Posted 28 May 2006

General Information

Mouse strain: Inbred AKR/J brothers/sisters led to 3 substrains labeled P for (accelerated senescence) prone and 3 substrains R for (senescence) resistant. From SAM-P/2 new strain SAM-P/8 was developed.

Phenotype

Neuropathological Analysis:

SAMP-8 has early onset, irreversible, severe deficits related to learning and memory (passive avoidance responses), but shows low incidence of senile amyloidosia (1).o 40-50% decrease in choline acetyltransferase (ChAT) activity (from 4-12 months) in 2/3 subregions of the hippocampus in the SAMP-8, but not the SAM-R1(resistant) strain.

Glucose accumulation normal at 1 month in SAMP-8 but decreases from 2-3 months and onward. Tyrosine accumulation unchanged from 1-5 months of age. The impairment of memory in mice at 2-3 months corresponds with the decrease in glucose but is not related to tyrosine.

There is also an increase amount of APP with cDNA sequence having 89.2% homology with human APP. No mutations similar to those reported in human familial AD were observed.

Availability

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References

Primary:

Yagi H, Katoh S, Akiguchi I, Takeda T. 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. 474 (1988), pp. 86-93. Abstract

Associated:

Cheng X-R, Zhou W-X, Zhang Y-X, Zhou D-S, Yang R-F, Chen L-F. Differential gene expression profiles in the hippocampus of senescence-accelerated mouse. Neurobiology Aging 2006 Mar 25; [Epub ahead of print]. Abstract

Canudas AM, Gutierrez-Cuesta J, Rodriguez MI, Acuna-Castroviejo D, Sureda FX, Camins A, Pallas M. Hyperphosphorylation of microtubule-associated protein tau in senescence-accelerated mouse (SAM). Mech Ageing Dev. 2005 Dec;126(12):1300-4. Abstract

Tomobe K, Isobe M, Okuma Y, Kitamura K, Oketani Y, Nomur Y. Genetic analysis of learning and memory deficits in senescence-accelerated mouse (SAM), Physiol Behav 84 (2005), pp. 505-510. Abstract

Butterfield DA, Poon HF. 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. Abstract

Poon HF, Castegena A, Farr SA, Thongboonkerd V, Lynn BC, Banks WA, Morley JE, Klein JB, Butterfield DA. Quantitative proteomics analysis of specific protein expression and oxidative modification in aged senescence-accelerated-prone 8 mice brain. Neuroscience 26 (2004), pp. 915-926. Abstract

Banks WA, Robinson SM, Verma S, Morley JE. 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. Abstract

Strong R, Reddyd V, Morley J E. Cholinergic deficits in the septal-hippocampal pathway of the SAM-P/8 senescence accelerated mouse. Brain Res. 2003 Mar 14;966(1):150-6. Abstract

Farr SA, Banks WA, Uezu K, Sano A, Gaskin, FS, Morley, JE. Antibody to ß-amyloid protein increases acetylcholine in the hippocampus of 12-month SAMP8 male mice. Life Sci 73 (2003), pp. 555-562. Abstract

Kumar VB, Vyas K, Franko M, Choudhary V, Buddhiraju C, Alvarez J, Morley JE. Molecular cloning, expression, and regulation of hippocampal amyloid precursor protein of senescence accelerated mouse (SAMP8).Biochem Cell Biol. 2001;79(1):57-67. Abstract

Kumar VB, Farr SA, Flood JF, Kamlesh V, Franko M, Banks WA, Morley JE 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. Abstract

Morley JE, Kumar VB, Bernardo AE, Farr SA, Uezu K, Tumosa N, Flood JF. Beta-amyloid precursor polypeptide in SAMP8 mice affects learning and memory. Peptides. 2000 Dec;21(12):1761-7. Abstract

Xiaolong W, Yongxiang Zh, Jinhuang Zh. Alzheimer's disease-related gene expression in the brain of senescence accelerated mouse. Neurosci Lett 268 (1999), pp. 139-142. Abstract

Takeda T. Senescence-accelerated mouse (SAM): a biogerontological resource in aging research. Neurobiol Aging 20 (1999) (2), pp. 105-110. Abstract

Wei X, Zhang Y, Zhou J. Alzheimer's disease-related gene expression in the brain of senescence accelerated mouse. Neurosci Lett. 1999 Jun 25;268(3):139-42. Abstract

Tomofumi N, Jun AT, Yasuhisa F, Hiromi F, Binghua Z, Yasumitsu N et al. An early stage mechanism of the age-associated mitochondrial dysfunction in the brain of SAMP8 mice; an age-associated neurodegeneration animal model. Neurosci Lett 254 (1998), pp. 69-72. Abstract

Kato A, Fukunari A, Sakai Y, Nakajima T. Prevention of amyloid-like deposition by a selective prolyl endopeptidase inhibitor, Y-29794, in senescence-accelerated mouse.J Pharmacol Exp Ther. 1997 Oct;283(1):328-35. Abstract

Jeong SJ, Kim K, Suh YH. Age-related changes in the expression of Alzheimer's beta APP in the brain of senescence accelerated mouse (SAM)-P/10. Neuroreport. 1997 May 6;8(7):1733-7. Abstract

Fujibayashi Y, Waki A, Wada K, Ueno M, Magata Y, Yonekura Y, Konishi J, Takeda T, Yokoyama A. Differential aging pattern of cerebral accumulation of radiolabeled glucose and amino acid in the senescence accelerated mouse (SAM), a new model for the study of memory impairment. Biol Pharm Bull. 17:102-5, l994. Abstract

Kuo H, Ingram DK, Walker LC, Tian M, Hengemihle JM, Jucker M. Similarities in the age-related hippocampal deposition of periodic acid-schiff-positive granules in the senescence-accelerated mouse P8 and C57BL/6 mouse strains. Neuroscience. 1996 Oct;74(3):733-40. Abstract

Strain JF, Morley JE. Age related impairment of aversive and appetitive learning in the SAMP P/8 mouse strain. A model of dementia of early onset. J Gerontol Biol Sci 47 (1992), pp. B52-B59. Abstract

Ohta, T. Hirano, H. Yagi, S. Tanaka, M. Hosokawa and T. Takeda. Behavioral characteristics of the SAM-P/8 strain in Sidman active avoidance task. Brain Res 498 (1989), pp. 195-198. Abstract