Efficacy of Long-Term Feeding of α-Glycerophosphocholine for Aging-Related Phenomena in Old Mice.

α-Glycerophosphocholine (GPC) is a natural source of choline. It reportedly prevents aging-related decline in cognitive function, but the underlying mechanism remains unclear. Although it is understood that aging influences taste sensitivity and energy regulation, whether GPC exerts antiaging effects on such phenomena requires further elucidation. Here, we used old C57BL/6J mice that were fed a GPC-containing diet, to investigate the molecular mechanisms underlying the prevention of a decline in cognitive function associated with aging and examine the beneficial effects of GPC intake on aging-related phenomena, such as taste sensitivity and energy regulation. We confirmed that GPC intake reduces the aging-related decline in the expression levels of genes related to long-term potentiation. Although we did not observe an improvement in aging-related decline in taste sensitivity, there was a notable improvement in the expression levels of ß-oxidation-associated genes in old mice. Our results suggest that the prevention of aging-related decline in cognitive function by GPC intake may be associated with the improvement of gene expression levels of long-term potentiation. Furthermore, GPC intake may positively influence lipid metabolism.

Comparison between the timing of the occurrence of taste sensitivity changes and short-term memory decline due to aging in SAMP1 mice.

Several studies have suggested that cognitive impairment affects taste sensitivity. However, the mechanism behind this is still unclear. In this study, we focused on short-term memory. Using senescence-accelerated mouse prone 1 (SAMP1) mice, we compared whether the effects of aging are observed earlier in taste sensitivity or short-term memory. We used 8-week-old mice as the young group, and 70- and 80-week-old mice as aged groups. Taste sensitivity was evaluated using a 48-hour two-bottle preference test, and short-term memory was evaluated using the Y-maze test. SAMP1 mice showed apparently changes in taste sensitivity at 70-weeks-old. However, the influence of aging on spontaneous alternation behavior, which is indicative of short-term memory alterations, was not observed in 70-week-old mice. At 80-weeks-old, the influence of aging was observed, and spontaneous alternation behavior was significantly decreased. This suggests that age-dependent changes in taste sensitivity occur prior to short-term memory function decline. In addition, there was no significant influence of aging on the mRNA expression of long-term potentiation-related genes in the hippocampus of 80-week-old mice. Therefore, the age-related decline of short-term memory may not affect taste sensitivity.

Analysis of aging-dependent changes in taste sensitivities of the senescence-accelerated mouse SAMP1.

To investigate aging-dependent changes in taste sensitivities, we performed behavioral tests regarding taste sensitivity among young and old SAMP1 mice. In this senescence-accelerated mice model, dramatic changes in taste sensitivities were observed at least 70 weeks old. As for in a brief access test, old mice showed significantly increased taste sensitivity to bitter, salty, sweet, and umami tastes. On the other hand, in a two-bottle test, avoidance of bitter and salty tastes increased, while preference for umami decreased with aging. To investigate the participation of peripheral taste detection systems in the observed changes, we analyzed both the expression of representative taste-related molecules and also turnover rates of taste bud cells. The mRNA expressions of the bitter taste receptor Tas2r105 and its coupled G protein gustducin were significantly decreased with aging. However, the majority of molecules tested did not show significant expression changes. In addition, no significant differences in the turnover rates of taste bud cells were observed between the two age groups. These results suggest that the changes in taste sensitivity of SAMP1 mice due to aging are caused by factors other than the deterioration of taste detection systems in the oral cavity.