Stroke and Alzheimer's disease have distinct consequences on neurovascular function but synergize to increase amyloid deposition
- 1Oregon Health & Science University
Abstract
INTRODUCTION: We examined whether stroke induces chronic cerebrovascular dysfunction and thereby exacerbates A{beta} pathology. METHODS: We exposed Tg2576 mice to a transient mild subcortical ischemia and examined cerebrovascular function at chronic timepoints as well as reactive astrocytes and A{beta} deposition post-mortem. RESULTS: Baseline cerebral blood flow and cerebrovascular reactivity (CVR) are both influenced by anesthesia regimen. A{beta} strongly impairs CVR at earlier ages, while mild ischemia impairs CVR at later ages. Mild ischemia reduces neurovascular coupling more strongly than A{beta} and synergistically increases A{beta} deposition in Tg2576 mice. DISCUSSION: Stroke-induced cerebrovascular dysfunction and astrocyte reactivity persist for long periods after the injury. Although there is variability in the spatiotemporal progression of ischemia- and A{beta}-induced vascular impairments, they generally follow the pattern of Thal staging. Surprisingly, the ischemia+A{beta} group showed the least cerebrovascular dysfunction yet an exacerbation of A{beta} deposition, suggesting that these pathologies are connected but not tightly coupled.
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BibTeX
@misc{ismail2026stroke,
title = {{Stroke and Alzheimer's disease have distinct consequences on neurovascular function but synergize to increase amyloid deposition}},
author = {O. Ismail and S. S. Woodruff and B. Zimmerman and W. Zhang and T. L. Stackhouse and M. M. Pike and R. L. Woltjer and A. Mishra},
howpublished = {bioRxiv},
year = {2026},
month = aug,
doi = {10.64898/2026.08.29.746901},
url = {https://www.biorxiv.org/content/10.64898/2026.08.29.746901v1},
note = {CC BY-NC-ND},
}
RIS
TY - UNPB
TI - Stroke and Alzheimer's disease have distinct consequences on neurovascular function but synergize to increase amyloid deposition
AU - O. Ismail
AU - S. S. Woodruff
AU - B. Zimmerman
AU - W. Zhang
AU - T. L. Stackhouse
AU - M. M. Pike
AU - R. L. Woltjer
AU - A. Mishra
PY - 2026
DA - 2026/08/29
PB - bioRxiv
DO - 10.64898/2026.08.29.746901
UR - https://www.biorxiv.org/content/10.64898/2026.08.29.746901v1
AB - INTRODUCTION: We examined whether stroke induces chronic cerebrovascular dysfunction and thereby exacerbates A{beta} pathology. METHODS: We exposed Tg2576 mice to a transient mild subcortical ischemia and examined cerebrovascular function at chronic timepoints as well as reactive astrocytes and A{beta} deposition post-mortem. RESULTS: Baseline cerebral blood flow and cerebrovascular reactivity (CVR) are both influenced by anesthesia regimen. A{beta} strongly impairs CVR at earlier ages, while mild ischemia impairs CVR at later ages. Mild ischemia reduces neurovascular coupling more strongly than A{beta} and synergistically increases A{beta} deposition in Tg2576 mice. DISCUSSION: Stroke-induced cerebrovascular dysfunction and astrocyte reactivity persist for long periods after the injury. Although there is variability in the spatiotemporal progression of ischemia- and A{beta}-induced vascular impairments, they generally follow the pattern of Thal staging. Surprisingly, the ischemia+A{beta} group showed the least cerebrovascular dysfunction yet an exacerbation of A{beta} deposition, suggesting that these pathologies are connected but not tightly coupled.
ER -