Journal Article

DZNE-2021-00215

http://join2-wiki.gsi.de/foswiki/pub/Main/Artwork/join2_logo100x88.png Medin aggregation causes cerebrovascular dysfunction in aging wild-type mice.

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

2020
National Acad. of Sciences Washington, DC

This record in other databases:    

Please use a persistent id in citations: doi:10.1073/pnas.2011133117

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.

Keyword(s): Aged, 80 and over (MeSH) ; Aging: metabolism (MeSH) ; Amyloid: genetics (MeSH) ; Amyloid: metabolism (MeSH) ; Animals (MeSH) ; Antigens, Surface: genetics (MeSH) ; Antigens, Surface: metabolism (MeSH) ; Aorta: metabolism (MeSH) ; Aorta: pathology (MeSH) ; Brain Chemistry: physiology (MeSH) ; Cerebrovascular Circulation: physiology (MeSH) ; Female (MeSH) ; Humans (MeSH) ; Male (MeSH) ; Mice (MeSH) ; Mice, Inbred C57BL (MeSH) ; Milk Proteins: genetics (MeSH) ; Milk Proteins: metabolism (MeSH) ; Vascular Diseases: metabolism (MeSH) ; Vascular Diseases: pathology (MeSH) ; MFG-E8 ; Medin ; aging ; amyloid ; cerebrovascular dysfunction ; Amyloid ; Antigens, Surface ; MFGE8 protein, human ; Mfge8 protein, mouse ; Milk Proteins

Note: ISSN 1091-6490 not unique: **3 hits**.

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Contributing Institute(s):

1. Cell Biology of Neurological Diseases (AG Jucker)
2. Neuroimmunology and Neurodegenerative Disease (AG Neher (Tübingen))
3. Parkinson Genetics (AG Gasser)
4. Functional Neuroproteomics and Translational Biomarkers in Neurodegenerative Diseases (AG Gloeckner)
5. Antibody Production (AG Feederle)
6. Functional Neurogenetics (AG Kahle)

Research Program(s):

1. 352 - Disease Mechanisms (POF4-352) (POF4-352)
2. 353 - Clinical and Health Care Research (POF4-353) (POF4-353)

Appears in the scientific report 2020

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Database coverage:
; BIOSIS Previews ; Biological Abstracts ; Clarivate Analytics Master Journal List ; Current Contents - Agriculture, Biology and Environmental Sciences ; Current Contents - Life Sciences ; Ebsco Academic Search ; Essential Science Indicators ; IF >= 10 ; JCR ; National-Konsortium ; SCOPUS ; Science Citation Index Expanded ; Web of Science Core Collection ; Zoological Record

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