Publication: Unaltered prion disease in mice lacking developmental endothelial locus–1
Unaltered prion disease in mice lacking developmental endothelial locus–1
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Zhu, C., Li, Z., Li, B., Pfammatter, M., Hornemann, S., & Aguzzi, A. (2019). Unaltered prion disease in mice lacking developmental endothelial locus–1. Neurobiology of Aging, 76, 208–213. https://doi.org/10.1016/j.neurobiolaging.2019.01.003
Abstract
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Abstract
Progression of prion diseases is driven by the accumulation of prions in the brain. Ablation of microglia or deletion of the eat-me-signal, milk-fat globule epidermal growth factor VIII (Mfge8), accelerates prion pathogenesis, suggesting that microglia defend the brain by phagocytosing prions. Similar to Mfge8, developmental endothelial locus–1 (Del-1) is a secreted protein that acts as an opsonin bridging phagocytes and apoptotic cells to facilitate phagocytosis. We therefore asked whether Del-1 might play a role in controlling prion
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- Zhu, Caihong
- Li, Zhihao
- Li, Bei
- Pfammatter, Manuela
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Zhu, C., Li, Z., Li, B., Pfammatter, M., Hornemann, S., & Aguzzi, A. (2019). Unaltered prion disease in mice lacking developmental endothelial locus–1. Neurobiology of Aging, 76, 208–213. https://doi.org/10.1016/j.neurobiolaging.2019.01.003
