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Degenhardt, K.* ; Wagner, J.* ; Skodras, A.* ; Candlish, M.* ; Koppelmann, A.J.* ; Wild, K.* ; Maxwell, R.* ; Rotermund, C.* ; von Zweydorf, F.* ; Gloeckner, C.J.* ; Davies, H.A.* ; Madine, J.* ; Del Turco, D.* ; Feederle, R. ; Lashley, T.* ; Deller, T.* ; Kahle, P.* ; Hefendehl, J.K.* ; Jucker, M.* ; Neher, J.J.*

Medin aggregation causes cerebrovascular dysfunction in aging wild-type mice.

Proc. Natl. Acad. Sci. U.S.A. 117, 23925-23931 (2020)
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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.
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Publication type Article: Journal article
Document type Scientific Article
Corresponding Author
Keywords Medin ; Mfg-e8 ; Cerebrovascular Dysfunction ; Aging ; Amyloid; Smooth-muscle-cells; Mouse Model; A-beta; Blood-flow; Amyloidosis; Growth; Mfg-e8; Vasculature; Dementia; Integrin
ISSN (print) / ISBN 0027-8424
e-ISSN 1091-6490
Journal Proceedings of the National Academy of Sciences of the United States of America
Quellenangaben Volume: 117, Issue: 38, Pages: 23925-23931 Article Number: , Supplement: ,
Publisher National Academy of Sciences
Publishing Place 2101 Constitution Ave Nw, Washington, Dc 20418 Usa
Non-patent literature Publications
Reviewing status Peer reviewed
Institute(s) CF Monoclonal Antibodies (CF-MAB)
Grants DFG
British Heart Foundation
German Research Foundation (DFG)