Overexpression of cellular prion protein (PrPC ) prevents cognitive dysfunction and apoptotic neuronal cell death induced by amyloid-β (Aβ1–40 ) administration in mice

Highlights ► Overexpression of PrPC prevents Aβ1–40 -induced spatial learning and memory deficits. ► Overexpression of PrPC prevents Aβ1–40 -induced hippocampal cell damage. ► PrPC inhibits programed cell death mechanisms activated by Aβ1–40 peptide in vivo.

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Bibliographische Detailangaben
Veröffentlicht in:	Neuroscience 2012-07, Vol.215, p.79-89
Hauptverfasser:	Rial, D, Piermartiri, T.C, Duarte, F.S, Tasca, C.I, Walz, R, Prediger, R.D
Format:	Artikel
Sprache:	eng
Schlagworte:	Alzheimer’s disease Amyloid beta-Peptides - administration & dosage amyloid-β protein Analysis of Variance Animals apoptosis Apoptosis - drug effects bcl-2-Associated X Protein - metabolism Caspase 3 - metabolism caspase-3 Cell Survival - drug effects cellular prion protein (PrPC) Cognition Disorders - chemically induced Cognition Disorders - pathology Gene Expression Regulation - drug effects Hippocampus - pathology In Vitro Techniques learning and memory Male Maze Learning - drug effects Mice Mice, Inbred C57BL Mice, Knockout Neurology Neurons - drug effects Peptide Fragments - administration & dosage Prion Proteins Prions - genetics Prions - metabolism Propidium Proto-Oncogene Proteins c-bcl-2 - metabolism Reaction Time - drug effects Tetrazolium Salts Thiazoles
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Beschreibung
Zusammenfassung:	Highlights ► Overexpression of PrPC prevents Aβ1–40 -induced spatial learning and memory deficits. ► Overexpression of PrPC prevents Aβ1–40 -induced hippocampal cell damage. ► PrPC inhibits programed cell death mechanisms activated by Aβ1–40 peptide in vivo.
ISSN:	0306-4522 1873-7544
DOI:	10.1016/j.neuroscience.2012.04.034