Amyloid Beta Influences Vascular Smooth Muscle Contractility and Mechanoadaptation

Eric S. Hald, Connor D. Timm, Patrick W. Alford

Research output: Contribution to journalArticlepeer-review

4 Scopus citations

Abstract

Amyloid beta accumulation in neuronal and cerebrovascular tissue is a key precursor to development of Alzheimer's disease and can result in neurodegeneration. While its persistence in Alzheimer's cases is well-studied, amyloid beta's direct effect on vascular function is unclear. Here, we measured the effect of amyloid beta treatment on vascular smooth muscle cell functional contractility and modeled the mechanoadaptive growth and remodeling response to these functional perturbations. We found that the amyloid beta 1-42 isoform induced a reduction in vascular smooth muscle cell mechanical output and reduced response to vasocontractile cues. These data were used to develop a thinwalled constrained mixture arterial model that suggests vessel growth, and remodeling in response to amyloid betamediated alteration of smooth muscle function leads to decreased ability of cerebrovascular vessels to vasodilate. These findings provide a possible explanation for the vascular injury and malfunction often associated with the development of neurodegeneration in Alzheimer's disease.

Original languageEnglish (US)
Article number111007
JournalJournal of biomechanical engineering
Volume138
Issue number11
DOIs
StatePublished - Nov 1 2016

Keywords

  • Alzheimer's disease
  • amyloid beta
  • cerebral amyloid angiopathy
  • growth and remodeling
  • vascular smooth muscle cells

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