The Transcellular Spread of Cytosolic Amyloids, Prions, and Prionoids

被引:352
作者
Aguzzi, Adriano [1 ]
Rajendran, Lawrence [2 ]
机构
[1] Univ Zurich Hosp, Inst Neuropathol, CH-8091 Zurich, Switzerland
[2] Univ Zurich, CH-8008 Zurich, Switzerland
关键词
FIBROBLAST-GROWTH-FACTOR; ALPHA-SYNUCLEIN DEPENDS; CELL-DERIVED EXOSOMES; PARKINSONS-DISEASE; INTRACELLULAR TRAFFICKING; ALZHEIMERS-DISEASE; PROTEIN SECRETION; FIBRIL FORMATION; MAMMALIAN-CELLS; PLASMA-MEMBRANE;
D O I
10.1016/j.neuron.2009.12.016
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
Recent reports indicate that a growing number of intracellular proteins are not only prone to pathological aggregation but can also be released and "infect" neighboring cells. Therefore, many complex diseases may obey a simple model of propagation where the penetration of seeds into hosts determines spatial spread and disease progression. We term these proteins prionoids, as they appear to infect their neighbors just like prions-but how can bulky protein aggregates be released from cells and how do they access other cells? The widespread existence of such prionoids raises unexpected issues that question our understanding of basic cell biology.
引用
收藏
页码:783 / 790
页数:8
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