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Neurological disorders

Eaten alive!

Nature Reviews Neuroscience volume 14, page 816 (2013)Cite this article

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In areas of the ischaemic brain in which the interruption of blood supply is most pronounced, rapid neuronal death ensues owing to energy depletion, but in surrounding areas, there is a delayed cell loss, which offers an opportunity for therapeutic intervention. Previous studies have shown that viable neurons exposed to toxic stimuli at sublethal levels can display the 'eat me' signal phosphatidylserine (PS), which induces their phagocytosis by macrophages. After ischaemia, neurons in the peri-infarct area have been shown to display PS at levels that peak after 3 days.

The PS signal is recognized by the phagocytic proteins Mer receptor tyrosine kinase (MERTK) and milk fat globule EGF-like factor 8 (MFGE8; also known as lactadherin), which are upregulated in brain macrophages in response to inflammation. Here, the authors showed that MERTK and MFGE8 were temporarily upregulated in rodent brain macrophages 3–7 days after transient, focal brain ischaemia and that peak expression of these proteins coincided with macrophage activation.

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References

  1. Neher, J. J. et al. Phagocytosis executes delayed neuronal death after focal brain ischemia. Proc. Natl Acad. Sci. USA http://dx.doi.org/10.1073/pnas.1308679110 (2013)

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Authors
  1. Monica Hoyos Flight
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Flight, M. Eaten alive!. Nat Rev Neurosci 14, 816 (2013). https://doi.org/10.1038/nrn3630

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