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Aguzzi, A; Rajendran, L (2009). The transcellular spread of cytosolic amyloids, prions, and prionoids. Neuron, 64(6):783-790.

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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.


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Additional indexing

Item Type:Journal Article, refereed, further contribution
Communities & Collections:04 Faculty of Medicine > Psychiatric University Hospital Zurich > Division of Psychiatric Research and Clinic for Psychogeriatric Medicine
04 Faculty of Medicine > University Hospital Zurich > Institute of Neuropathology
Dewey Decimal Classification:570 Life sciences; biology
610 Medicine & health
Deposited On:24 Jan 2011 20:13
Last Modified:28 Oct 2014 16:00
Free access at:Publisher DOI. An embargo period may apply.
Publisher DOI:10.1016/j.neuron.2009.12.016
PubMed ID:20064386

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