Grading score system: A method for evaluation of the degree of senescence in Senescence Accelerated Mouse (SAM)

Hosokawa, Masanori; Kasai, Rinshi S.; Higuchi, Kenichi; Takeshita, S; Shimizu, Katsuji; Hamamoto, Hiromi; Honma, Atsuko; Irino, Mika; Toda, Keiichi; Matsumura, Akitaka

doi:10.1016/0047-6374(84)90168-4

Cited by 196 publications

(98 citation statements)

References 7 publications

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“…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: 98%

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

confidence: 98%

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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“…All the SAMP strains develop degenerative joint disease at different frequency and severity (Hosokawa et al, 1984). Among the SAMP lines, the SAMP8 strain displays early-onset age-related degenerative changes in TMJ's articular surface, including roughness, fissures, and erosion (Chen et al, 1989).…”

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confidence: 99%

TMJ Degeneration in SAMP8 Mice is Accompanied by Deranged Ihh Signaling

et al. 2014

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The temporomandibular joint (TMJ) functions as a loadbearing diarthrodial joint during mastication, and its continuous use and stress can lead to degeneration over age. Using senescence-accelerated (SAMP8) mice that develop early osteoarthritis-like changes in synovial joints at high frequency, we analyzed possible molecular mechanisms of TMJ degeneration and tested whether and how malocclusion may accelerate it. Condylar articular cartilage in young SAMP8 mice displayed early-onset osteoarthritic changes that included reductions in superficial/chondroprogenitor cell number, proteoglycan/collagen content, and Indian hedgehog (Ihh)-expressing chondrocytes. Following malocclusion induced by tooth milling, the SAMP8 condyles became morphologically defective, displayed even lower proteoglycan levels, and underwent abnormal chondrocyte maturation compared with malocclusion-treated condyles in wild-type mice. Malocclusion also induced faster progression of pathologic changes with increasing age in SAMP8 condyles as indicated by decreased PCNA-positive proliferating chondroprogenitors and increased TUNELpositive apoptotic cells. These changes were accompanied by steeper reductions in Ihh signaling and by expression of matrix metalloproteinase 13 at the chondro-osseous junction in SAMP8 articular cartilage. In sum, we show for the first time that precocious TMJ degeneration in SAMP8 mice is accompanied by-and possibly attributable toaltered Ihh signaling and that occlusal dysfunction accelerates progression toward degenerative TMJ disease in this model.

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“…All of the SAMP1 mice were kept at room temperature (20 ± 1 °C), at a relative humidity of about 50% and with a light-dark cycle of 12 hours; food (CE-2, CLEA Japan, Inc.) and tap water were provided ad libitum. The SAM used in this study was a useful model in that senescence was accelerated after it grew up, and it was assumed to live for 50% of its survival time (297 days on average) 10,11) . In this study, running time (exercise capacity), the oxidative stress regulation system, senescence grading scores and weight were measured at 38 to 39 weeks of age.…”

Section: Methodsmentioning

confidence: 99%

Effect of Ubiquinol on Exercise and the Oxidative Stress Regulation System in SMAP1 Mice

2013

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Abstract. [Purpose] This study examined how exercise capacity and the oxidative stress regulation system are affected by different amounts of consumed ubiquinol (reduced coenzyme Q10, H 2 CoQ10: QH) through experiments on 23 SAMP1 mice.[Methods] The mice were randomly divided into two groups: one consuming a high amount of QH (300 mg/Kg) and the other consuming a low amount of QH (30 mg/Kg). Both groups were made to run up to their limit on a treadmill (TM) before/after consuming QH, and then each running time was measured. For the oxidative stress regulation system, the d-ROM test value (degree of oxidative stress) and BAP test value (anti-oxidant potential) were measured both in a resting state before QH consumption and after running up to the limit, and then the BAP/d-ROM ratio was calculated. The values of plasma QH and plasma ubiquinone (plasma oxidized CoQ10) were also measured, and the reduced ratio was calculated.[Results] Both groups showed a significant extension of running time. Also, a more significant extension was seen in the group consuming a high amount of QH than in the group consuming a low amount. With regard to the oxidative stress regulation system, the group consuming a high amount also showed a significant increase in d-ROM test value, plasma QH value and reduced ratio. [Conclusion] The difference in the amount of consumed ubiquinol led to an extension of running time and an increase in reduced ratio and other values.

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Grading score system: A method for evaluation of the degree of senescence in Senescence Accelerated Mouse (SAM)

Cited by 196 publications

References 7 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

TMJ Degeneration in SAMP8 Mice is Accompanied by Deranged Ihh Signaling

Effect of Ubiquinol on Exercise and the Oxidative Stress Regulation System in SMAP1 Mice

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