Journal
EMBO MOLECULAR MEDICINE
Volume 2, Issue 8, Pages 306-314Publisher
WILEY
DOI: 10.1002/emmm.201000082
Keywords
Alzheimer's disease; amyloid; prion protein; synaptic plasticity
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Funding
- European Union
- Swiss National Research Foundation
- Novartis Foundation
- European Research Council
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Alzheimer's disease (AD), the most common neurodegenerative disorder, goes along with extracellular amyloid-beta (A beta) deposits. The cognitive decline observed during AD progression correlates with damaged spines, dendrites and synapses in hippocampus and cortex. Numerous studies have shown that A beta oligomers, both synthetic and derived from cultures and AD brains, potently impair synaptic structure and functions. The cellular prion protein (PrPc) was proposed to mediate this effect. We report that ablation or overexpression of PrPc had no effect on the impairment of hippocampal synaptic plasticity in a transgenic model of AD. These findings challenge the role of PrPc as a mediator of A beta toxicity.
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