Journal
INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
Volume 22, Issue 24, Pages -Publisher
MDPI
DOI: 10.3390/ijms222413442
Keywords
stroke; cell death; neuronal death; delayed neuronal death; selective neuronal loss; secondary neurodegeneration; phagocytosis; microglia; phagoptosis; ischemia
Funding
- Medical Research Council UK [MR/L010593]
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After a stroke, rapid necrosis of cells in the infarct occurs, followed by delayed loss of neurons due to microglial phagocytosis, which may be prevented by targeting phagocytic receptors on microglia.
After stroke, there is a rapid necrosis of all cells in the infarct, followed by a delayed loss of neurons both in brain areas surrounding the infarct, known as 'selective neuronal loss', and in brain areas remote from, but connected to, the infarct, known as 'secondary neurodegeneration'. Here we review evidence indicating that this delayed loss of neurons after stroke is mediated by the microglial phagocytosis of stressed neurons. After a stroke, neurons are stressed by ongoing ischemia, excitotoxicity and/or inflammation and are known to: (i) release find-me signals such as ATP, (ii) expose eat-me signals such as phosphatidylserine, and (iii) bind to opsonins, such as complement components C1q and C3b, inducing microglia to phagocytose such neurons. Blocking these factors on neurons, or their phagocytic receptors on microglia, can prevent delayed neuronal loss and behavioral deficits in rodent models of ischemic stroke. Phagocytic receptors on microglia may be attractive treatment targets to prevent delayed neuronal loss after stroke due to the microglial phagocytosis of stressed neurons.
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