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Review
. 2021 Apr 23;22(9):4405.
doi: 10.3390/ijms22094405.

Neuroinflammation in Post-Ischemic Neurodegeneration of the Brain: Friend, Foe, or Both?

Ryszard Pluta  1 , Sławomir Januszewski  1 , Stanisław J Czuczwar  2
Affiliations
Review

Neuroinflammation in Post-Ischemic Neurodegeneration of the Brain: Friend, Foe, or Both?

Ryszard Pluta et al. Int J Mol Sci. .

Abstract

One of the leading causes of neurological mortality, disability, and dementia worldwide is cerebral ischemia. Among the many pathological phenomena, the immune system plays an important role in the development of post-ischemic degeneration of the brain, leading to the development of neuroinflammatory changes in the brain. After cerebral ischemia, the developing neuroinflammation causes additional damage to the brain cells, but on the other hand it also plays a beneficial role in repair activities. Inflammatory mediators are sources of signals that stimulate cells in the brain and promote penetration, e.g., T lymphocytes, monocytes, platelets, macrophages, leukocytes, and neutrophils from systemic circulation to the brain ischemic area, and this phenomenon contributes to further irreversible ischemic brain damage. In this review, we focus on the issues related to the neuroinflammation that occurs in the brain tissue after ischemia, with particular emphasis on ischemic stroke and its potential treatment strategies.

Keywords: T lymphocytes; astrocytes; brain ischemia; leukocytes; macrophages; microglia; monocytes; neuroinflammation; neutrophils; platelets; stroke.

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Conflict of interest statement

The authors declare no conflict of interest.

Figures

Figure 1
Figure 1
There is a delicate balance between the beneficial and harmful effects of neuroinflammation in post-ischemic brain neurodegeneration. Some neuroinflammation phenomena are protective, such as phagocytosis, but others, such as pro-inflammatory mediators, are detrimental.
See this image and copyright information in PMC

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