Age-related changes in learning and memory in the senescence-accelerated mouse (SAM)

Miyamoto, Masaomi; Kiyota, Yoshihiro; Yamazaki, Naoki; Nagaoka, Akinobu; Matsuo, Takao; Nagawa, Yuji; Takeda, Takeshi

doi:10.1016/0031-9384(86)90112-5

Cited by 354 publications

(166 citation statements)

References 20 publications

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“…Consequently, SAMP8 has been extensively phenotyped for behavioral abnormalities. The results indicate that cognitive abnormalities in this model are abundant and the mimic behavioral/cognitive deficits observed in AD patients and other transgenic models [50,100,101]. SAMP8 also demonstrated impairment of aversive and appetitive training [101].…”

Section: Behavioral Characteristicssupporting

confidence: 51%

“…SAMP8 presented not only similar characteristics to aged humans, such as shorter lifespan, lordosis, reduced physical activity, and hair loss [46,47], but also some neurodegenerative features, such as early onset of learning and memory deficits [48], altered emotions and abnormal circadian rhythm [49,50], neuronal cell loss [51], and reduction in the release of neurotransmitters in the brain [52,53]. Besides, impairment of mitochondrial functions has been shown in SAMP8 brain at a relatively early age compared to SAMR1 mice [29].…”

Section: Samp8 Postulated As An Early Model Of Alzheimer's Diseasementioning

confidence: 96%

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

Pallàs

2012

ISRN Cell Biology

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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.

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Section: Behavioral Characteristicssupporting

confidence: 51%

Section: Samp8 Postulated As An Early Model Of Alzheimer's Diseasementioning

confidence: 96%

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

Pallàs

2012

ISRN Cell Biology

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“…Carp. Fax j1 718 698 3803. e-mail carpri!nysomr.emi.com The brain is also the key organ involved in a mouse model of accelerated ageing in which early deficits in learning and memory are a salient feature (Miyamoto et al, 1986 ;Takeda et al, , 1997Flood et al, 1995 ;Flood & Morley, 1998). The SAMP8 mouse strain was one of a number of strains produced by an inadvertent cross between AKR mice and an unknown strain or strains, and subsequent inbreeding of the resultant litters (Takeda et al, 1997).…”

Section: Introductionmentioning

confidence: 99%

Scrapie strain-specific interactions with endogenous murine leukaemia virus.

Carp¹,

Meeker²,

Caruso³

et al. 1999

Journal of General Virology

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The finding that a senescence-accelerated mouse (SAMP8) shows early brain ageing, with histopathological changes resembling those seen in scrapie, combined with the discovery of high levels of endogenous murine leukaemia virus (MuLV) in brains of SAMP8 mice prompted us to examine the effect of scrapie infection on MuLV titres in this strain and in one of its progenitors, the AKR strain. Three scrapie strains (ME7, 22L and 139A) that had a comparatively short incubation period in SAMP8 and AKR mice caused an increase in brain MuLV titres that was scrapie strainspecific : in each mouse strain, the greatest effect was with 139A, and the least with ME7. The 22A scrapie strain, which has a long incubation period in SAMP8 mice, did not affect MuLV titres in brains of this mouse strain. Previous analyses of scrapie incubation periods in AKR, SAMP8 and another strain derived from an AKR cross (SAMR1) showed an inverse relationship between brain MuLV titres and scrapie incubation periods. This finding, combined with the effect of scrapie on MuLV titres, suggests an interaction between the scrapie infectious process and MuLV replication.

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“…50 The increase in HCNP in senescence-accelerated mice from three to five months correlated with memory deterioration that is evident in this strain. 51 Additional evidence for a role of HCNP and its precursor in neural development comes from a number of in vitro studies. Proteomic analysis of conditioned medium from cultured adult rat hippocampal progenitor cells (AHPs) revealed that RKIP is secreted by AHPs.…”

Section: Rkip Hcnp and Neural Developmentmentioning

confidence: 99%

Raf Kinase Inhibitory Protein (RKIP): Functional Pleiotropy in the Mammalian Brain

et al. 2014

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In 1984, a cytosolic protein was isolated from bovine brain and coined phosphatidylethanolamine binding protein (PEBP) to describe its phospholipid-binding potential. Its cellular function remained elusive for more than a decade until it was discovered that PEBP had the ability to suppress the Raf1-mitogen activated protein kinase (MAPK) pathway, earning it the new name of Raf1 kinase inhibitory protein (RKIP). This milestone discovery has paved the way for numerous studies that have now extended the reach of RKIP's function to other signaling cascades, within the context of various physiological and pathophysiological systems. This review will summarize our current knowledge of the neurophysiological roles of RKIP in the mammalian brain, including its function in the circadian clock and synaptic plasticity. It will also discuss evidence for an involvement of RKIP and its derived neuropeptide, hippocampal cholinergic neurostimulating peptide (HCNP), in neural development and differentiation. Implications in certain pathologies such as Alzheimer's disease and brain cancer will be highlighted. By chronicling the diverse functions of RKIP in the brain, we hope that this review will serve as a timely resource that ignites future studies on this versatile, multifaceted protein in the nervous system.

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Age-related changes in learning and memory in the senescence-accelerated mouse (SAM)

Cited by 354 publications

References 20 publications

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

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

Scrapie strain-specific interactions with endogenous murine leukaemia virus.

Raf Kinase Inhibitory Protein (RKIP): Functional Pleiotropy in the Mammalian Brain

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