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.
Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call
