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EMBO Mol Med. 2010 Aug;2(8):306-14. doi: 10.1002/emmm.201000082.

Prion protein and Abeta-related synaptic toxicity impairment.

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  • 1Institute of Neuropathology, University Hospital Zürich, Zürich, Switzerland.

Abstract

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.

PMID:
20665634
PMCID:
PMC2962809
DOI:
10.1002/emmm.201000082
[PubMed - indexed for MEDLINE]
Free PMC Article
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