Table of Contents
ISRN Cell Biology
Volume 2012, Article ID 917167, 12 pages
Review Article

Senescence-Accelerated Mice P8: A Tool to Study Brain Aging and Alzheimer's Disease in a Mouse Model

Unitat de Farmacologia i Farmacognòosia, Facultat de Farmàcia, Institut de Biomedicina (IBUB), Universitat de Barcelona y Centros de Investigación Biomédica en Red de Enfermedades Neurodegenerativas (CIBERNED), Nucli Universitari de Pedralbes, 08028 Barcelona, Spain

Received 23 September 2012; Accepted 15 October 2012

Academic Editors: A. Chiarini, E. Kolettas, and D. Scholz

Copyright © 2012 Mercè Pallàs. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


The causes of aging remain unknown, but they are probably intimately linked to a multifactorial process that affects cell networks to varying degrees. Although a growing number of aging and Alzheimer’s disease (AD) animal models are available, a more comprehensive and physiological mouse model is required. In this context, the senescence-accelerated mouse prone 8 (SAMP8) has a number of advantages, since its rapid physiological senescence means that it has about half the normal lifespan of a rodent. In addition, according to data gathered over the last five years, some of its behavioral traits and histopathology resemble AD human dementia. SAMP8 has remarkable pathological similarities to AD and may prove to be an excellent model for acquiring more in-depth knowledge of the age-related neurodegenerative processes behind brain senescence and AD in particular. We review these facts and particularly the data on parameters related to neurodegeneration. SAMP8 also shows signs of aging in the immune, vascular, and metabolic systems, among others.