Neurochemical Research

, Volume 34, Issue 4, pp 639–659

Senescence-Accelerated Mouse (SAM) with Special References to Neurodegeneration Models, SAMP8 and SAMP10 Mice


DOI: 10.1007/s11064-009-9922-y

Cite this article as:
Takeda, T. Neurochem Res (2009) 34: 639. doi:10.1007/s11064-009-9922-y


The SAM strains, a group of related inbred strains consisting of senescence-prone inbred strains (SAMP) and senescence-resistant inbred strains (SAMR), have been successfully developed by selective inbreeding of the AKR/J strain of mice donated by the Jackson laboratory in 1968. The characteristic feature of aging common to the SAMP and SAMR is accelerated senescence and normal aging, respectively. Furthermore, SAMP and SAMR strains of mice manifest various pathobiological phenotypes spontaneously. Among SAMP strains, SAMP8 and SAMP10 mice show age-related behavioral deterioration such as deficits in learning and memory, emotional disorders (reduced anxiety-like behavior and depressive behavior) and altered circadian rhythm associated with certain pathological, biochemical and pharmacological changes. Here, the previous and recent literature on SAM mice are reviewed with an emphasis on SAMP8 and SAMP10 mice. A spontaneous model like SAM with distinct advantages over the gene-modified model is hoped by investigators to be used more widely as a biogerontological resource to explore the etiopathogenesis of accelerated senescence and neurodegenerative disorders.


Animal model Neurodegeneration model Senescence-accelerated mouse (SAM) SAM SAMP8 SAMP10 SAMR1 Aging Accelerated senescence Lifespan Genetic profile Behavior Neurobiology Deficits in learning and memory Emotional disorders Circadian rhythm Anxiety Reduced anxiety-like behavior, depressive behavior Passive avoidance test Active avoidance test Morris water maze test Radial maze test Tail suspension test Neuropathology Neurochemistry Neurotransmitter Brain atrophy Blood-brain barrier (BBB) Neurodegenerative disorders Agerelated pathologies Alzheimer’s disease Aβ Oxidative stress Mitochondrial dysfunction Gene expression Proteomics LTP 

Copyright information

© Springer Science+Business Media, LLC 2009

Authors and Affiliations

  1. 1.The Council for SAM ResearchKyotoJapan

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