Research Models

Senescence Accelerated Mouse (SAMP8)

Synonyms: SAMP-8, SAM-P/8, SAM-P8


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Species: Mouse
Modification: Spontaneous
Disease Relevance: Alzheimer's Disease
Strain Name: N/A
Genetic Background: AKR/J, suspected outbreeding to unknown line
Availability: Envigo (formerly Harlan): SAMP8-TaHsd


The Senescence Accelerated Mouse-Prone 8 (SAMP8) is a naturally occuring mouse line that displays a phenotype of accelerated aging. While maintaining an inbred AKR/J line in the early 1970's, researchers at Kyoto University became aware that some of the progeny exhibited a moderate to severe degree of activity loss, hair loss, lordokyphosis and early death. Several lines of senescence accelrated animals were established (SAM-P/1, SAM-P/2, SAM-P/3, and SAM-P/4) along with several lines of senescence resistant strains (with normal aging). The SAMP8 line is derived from the SAM-P/2 line.

The SAMP mice, including SAMP8, have been widely used in aging research to study phenotypes such as immune dysfunction, osteoporosis, and brain atrophy. The mice have apparently normal early development with no evidence of growth retardation. Despite intense characterization of SAMP strains, the genes responsible for the accelerated senescence and pathologic changes remain largely unknown.


Age-associated increase in hippocampal Aβ from four to twelve months, but no plaque-like structures by Congo red or thioflavine S. Spongiform degeneration: vacuoles of various size in the neuropil in the brain stem (Yagi et al., 1989). Microglial cell proliferation (Amano et al., 1995). Degeneration of dopamine neurons in the substantia nigra and noradrenaline neurons in the locus coeruleus (Karasawa et al., 1997).


Age-associated behavioral impairments including learning and memory difficulties (Miyamoto et al., 1986), emotional disorders, such as reduced anxiety-like behavior and depressive behavior (Miyamoto et al., 1992) and altered circadian rhythms of spontaneous motor activity and water consumption (Miyamoto, 1997).

Last Updated: 25 Nov 2019


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Paper Citations

  1. . Spontaneous spongy degeneration of the brain stem in SAM-P/8 mice, a newly developed memory-deficient strain. J Neuropathol Exp Neurol. 1989 Sep;48(5):577-90. PubMed.
  2. . Increased expression of cathepsins E and D in reactive microglial cells associated with spongiform degeneration in the brain stem of senescence-accelerated mouse. Exp Neurol. 1995 Dec;136(2):171-82. PubMed.
  3. . Immunocytochemical study of catecholaminergic neurons in the senescence-accelerated mouse (SAM-P8) brain. J Neural Transm. 1997;104(11-12):1267-75. PubMed.
  4. . Age-related changes in learning and memory in the senescence-accelerated mouse (SAM). Physiol Behav. 1986;38(3):399-406. PubMed.
  5. . Senescence-accelerated mouse (SAM): age-related reduced anxiety-like behavior in the SAM-P/8 strain. Physiol Behav. 1992 May;51(5):979-85. PubMed.
  6. . Characteristics of age-related behavioral changes in senescence-accelerated mouse SAMP8 and SAMP10. Exp Gerontol. 1997 Jan-Apr;32(1-2):139-48. PubMed.

External Citations

  1. Envigo (formerly Harlan): SAMP8-TaHsd

Further Reading


  1. . Differential gene expression profiles in the hippocampus of senescence-accelerated mouse. Neurobiol Aging. 2007 Apr;28(4):497-506. PubMed.
  2. . Hyperphosphorylation of microtubule-associated protein tau in senescence-accelerated mouse (SAM). Mech Ageing Dev. 2005 Dec;126(12):1300-4. PubMed.
  3. . Genetic analysis of learning and memory deficits in senescence-accelerated mouse (SAM). Physiol Behav. 2005 Mar 31;84(4):505-10. PubMed.
  4. . The senescence-accelerated prone mouse (SAMP8): a model of age-related cognitive decline with relevance to alterations of the gene expression and protein abnormalities in Alzheimer's disease. Exp Gerontol. 2005 Oct;40(10):774-83. PubMed.
  5. . Quantitative proteomics analysis of specific protein expression and oxidative modification in aged senescence-accelerated-prone 8 mice brain. Neuroscience. 2004;126(4):915-26. PubMed.
  6. . Efflux of human and mouse amyloid beta proteins 1-40 and 1-42 from brain: impairment in a mouse model of Alzheimer's disease. Neuroscience. 2003;121(2):487-92. PubMed.
  7. . Cholinergic deficits in the septal-hippocampal pathway of the SAM-P/8 senescence accelerated mouse. Brain Res. 2003 Mar 14;966(1):150-6. PubMed.
  8. . Antibody to beta-amyloid protein increases acetylcholine in the hippocampus of 12 month SAMP8 male mice. Life Sci. 2003 Jun 20;73(5):555-62. PubMed.
  9. . Age-related deterioration of ability of acquisition in memory and learning in senescence accelerated mouse: SAM-P/8 as an animal model of disturbances in recent memory. Brain Res. 1988 Nov 22;474(1):86-93. PubMed.
  10. . Site-directed antisense oligonucleotide decreases the expression of amyloid precursor protein and reverses deficits in learning and memory in aged SAMP8 mice. Peptides. 2000 Dec;21(12):1769-75. PubMed.
  11. . Behavioral characteristics of the SAM-P/8 strain in Sidman active avoidance task. Brain Res. 1989 Sep 25;498(1):195-8. PubMed.
  12. . Early onset of age-related impairment of aversive and appetitive learning in the SAM-P/8 mouse. J Gerontol. 1992 Mar;47(2):B52-9. PubMed.
  13. . The behavioral, pathological and therapeutic features of the senescence-accelerated mouse prone 8 strain as an Alzheimer's disease animal model. Ageing Res Rev. 2014 Jan;13:13-37. Epub 2013 Nov 21 PubMed.