Differential aging pattern of cerebral accumulation of radiolabeled glucose and amino acid in the senescence accelerated mouse (SAM), a new model for the study of memory impairment.

Using an accelerated senescence-prone model mouse strain, SAMP8, with spontaneously occurring age-related deficits in learning and memory, cerebral glucose and amino acid accumulation were investigated to study the metabolic abnormalities in relation to age. The findings were compared with those in an accelerated senescence-resistant mouse strain, SAMR1, without deterioration of ability in learning and memory. [14C]-2-Deoxyglucose accumulation in the SAMP8 brain was normal at 1 month of age but decreased from 2-3 months of age onwards. In contrast, tyrosine accumulation was unchanged from 1 to 5 months of age. The impairment of memory in the SAMP8 at 2-3 months of age corresponded with the decrease in [14C]-2-deoxyglucose accumulation, but was not related to Tyr. This animal model may help provide new information on the metabolic changes in aging.