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

Karoline Degenhardt1,2,3, Jessica Wagner1,2,3, Angelos Skodras1,2

  • 1German Center for Neurodegenerative Diseases (DZNE), 72076 Tübingen, Germany.

Proceedings of the National Academy of Sciences of the United States of America
|September 9, 2020
PubMed
Summary

Medin amyloid aggregates are common in aging humans and mice. Targeting the Medin precursor protein MFG-E8 prevents age-related vascular dysfunction in mice, suggesting a new approach for healthy aging.

Keywords:
MFG-E8Medinagingamyloidcerebrovascular dysfunction

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Area of Science:

  • Cardiovascular Science
  • Neuroscience
  • Aging Research

Background:

  • Medin is the most prevalent human amyloid, found in blood vessels of individuals over 50.
  • The role of Medin deposition in age-related vascular dysfunction is currently unknown.

Purpose of the Study:

  • To investigate the role of Medin in age-dependent vascular dysfunction.
  • To determine if targeting Medin or its precursor impacts vascular aging.

Main Methods:

  • Age-dependent development of Medin aggregates was studied in wild-type mice aortas and brain vasculature.
  • The effect of genetic deficiency of MFG-E8 (Medin precursor) on vascular aggregates and cerebrovascular function was assessed.

Main Results:

  • Medin aggregates were found to develop in mouse aorta and brain vasculature in an age-dependent manner.
  • Genetic deficiency of MFG-E8 prevented Medin aggregate formation and age-associated decline in cerebrovascular function.
  • This suggests MFG-E8 is crucial for Medin aggregation and subsequent vascular dysfunction.

Conclusions:

  • Medin aggregation is linked to age-related vascular dysfunction.
  • Targeting MFG-E8 may be a promising therapeutic strategy to maintain vascular health during aging.
  • This research opens new avenues for interventions promoting healthy aging.