Neurochemical Research

, Volume 34, Issue 4, pp 639–659

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

ORIGINAL PAPER

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
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Abstract

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.

Keywords

Animal modelNeurodegeneration modelSenescence-accelerated mouse (SAM)SAMSAMP8SAMP10SAMR1AgingAccelerated senescenceLifespanGenetic profileBehaviorNeurobiologyDeficits in learning and memoryEmotional disordersCircadian rhythmAnxietyReduced anxiety-like behavior, depressive behaviorPassive avoidance testActive avoidance testMorris water maze testRadial maze testTail suspension testNeuropathologyNeurochemistryNeurotransmitterBrain atrophyBlood-brain barrier (BBB)Neurodegenerative disordersAgerelated pathologiesAlzheimer’s diseaseOxidative stressMitochondrial dysfunctionGene expressionProteomicsLTP

Copyright information

© Springer Science+Business Media, LLC 2009

Authors and Affiliations

  1. 1.The Council for SAM ResearchKyotoJapan