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Vascular amyloidosis impairs the gliovascular unit in a mouse model of Alzheimer's disease. | LitMetric

Vascular amyloidosis impairs the gliovascular unit in a mouse model of Alzheimer's disease.

Brain

1 Department of Neurobiology, University of Alabama at Birmingham, Birmingham, AL, USA 2 Center for Glial Biology in Medicine, University of Alabama at Birmingham, Birmingham, AL, USA

Published: December 2015

AI Article Synopsis

  • Reduced cerebral blood flow impairs cognitive functions and damages brain tissue, particularly in conditions like Alzheimer's disease, where the gliovascular unit struggles to regulate blood flow effectively.
  • The study utilized dual imaging techniques to investigate how vascular amyloid deposits influenced the function of the gliovascular unit in a mouse model of Alzheimer's, revealing that these deposits disrupt the connection between astrocytes and blood vessel walls.
  • Results indicated that while astrocytes can still release substances that affect blood flow, the presence of vascular amyloid makes blood vessels more rigid, leading to diminished vascular responses in affected areas compared to unaffected segments.

Article Abstract

Reduced cerebral blood flow impairs cognitive function and ultimately causes irreparable damage to brain tissue. The gliovascular unit, composed of neural and vascular cells, assures sufficient blood supply to active brain regions. Astrocytes, vascular smooth muscle cells, and pericytes are important players within the gliovascular unit modulating vessel diameters. While the importance of the gliovascular unit and the signals involved in regulating local blood flow to match neuronal activity is now well recognized, surprisingly little is known about this interface in disease. Alzheimer's disease is associated with reduced cerebral blood flow. Here, we studied how the gliovascular unit is affected in a mouse model of Alzheimer's disease, using a combination of ex vivo and in vivo imaging approaches. We specifically labelled vascular amyloid in living mice using the dye methoxy-XO4. We elicited vessel responses ex vivo using either pharmacological stimuli or cell-specific calcium uncaging in vascular smooth muscle cells or astrocytes. Multi-photon in vivo imaging through a cranial window allowed us to complement our ex vivo data in the presence of blood flow after label-free optical activation of vascular smooth muscle cells in the intact brain. We found that vascular amyloid deposits separated astrocyte end-feet from the endothelial vessel wall. High-resolution 3D images demonstrated that vascular amyloid developed in ring-like structures around the vessel circumference, essentially forming a rigid cast. Where vascular amyloid was present, stimulation of astrocytes or vascular smooth muscle cells via ex vivo Ca(2+) uncaging or in vivo optical activation produced only poor vascular responses. Strikingly, vessel segments that were unaffected by vascular amyloid responded to the same extent as vessels from age-matched control animals. We conclude that while astrocytes can still release vasoactive substances, vascular amyloid deposits render blood vessels rigid and reduce the dynamic range of affected vessel segments. These results demonstrate a mechanism that could account in part for the reduction in cerebral blood flow in patients with Alzheimer's disease.media-1vid110.1093/brain/awv327_video_abstractawv327_video_abstract.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5006220PMC
http://dx.doi.org/10.1093/brain/awv327DOI Listing

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