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Updated: Dec 22, 2025

A Middle Cerebral Artery Occlusion Technique for Inducing Post-stroke Depression in Rats

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Published on: May 22, 2019

COVID-19-Related Stroke.

David C Hess¹, Wael Eldahshan², Elizabeth Rutkowski³

¹Department of Neurology, Medical College of Georgia, Augusta University, Augusta, GA, 30912, USA. Dhess@augusta.edu.

Translational Stroke Research

|May 8, 2020

Summary

This summary is machine-generated.

COVID-19 can cause stroke due to hypercoagulability, potentially linked to sepsis-induced coagulopathy. SARS-CoV-2 virus interaction with ACE2 may disrupt the renin-angiotensin system, favoring harmful pathways that lead to stroke.

Keywords:

Angiotensin-converting enzyme 2 (ACE2)COVID-19 Coagulopathy SARS-CoV-2 Sepsis Stroke

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A Thrombotic Stroke Model Based On Transient Cerebral Hypoxia-ischemia

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Area of Science:

Neurology
Virology
Cardiovascular Science

Background:

COVID-19 is linked to neurological complications, notably stroke.
Hypercoagulability in COVID-19 patients resembles sepsis-induced coagulopathy, increasing stroke risk.

Discussion:

SARS-CoV-2 binds to ACE2 on brain cells, disrupting the renin-angiotensin system (RAS).
This interaction may shift the balance towards the pro-inflammatory and vasoconstrictive ACE1/angiotensin II axis, promoting stroke.
ACE2 depletion by SARS-CoV-2 could be a mechanism for COVID-19-related neurological injury.

Key Insights:

COVID-19-associated stroke may stem from viral disruption of the ACE2/RAS pathway.
Understanding this mechanism provides rationale for specific stroke treatments in COVID-19 patients.

Outlook:

Continued use of tissue plasminogen activator for COVID-19 stroke is supported.
Low molecular weight heparinoids show promise in mitigating thrombosis and mortality in sepsis-induced coagulopathy, including COVID-19 cases.