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Permanent URL to this publication: http://dx.doi.org/10.5167/uzh-39973

Calella, A M; Farinelli, M; Nuvolone, M; Mirante, O; Moos, R; Falsig, J; Mansuy, I M; Aguzzi, A (2010). Prion protein and Abeta-related synaptic toxicity impairment. EMBO Molecular Medicine, 2(8):306-314.

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Alzheimer's disease (AD), the most common neurodegenerative disorder, goes along with extracellular amyloid-beta (Abeta) deposits. The cognitive decline observed during AD progression correlates with damaged spines, dendrites and synapses in hippocampus and cortex. Numerous studies have shown that Abeta oligomers, both synthetic and derived from cultures and AD brains, potently impair synaptic structure and functions. The cellular prion protein (PrP(C)) was proposed to mediate this effect. We report that ablation or overexpression of PrP(C) had no effect on the impairment of hippocampal synaptic plasticity in a transgenic model of AD. These findings challenge the role of PrP(C) as a mediator of Abeta toxicity.

Item Type:Journal Article, refereed, original work
Communities & Collections:04 Faculty of Medicine > University Hospital Zurich > Institute of Neuropathology
DDC:570 Life sciences; biology
610 Medicine & health
Deposited On:19 Jan 2011 13:24
Last Modified:27 Nov 2013 21:52
Free access at:PubMed ID. An embargo period may apply.
Publisher DOI:10.1002/emmm.201000082
PubMed ID:20665634
Citations:Web of Science®. Times Cited: 99
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Scopus®. Citation Count: 102

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