Spermidine boosts autophagy to protect from synapse aging

Abstract

All animals form memories to adapt their behavior in a context-dependent manner. With increasing age, however, forming new memories becomes less efficient. While synaptic plasticity promotes memory formation, the etiology of age-induced memory formation remained enigmatic. Previous work showed that simple feeding of polyamine spermidine protects from age-induced memory impairment in Drosophila. Most recent work now shows that spermidine operates directly at synapses, allowing for an autophagy-dependent homeostatic regulation of presynaptic specializations. How exactly autophagic regulations intersect with synaptic plasticity should be an interesting subject for future research.

Keywords: Drosophila melanogaster; aging; autophagy; memory impairment; synapse.

Figure 1.

Spermidine operates directly at presynaptic active zone scaffolds (composed of Brp/bruchpilot protein) to allow for an autophagy-dependent homeostatic regulation of these specializations. In effect, spermdine protects learning efficacy from aging-induced decline.