RT Journal Article
T1 Cellular prion protein modulates β-amyloid deposition in aged APP/PS1 transgenic mice
A1 Ordóñez Gutiérrez, Lara
A1 Torres, Juan María
A1 Gavín, Rosalina
A1 Antón, Marta
A1 Arroba Espinosa, Ana Isabel
A1 Espinosa, Juan Carlos
A1 Vergara, Cristina
A1 Río, José A. del
A1 Wandosell, Francisco
AB Alzheimer’s disease and prion diseases are neuropathological disorders that are caused by abnormal processing and aggregation of amyloid and prion proteins. Interactions between amyloid precursor protein (APP) and PrPc proteins have been described at the neuron level. Accordingly to this putative interaction, we investigated whether b-amyloid accumulation may affect prion infectivity and, conversely, whether different amounts of PrP may affect b-amyloid accumulation. For this purpose, we used the APPswe/PS1dE9 mouse line, a common model of Alzheimer’s disease, crossed with mice that either overexpress (Tga20) or that lack prion protein (knock-out) to generate mice that express varying amounts of prion protein and deposit b-amyloid. On these mouse lines, we investigated the influence of each protein on the evolution of both diseases. Our results indicated that although the presence of APP/PS1 and b-amyloid accumulation had no effect on prion infectivity, the accumulation of b-amyloid deposits was dependent on PrPc, whereby increasing levels of prion protein were accompanied by a significant increase in b-amyloid aggregation associated with aging.
PB Elsevier
SN 0197-4580
YR 2013
FD 2013
LK https://hdl.handle.net/20.500.14352/95898
UL https://hdl.handle.net/20.500.14352/95898
LA eng
NO Ordóñez-Gutiérrez L, Torres JM, Gavín R, Antón M, Arroba-Espinosa AI, Espinosa JC, Vergara C, Del Río JA, Wandosell F. Cellular prion protein modulates β-amyloid deposition in aged APP/PS1 transgenic mice. Neurobiol Aging. 2013 Dec;34(12):2793-804. doi: 10.1016/j.neurobiolaging.2013.05.019. Epub 2013 Jul 4. PMID: 23831375.
DS Docta Complutense
RD 16 abr 2025