title: Prion protein and Abeta-related synaptic toxicity impairment.
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.
authors.affiliation: Institute of Neuropathology, University Hospital Zürich, Zürich, Switzerland.
authors.forename: Anna Maria
authors.initials: AM
authors.lastname: Calella
authors.forename: Mélissa
authors.initials: M
authors.lastname: Farinelli
authors.forename: Mario
authors.initials: M
authors.lastname: Nuvolone
authors.forename: Osvaldo
authors.initials: O
authors.lastname: Mirante
authors.forename: Rita
authors.initials: R
authors.lastname: Moos
authors.forename: Jeppe
authors.initials: J
authors.lastname: Falsig
authors.forename: Isabelle M
authors.initials: IM
authors.lastname: Mansuy
authors.forename: Adriano
authors.initials: A
authors.lastname: Aguzzi
mesh_terms: D000544:Alzheimer Disease / Q000473:pathology* / Q000503:physiopathology; D016229:Amyloid beta-Peptides / Q000378:metabolism*; D000818:Animals; D004195:Disease Models, Animal; D006624:Hippocampus / Q000473:pathology*; D006801:Humans; D051379:Mice; D008822:Mice, Transgenic; D011328:Prions / Q000235:genetics / Q000378:metabolism*; D013569:Synapses / Q000473:pathology*
chemical_list: D016229:Amyloid beta-Peptides; D011328:Prions