Please use this identifier to cite or link to this item: http://hdl.handle.net/2445/125694
Title: Amyloid and tau pathology of familial Alzheimer's disease APP/PS1 mouse model in a senescence phenotype background (SAMP8)
Author: Porquet Costa, David
Andrés Benito, Pol
Griñán Ferré, Christian
Camins Espuny, Antoni
Ferrer, Isidro (Ferrer Abizanda)
Canudas Teixidó, Anna-Maria
Valle i Macià, Jaume del
Pallàs i Llibería, Mercè, 1964-
Keywords: Malaltia d'Alzheimer
Malalties neurodegeneratives
Alzheimer's disease
Neurodegenerative diseases
Issue Date: 8-Feb-2015
Publisher: Springer Verlag
Abstract: The amyloid precursor protein/presenilin 1 (APP/PS1) mouse model of Alzheimer's disease (AD) has provided robust neuropathological hallmarks of familial AD-like pattern at early ages, whereas senescence-accelerated mouse prone 8 (SAMP8) has a remarkable early senescence phenotype with pathological similarities to AD. The aim of this study was the investigation and characterization of cognitive and neuropathological AD markers in a novel mouse model that combines the characteristics of the APP/PS1 transgenic mouse model with a senescence-accelerated background of SAMP8 mice. Initially, significant differences were found regarding amyloid plaque formation and cognitive abnormalities. Bearing these facts in mind, we determined a general characterization of the main AD brain molecular markers, such as alterations in amyloid pathway, neuroinflammation, and hyperphosphorylation of tau in these mice along their lifetimes. Results from this analysis revealed that APP/PS1 in SAMP8 background mice showed alterations in the pathways studied in comparison with SAMP8 and APP/PS1, demonstrating that a senescence-accelerated background exacerbated the amyloid pathology and maintained the cognitive dysfunction present in APP/PS1 mice. Changes in tau pathology, including the activity of cyclin-dependent kinase 5 (CDK5) and glycogen synthase kinase 3 β (GSK3β), differs, but not in a parallel manner, with amyloid disturbances.
Note: Versió postprint del document publicat a: https://doi.org/10.1007/s11357-015-9747-3
It is part of: AGE, 2015, vol. 37, num. 1, p. 12
URI: http://hdl.handle.net/2445/125694
Related resource: https://doi.org/10.1007/s11357-015-9747-3
ISSN: 0161-9152
Appears in Collections:Articles publicats en revistes (Patologia i Terapèutica Experimental)
Articles publicats en revistes (Institut d'lnvestigació Biomèdica de Bellvitge (IDIBELL))

Files in This Item:
File Description SizeFormat 
647694.pdf3.61 MBAdobe PDFView/Open


Items in DSpace are protected by copyright, with all rights reserved, unless otherwise indicated.