Abstract
Recent demographic trends toward a markedly aging population have led to concerns about more people developing age-associated diseases, in particular senile dementia. Therefore, it is important to clarify the basic mechanism of age-related changes in brain functions such as learning and cognitive deficiency and to develop safe and effective means of prevention and treatment of age-associated diseases. To do so, a useful animal model of age-associated diseases is essential. As one alternative model, Takeda et al. (1,2) developed the senescence-accelerated mouse (SAM) as a murine model of accelerated aging. SAM strains have a shortened life-span and develop early manifestations of senescence, including decreased activity, alopecia, lack of hair glossiness, skin coarseness, periophthalmic lesions, increased lordokyphosis, and systemic senile amyloidosis. The SAMP8 strain of senescence-related prone mice (SAMP) shows an age-related deterioration in learning ability compared with the control strain SAMR1, senescence-resistant mice (SAMR) (3–5). We studied neurochemical changes in the SAMP8 brain compared to the SAMR1 brain during aging (6,7) and the effectiveness of several drugs in preventing age-related changes in the SAMP8 brain. In this chapter, we report the neurochemical and pharmacological findings of a study of SAMP8 and SAMR1 mice and discuss the significance and limitations of SAMP8 in basic studies of the aging mechanism and the screening and development of novel cognitive enhancers.
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