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Alzheimer's disease (AD), the most common neurodegenerative disorder, goes along with extracellular amyloid‐β (Aβ) deposits. The cognitive decline observed during AD progression correlates with damaged spines, dendrites and synapses in hippocampus and cortex. Numerous studies have shown that Aβ 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 Aβ toxicity.
|Item Type:||Journal Article, refereed, original work|
|Communities & Collections:||04 Faculty of Medicine > Brain Research Institute|
|DDC:||570 Life sciences; biology|
610 Medicine & health
|Deposited On:||04 Jan 2011 09:16|
|Last Modified:||27 Nov 2013 18:47|
|Free access at:||PubMed ID. An embargo period may apply.|
|Citations:||Web of Science®. Times Cited: 96|
Scopus®. Citation Count: 101
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