Anatomy and Cell Biology Publications
Document Type
Article
Publication Date
3-27-2019
Issue
11
Journal
Frontiers in Aging Neuroscience
Volume
11
First Page
1
Last Page
9
URL with Digital Object Identifier
https://doi.org/10.3389/fnagi.2019.00047
Abstract
Aberrations in brain microcirculation and the associated increase in blood-brain-barrier (BBB) permeability in addition to neuroinflammation and A beta deposition observed in Alzheimer's disease (AD) and ischemia have gained considerable attention recently. However, the role of microvascular homeostasis as a pathogenic substrate to disturbed microperfusion as well as an overlapping etiologic mechanism between AD and ischemia has not been thoroughly explored. In this study, we employ temporal histopathology of cerebral vasculature in a rat model of beta-amyloid (A beta) toxicity and endothelin-1 induced-ischemia (ET1) to investigate the panorama of cerebral pathology and the protein expression on d1, d7, and d28 post-injury. The combination of A beta and ET1 pathological states leads to an alteration in microvascular anatomy, texture, diameter, density, and protein expression, in addition to disturbed vessel-matrix-connections, inter-compartmental water exchange and basement membrane profile within the lesion epicenter localized in the striatum of A beta+ET1 brains compared to A beta and ET1 rats. We conclude that the neural microvascular network, in addition to the neural tissue, is not only sensitive to structural deterioration but also serves as an underlying vascular etiology between ischemia and AD pathologies. Such investigation can provide prospects to appreciate the interrelationships between structure and responses of cerebral microvasculature and to provide a venue for vascular remodeling as a new treatment strategy.
Creative Commons License
This work is licensed under a Creative Commons Attribution 4.0 License.
Notes
First published by Frontiers Media on March 27, 2019.
Amtul, Zareen; Yang, Jun; Lee, Ting-Yim; Cechetto, David F. (2019). Pathological Changes in Microvascular Morphology, Density, Size and Responses Following Comorbid Cerebral Injury. Frontiers in Aging Neuroscience, issue 11.pp1-9