K aging (Other)
%K amyloid (Other)
%K cerebrovascular dysfunction (Other)
%K Amyloid (NLM Chemicals)
%K Antigens, Surface (NLM Chemicals)
%K MFGE8 protein, human (NLM Chemicals)
%K Mfge8 protein, mouse (NLM Chemicals)
%K Milk Proteins (NLM Chemicals)
%F PUB:(DE-HGF)16
%9 Journal Article
%$ pmid:32900929
%2 pmc:PMC7519322
%R 10.1073/pnas.2011133117
%U https://pub.dzne.de/record/154362