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Published in: Current Neurology and Neuroscience Reports 8/2023

03-07-2023 | Stroke

Neuroinflammation in Acute Ischemic and Hemorrhagic Stroke

Authors: Diana L. Alsbrook, Mario Di Napoli, Kunal Bhatia, José Biller, Sasan Andalib, Archana Hinduja, Roysten Rodrigues, Miguel Rodriguez, Sara Y. Sabbagh, Magdy Selim, Maryam Hosseini Farahabadi, Alibay Jafarli, Afshin A. Divani

Published in: Current Neurology and Neuroscience Reports | Issue 8/2023

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Abstract

Purpose of Review

This review aims to provide an overview of neuroinflammation in ischemic and hemorrhagic stroke, including recent findings on the mechanisms and cellular players involved in the inflammatory response to brain injury.

Recent Findings

Neuroinflammation is a crucial process following acute ischemic stroke (AIS) and hemorrhagic stroke (HS). In AIS, neuroinflammation is initiated within minutes of the ischemia onset and continues for several days. In HS, neuroinflammation is initiated by blood byproducts in the subarachnoid space and/or brain parenchyma. In both cases, neuroinflammation is characterized by the activation of resident immune cells, such as microglia and astrocytes, and infiltration of peripheral immune cells, leading to the release of pro-inflammatory cytokines, chemokines, and reactive oxygen species. These inflammatory mediators contribute to blood-brain barrier disruption, neuronal damage, and cerebral edema, promoting neuronal apoptosis and impairing neuroplasticity, ultimately exacerbating the neurologic deficit. However, neuroinflammation can also have beneficial effects by clearing cellular debris and promoting tissue repair. The role of neuroinflammation in AIS and ICH is complex and multifaceted, and further research is necessary to develop effective therapies that target this process. Intracerebral hemorrhage (ICH) will be the HS subtype addressed in this review.

Summary

Neuroinflammation is a significant contributor to brain tissue damage following AIS and HS. Understanding the mechanisms and cellular players involved in neuroinflammation is essential for developing effective therapies to reduce secondary injury and improve stroke outcomes. Recent findings have provided new insights into the pathophysiology of neuroinflammation, highlighting the potential for targeting specific cytokines, chemokines, and glial cells as therapeutic strategies.
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Metadata
Title
Neuroinflammation in Acute Ischemic and Hemorrhagic Stroke
Authors
Diana L. Alsbrook
Mario Di Napoli
Kunal Bhatia
José Biller
Sasan Andalib
Archana Hinduja
Roysten Rodrigues
Miguel Rodriguez
Sara Y. Sabbagh
Magdy Selim
Maryam Hosseini Farahabadi
Alibay Jafarli
Afshin A. Divani
Publication date
03-07-2023
Publisher
Springer US
Published in
Current Neurology and Neuroscience Reports / Issue 8/2023
Print ISSN: 1528-4042
Electronic ISSN: 1534-6293
DOI
https://doi.org/10.1007/s11910-023-01282-2