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Spermadine Grants Insight into a Mechanism of Age-Related Memory Dysfunction

Spermadine induces greater autophagy, the collection of cellular housekeeping processes that is associated with many of the methods demonstrated to modestly slow aging in laboratory species. Researchers here use dietary spermadine in flies to investigate one specific mechanism involved in age-related neurodegeneration. When it comes down to it, a great deal of fundamental life science research is a matter of finding or creating two similar situations and then using the small differences between them as a tool to probe the complexities of biology. Here one set of flies has a greater loss of memory, and that can be traced to specific functional changes in the synapses:

Neurons communicate by sending impulses, in the form of secretion of neurotransmitters, across small spaces called synapses. It is these synapses that undergo structural and functional changes during formation and retrieval of memories. Though alterations in synaptic performance are believed to accompany aging, the causal relationship between age-dependent memory impairment and synaptic changes remains largely unknown. Using the fly Drosophila melanogaster as a model, we found that feeding them spermidine - a polyamine compound - suppresses age-induced decline in olfactory memory, providing us with a tool to further decipher mechanisms associated with age-dependent memory impairment.

In this study, we investigated the relationship between synaptic changes and age-dependent memory impairment by studying the olfactory circuitry. We observed an age-related increase in the levels of the synaptic proteins Bruchpilot and Rim-binding protein, which caused an enlargement of the presynaptic active zone - the complex of proteins that mediate neurotransmitter release - and enhanced synaptic transmission. Interestingly, feeding of spermidine was sufficient to abolish these age-associated presynaptic changes, further emphasizing the relationship between presynaptic performance and age-dependent memory impairment. Furthermore, flies engineered to express an excess of the core active zone protein Bruchpilot showed a premature impairment in memory formation in young flies. Based on our data, aging plausibly steers the synapses towards the upper limit of their operational range, limiting synaptic plasticity and contributing to impairment of memory formation.

Link: http://dx.doi.org/10.1371/journal.pbio.1002563

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