Age-Related Changes in Insulin-like Signaling Lead to Intermediate-Term Memory Impairment in Drosophila

Publication date: 14 February 2017
Source:Cell Reports, Volume 18, Issue 7
Author(s): Kento Tanabe, Motoyuki Itoh, Ayako Tonoki
Insulin and insulin-growth-factor-like signaling (IIS) plays important roles in the regulation of development, growth, metabolic homeostasis, and aging, as well as in brain functions such as learning and memory. The temporal-spatial role of IIS in learning and memory and its effect on age-dependent memory impairment remain unclear. Here, we report that intermediate-term memory (ITM), but not short-term memory (STM), in Drosophila aversive olfactory memory requires transient IIS during adulthood. The expression of Drosophila insulin-like peptide 3 (Dilp3) in insulin-producing cells and insulin receptor function in the fat body are essential for ITM. Although the expression of dilp3 decreases with aging, which is unique among dilp genes, the transient expression of dilp3 in aged flies enhances ITM. These findings indicate that ITM is systemically regulated by communication between insulin-producing cells and fat body and that age-dependent changes in IIS contribute to age-related memory impairment.

Graphical abstract

Teaser

Tanabe et al. find that insulin signaling in the adult Drosophila fat body is required for intermediate-term memory in Drosophila. In addition, they show that age-related changes in insulin signaling contribute to age-related memory impairment.


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