Deficits in learning ability and aging of skin in both strains of senescence-accelerated mouse (SAM) P8 and P10 : neuropathological, neurochemical, histological and pharmacological analysis(Chemical & Pharmacological study)

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  • Deficits in learning ability and aging of skin in both strains of senescence accelerated mouse SAM P8 and P1O neuropathological neurochemical histological and pharmacological analysis

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Animal models of age-related deficiencies are required to elucidate the fundamental mechanisms of age-related deficiencies of learning or aging of skin, the establishment of pertinent animal models that have characteristics very similar to those of human dysfunctions is needed to develop prophylactics/therapeutics against age-related disease. The SAM (senescence-accelerated mouse) has been established as a murine model of SAM strains, groups of related-inbred strains including nine strains of accelerated senescence-prone, short-lived mice (SAMP) and three strains of accelerated senescence-resistant, long-lived mice (SAMR). SAMP strain mice show relatively strain-specific age-associated phenotypic pathologies such as shortened life span and early manifestation of senescence. Among SAMP strain mice, SAMP8 and SAMP10 mice show an age-related deterioration in learning ability and skin aging. We review the neuropathological, neurochemical, histological and pharmacological features of SAM strains, particularly those of SAMP8 and SAMP10 strains, and the effects of several drugs on biochemical, behavioral and histological alterations in the SAMP8.

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