| First Author | Degenhardt K | Year | 2020 |
| Journal | Proc Natl Acad Sci U S A | Volume | 117 |
| Issue | 38 | Pages | 23925-23931 |
| PubMed ID | 32900929 | Mgi Jnum | J:296359 |
| Mgi Id | MGI:6459211 | Doi | 10.1073/pnas.2011133117 |
| Citation | Degenhardt K, et al. (2020) Medin aggregation causes cerebrovascular dysfunction in aging wild-type mice. Proc Natl Acad Sci U S A 117(38):23925-23931 |
| abstractText | 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. |
