Genetic Rescue of Functional Senescence in Synaptic and Behavioral Plasticity

• DOI: 10.5665/sleep.3988
• Publication Date: 2014-08-29T15:00:52Z
• Authors: Jeffrey M. Donlea; Narendrakumar Ram...; Neal Silverman; Paul J. Shaw
• Keywords: Senescence

Aging has been linked with decreased neural plasticity and memory formation in humans laboratory model species such as the fruit fly, Drosophila melanogaster. Here, we examine plastic responses following social experience a high-throughput method to identify interventions that prevent these impairments.Wild-type transgenic melanogaster.Young (5-day old) or aged (20-day adult female were housed socially enriched (n = 35-40) isolated environments, then assayed for changes sleep structural markers of synaptic terminal growth ventral lateral neurons (LNVs) circadian clock.When young flies are environment, they exhibit elaboration within component circuitry, LNVs, which is followed by increased sleep. Aged flies, however, no longer either changes. Because tight correlation between ensuing increases sleep, use after enrichment marker prolong youthful flies. To validate this strategy, find three independent genetic manipulations delay age-related losses plasticity: (1) elevation dopaminergic signaling, (2) over-expression transcription factor blistered (bs) (3) reduction Imd immune signaling pathway. These findings provide proof-of-principle evidence measuring may highly scalable assay study deficits plasticity.These studies demonstrate provides promising loss begin genes might be manipulated onset functional senescence.