Evidence map›Paper›PMID 32900929›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2020

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

Karoline Degenhardt, Jessica Wagner, Angelos Skodras, Michael Candlish, Anna Julia Koppelmann, Katleen Wild, Rusheka Maxwell, Carola Rotermund, Felix von Zweydorf, Christian Johannes Gloeckner and 10 more

Open access · greenAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
2.4field-weighted citation impact, top 10% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

28 citing papers in PubMed, 44 citations in OpenAlex.

  1. Vascular Aging.Circulation · 2026
    Review
  2. Article
  3. Article
  4. Review
  5. Chemical Synthesis of Medin via a Removable Aggregation-Suppressing Linker.Journal of peptide science : an official publication of the European Peptide Society · 2025
    Article
  6. Medin drives Aβ40 to adopt Aβ42-like fibril polymorphs in vitro.bioRxiv : the preprint server for biology · 2025
    Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Exercise to Mitigate Cerebrovascular Aging: A Geroscience Perspective.The journals of gerontology. Series A, Biological sciences and medical sciences · 2024
    Review
  12. Review
  13. Article
  14. Article
  15. Article
  16. Hallmarks of cardiovascular ageing.Nature reviews. Cardiology · 2023
    Review
  17. Article
  18. Article
  19. Article
  20. Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

20 authors at 6 institutions in 2 countries.

Karoline DegenhardtGerman Center for Neurodegenerative Diseases (DZNE), 72076 Tübingen, Germany.
Jessica WagnerGerman Center for Neurodegenerative Diseases (DZNE), 72076 Tübingen, Germany.
Angelos SkodrasGerman Center for Neurodegenerative Diseases (DZNE), 72076 Tübingen, Germany.
Michael CandlishBuchmann Institute for Molecular Life Sciences and Institute of Cell Biology and Neuroscience, Goethe University Frankfurt, 60438 Frankfurt, Germany.
Anna Julia KoppelmannDepartment of Cellular Neurology, Hertie Institute for Clinical Brain Research, University of Tübingen, 72072 Tübingen, Germany.
Katleen WildGerman Center for Neurodegenerative Diseases (DZNE), 72076 Tübingen, Germany.
Rusheka MaxwellDepartment of Cellular Neurology, Hertie Institute for Clinical Brain Research, University of Tübingen, 72072 Tübingen, Germany.
Carola RotermundGerman Center for Neurodegenerative Diseases (DZNE), 72076 Tübingen, Germany.
Felix von ZweydorfGerman Center for Neurodegenerative Diseases (DZNE), 72076 Tübingen, Germany.
Christian Johannes GloecknerGerman Center for Neurodegenerative Diseases (DZNE), 72076 Tübingen, Germany.ORCID 0000-0001-6494-6944
Hannah A DaviesDepartment of Cardiovascular and Metabolic Medicine, Institute of Life Course and Medical Sciences, University of Liverpool, Liverpool L69 3BX, United Kingdom.
Jillian MadineDepartment of Cardiovascular and Metabolic Medicine, Institute of Life Course and Medical Sciences, University of Liverpool, Liverpool L69 3BX, United Kingdom.ORCID 0000-0001-9963-5871
Domenico Del TurcoInstitute of Clinical Neuroanatomy, Dr. Senckenberg Anatomy, Neuroscience Center, Goethe University, D-60590 Frankfurt/Main, Germany.
Regina FeederleMonoclonal Antibody Core Facility, Institute for Diabetes and Obesity, Helmholtz Zentrum München, Research Center for Environmental Health, 85764 Neuherberg, Germany.ORCID 0000-0002-3981-367X
Tammaryn LashleyQueen Square Brain Bank for Neurological Disorders, University College London Queen Square Institute of Neurology, London WC1N 1PJ, United Kingdom.ORCID 0000-0001-7389-0348
Thomas DellerInstitute of Clinical Neuroanatomy, Dr. Senckenberg Anatomy, Neuroscience Center, Goethe University, D-60590 Frankfurt/Main, Germany.
Philipp KahleGerman Center for Neurodegenerative Diseases (DZNE), 72076 Tübingen, Germany.ORCID 0000-0002-8587-1731
Jasmin K HefendehlBuchmann Institute for Molecular Life Sciences and Institute of Cell Biology and Neuroscience, Goethe University Frankfurt, 60438 Frankfurt, Germany.
Mathias JuckerGerman Center for Neurodegenerative Diseases (DZNE), 72076 Tübingen, Germany.ORCID 0000-0001-9045-1072
Jonas J NeherGerman Center for Neurodegenerative Diseases (DZNE), 72076 Tübingen, Germany; jonas.neher@dzne.de.ORCID 0000-0003-1346-8924
German Center for Neurodegenerative Diseases · DEGoethe University Frankfurt · DEHertie Institute for Clinical Brain Research · DEUniversity of Liverpool · GBHelmholtz Zentrum München · DENational Hospital for Neurology and Neurosurgery · GB

Funding

British Heart Foundation FS/12/61/29877
6 · The paper itself

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.

Indexed as

Aged, 80 and overAgingAmyloidAnimalsAntigens, SurfaceAortaBrain ChemistryCerebrovascular CirculationFemaleHumansMaleMiceMice, Inbred C57BLMilk ProteinsVascular DiseasesAmyloidAntigens, SurfaceMFGE8 protein, humanMfge8 protein, mouseMilk Proteinsagingamyloidcerebrovascular dysfunctionMedinMFG-E8

Identifiers

PMID32900929
PMCPMC7519322
OpenAlexW3084114732

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.